Title of Invention

DIARYL UREA DERIVATIVES

Abstract

The invention relates to the use of diaryl urea derivatives in the treatment of protein kinase dependent diseases or for the manufacture of pharmaceutical compositions for use in the treatment of said diseases, methods of use of diaryl urea derivatives in the treatment of said diseases, pharmaceutical preparations comprising diaryl urea derivatives for the treatment of said diseases, diaryl urea derivatives for use in the treatment of said diseases, novel diaryl urea derivatives, pharmaceutical preparations comprising these novel diaryl urea derivatives, processes for the manufacture of the novel diaryl urea derivatives, the use or methods of use of the novel diaryl urea derivatives as mentioned above, and/or these novel diaryl urea derivatives for use in the treatment of the animal or human body.

Full Text

Diaryi urea ciesvatives useful for the treatment of protein kinase dependent diseases Summary of the Invention The invent-on relates to the use of diaryi urea derivatives in the ireo!mes: of protein kinase dependent diseases or for the manufacture of pharmaceutical compose'ens for use in the treatment of said diseases, methods of use of diaryi urea derivatives in tee treatment of said diseases, shaenaceutical preparations comprising diaryi urea derivative-? for the treatment of said diseases, diaryi urea derivatives for use in the treatment of said diseases, novel diaryi area derivatives, pharmaceutical preparations comprising these novel c'aryl urea derivatives, processes \or the manufacture of ihe novel diaryi urea derivatives, the use or methods of use of the novel diaryi urea derivatives as mentioned above, and/or these novel diaryi urea derivatives for use in the treatment of the animal or human body. Background of the Invention Protein kinases (PKs) are enzymes which catalyze the phosphorylation of specific serine, threonine or tyrosine residues in cellular proteins. These post-translational modifications o\ substrate proteins act as molecular switch regulating cell proliferation, activation and/or differentiation. Aberrant or excessive PK activity has been observed in many disease states including benign and malignant proliferative disorders. In many cases, it has been possible to treat diseases in vitro and in many cases in vivo, such as proliferative disorders, by making use of PK inhibitors. In view of the large number of protein kinase inhibitors and the multitude of proliferative and other PK-related diseases, there is an ever-existing need to provide novel classes of compounds that are useful as PK inhibitors and thus in the treatment of these PTK related diseases. What is required are new classes of pharmaceutical^ advantageous PK inhibiting compounds. General Description of the Invention It has now been found that various compounds of the diaryi urea derivative class show inhibition of a number of protein tyrosine kinases. Among the advantages, a good bioavailability and, especially where substituents at the ring with A and A' in formula ! or I* given below are present, lower accessibility to metabolism are to be mentioned. The compounds of formula I or I*, described below in more detail, especially show inhibition of one or more of the following protein tyrosine kinases: c-Abl, Bcr-Abi, the receptor tyrosine kinases Fit3, VEGF-R or c-Kit, as we!! as combinations of tow or mora of these; in the case c" novel clian/i urea derivatives according to the invention, the compounds are appropriate *or the inhibition of these and'or other protein tyrosine kineses, especially those mentioned above and/or, in addition, the non-receptor tyros'ne kinase Rah and/or for the inhibition :f mutants of these enzymes, especially of Bcr-A::'. 'or example tne G!u255 -> Lysine mutant, in view of these activities, the compounds can be used for the treatment of diseases re eted to esoeciaiiy aberrant or excessive activity o* such types of kinases, especially those mentioned. Detailed Pescription of the Invention The invention especially relates to the use of diary! urea derivatives the; are compounds of the formula I wherein G is either not present, lower alkylene or C3-C5cycloalkylene and Z is a radical of the formula la or G is not present and Z is a radical of the formula lb A is CM, X c: N->0 and A' is X or \4->0} v.-i-h tea proviso that not ;:iorc than one of A arc A' can be N->0: r, is 1 or 2; ; il i .j U, i Ol _ . r is 0 to 5; X is MR i' p \s 0, wherein R is hydrogen o\ an organic mc-ely, or if p is 2 or 3, X is nitrogen which tcnether with (CHXP and the bonds represented in dotted (ircerrepted) lines (including the atoms to which they are bound) forms a rim;. or X is CHK wherein K is lower aikv! or hydrogen and p is zero, with the proviso that the bonds represented in dotted lines, if p is zero, are absent; Yi isO. Sor CH2; Y2 is O, S or XH; with the proviso that (Y1)n-(Y2)n does not include O-O, S-S, NH-O, NH-S or S-0 groups; each of R1( R?, R3 and R5l independently of the others, is hydrogen or an inorganic or organic moiety or any two of them together form a lower alkylene-dioxy bridge bound via the oxygen atoms, and the remaining one of these moieties is hydrogen or an inorganic or organic moiety; and R4 (if present, that is, if r is not zero) is an inorganic or organic moiety; or a tautomer thereof; or a pharmaceutical^ acceptable salt thereof; in the treatment of protein kinase (especially tyrosine protein kinase) dependent diseases or for the manufacture of pharmaceutical compositions for use in the treatment of said diseases, methods of use of diaryl urea derivatives in the treatment of said diseases, pharmaceutical preparations comprising diaryl urea derivatives for the treatment of said diseases, diaryl urea derivatives for use in the treatment of said diseases. The invention further also relates to the use or diaryl urea derivatives as described above, wherein the diaryl urea derivative is a compound of the formula I* and with the further proviso that if one of R1f R2 and R3 is halo, the other two cannot both be hydrogen; R4 is lower alkoxy, especially methoxy, lower alkanoylamino, especially acetylamino, hydroxyphenylamino, especially p-hydroxyphenylamino, amino-lower alkyl-oxyphenyl-amino, especially 4-[(2-aminoethyl)-oxyphenyl]-amino, sulfamoylphenylamino, especially 4- sulfamoylphenylamino, carbamoylphenylamino, especially 4-carbamoylphenylamino, [N- (hydroxy-lower alkyl)-carbamoyI]-phenylamino, especially [N-(2-hydroxyethyl)-carbamoyl]- phenylamino, or halo, especially chloro; and R5 is hydrogen, lower alkyl or halo, especially hydrogen; or a tautomer thereof; or pharmaceutical^ acceptable salts thereof; to pharmaceutical preparations comprising these novel diaryl urea derivatives or pharmaceutical^ acceptable salts thereof, processes for the manufacture of the novel diaryl urea derivatives or pharmaceutical^ acceptable salts thereof, the use or methods of use of the novel diaryl urea derivatives or pharmaceutical^ acceptable salts thereof as mentioned above, and/or these novel diaryl urea derivatives or pharmaceutically acceptable salts thereof for use in the treatment of the animal or human body. The general terms used hereinbefore and hereinafter preferably have, within this disclosure, the following meanings, unless otherwise indicated: The prefix "lower" denotes a radical having 1 up to and including a maximum of 7, especially 1 up to and including a maximum of 4 carbon atoms, the radicals in question being either linear or branched with single or multiple branching. Lower alkyl, for example, is methyl, ethyl, n-propyl, sec-propyl, n-butyl, isobutyl, sec-butyl, tert-butyl, n-pentyl, n-hexyl or n-heptyl. Where the plural form is used for compounds, salts, pharmaceutical preparations, diseases and the like, this is intended to mean also a single compound, salt, or the like. Halo(geno) is preferably iodo, bromo, chloro or fluoro, especially fluoro, chloro or bromo. In view of the close relationship between the diaryl urea derivatives in free form and in the form of their salts, including those salts that can be used as intermediates, for example in the purification or identification of the novel compounds, tautomers or tautomeric mixtures and their salts, any reference hereinbefore and hereinafter to these compounds, especially the compounds of the formula I or I*, is to be understood as referring also to the corresponding tautomers of these compounds, especially of compounds of the formula I or 1*, tautomeric mixtures of these compounds, especially of compounds of the formula I or I*, or salts of any of these, as appropriate and expedient and if not mentioned otherwise. Tautomers can, e.g., be present in cases where amino or hydroxy, each with a least one bound hydrogen, are boundlo carbon atoms that are bound to adjacent atoms by double bonds (e.g. keto-enol or imine-enamine tautoemerism). Preferred tautomers are the pyridin-on-yl or pyrimidin-on-yl forms of compounds wherein R* is hydroxy and the other moieties are defined as for compounds of the formula I or I*, respectively. Where "a compound ..., a tautomer thereof; or a salt thereof or the like is mentioned, this means "a compound ..., a tautomer thereof, or a salt of the compound or the tautomer". Any asymmetric carbon atom may be present in the (R)-, (S)- or (Reconfiguration, preferably in the (R)- or (S)-configuration. Substituents at a ring at atoms with saturated bonds may, if possible, be present in cis- (= Z-) or trans (= E-) form. The compounds may thus be present as mixtures of isomers or preferably as pure isomers, preferably as enantiomer-pure diastereomers or pure enantiomers. Salts are preferably the pharmaceutical^ acceptable salts of the diary! urea derivatives, especially of compounds of the formula I or I* if they are carrying salt-forming groups. Salt-forming groups are groups or radicals having basic or acidic properties. Compounds having at least one basic group or at least one basic radical, for example amino, a secondary amino group not forming a peptide bond or a pyridyl radical, may form acid addition salts, for example with inorganic acids, such as hydrochloric acid, sulfuric acid or a phosphoric acid, or with suitable organic carboxylic or sulfonic acids, for example aliphatic mono- or di-carbo-xylic acids, such as trifluoroacetic acid, acetic acid, propionic acid, glycolic acid, succinic acid, maleic acid, fumaric acid, hydroxymaleic acid, malic acid, tartaric acid, citric acid or oxalic acid, or amino acids such as arginine or lysine, aromatic carboxylic acids, such as benzoic acid, 2-phenoxy-benzoic acid, 2-acetoxy-benzoic acid, salicylic acid, 4-aminosalicylic acid, aromatic-aliphatic carboxylic acids, such as mandelic acid or cinnamic acid, hetero- aromatic carboxylic acids, such as nicotinic acid or isonicotinic acid, aliphatic sulfonic acids, such as methane-, ethane- or 2-hydroxyethanesulfonic acid, or aromatic sulfonic acids, for example benzene-, p-toluene- or naphthaIene-2-sulfonic acid. When several basic groups are present mono- or poly-acid addition salts may be formed. Compounds having acidic groups, a carboxy group or a phenolic hydroxy group, may form metal or ammonium salts, such as alkali metal or alkaline earth metal salts, for example sodium, potassium, magnesium or calcium salts, or ammonium salts with ammonia or suitable organic amines, such as tertiary monoamines, for example triethylamine or tri-(2-hydroxy-ethyl)-amine, or heterocyclic bases, for example /V-ethyl-piperidine or A/t/V-dimethylpiper-azine. Mixtures of salts are possible. Compounds having both acidic and basic groups can form internal salts. For the purposes of isolation or purification, as well as in the case of compounds that are used further as intermediates, it is also possible to use pharmaceutical^ unacceptable salts, e.g. the picrates. Only pharmaceutical acceptable, non-toxic salts may be used for therapeutic purposes, however, and those salts are therefore preferred. An organic moiety R is preferably unsubstituted or substituted alkyl, unsubstituted or substituted alkenyl, unsubstituted or substituted aikynyl, unsubstituted or substituted aryl, unsubstituted or substituted heterocyclyl, unsubstituted or substituted cycloalkyl or unsubstituted or substituted cycloalkenyl; preferred is unsubstituted alkyl. "Substituted", whereever used for a moiety, means that one or more hydrogen atoms in the respective moiety, especially up to 5, more especially up to three, of the hydrogen atoms are replaced independently of each other by the corresponding number of substituents which preferably are independently selected from the group consisting of lower alkyl, for example methyl, ethyl or propyl, halo-lower alkyl, for example trifluoromethyl, C6-C16-aryl, especially phenyl or naphthyl (where C6-C16-aryl, especially phenyl or napthyl, is unsubstituted or substituted by one or more, especially up to three moieties selected from halogen, carboxy, lower alkoxycarbonyl, hydroxy, lower alkoxy, phenyl-Iower alkoxy, lower alkanoyloxy, lower alkanoyl, amino, N-lower alkylamino, N,N-di-lower alkylamino, N-phenyl-lower alkylamino, N,N-bis(phenyl-lower alkyl)-amino, lower alkanoylamino, halo, halo-lower alkyl, e.g. trifluoro- methyl, sulfo, sulfamoyl, carbamoyl, N-loweralkyl-carbamoyl, N-(hydrcxy-!ower aikyl)-carb-amoyl, such as N-(2-hydroxyethyl)-carbarnoyl, cyano, cyano-lower alkyl and nitro), C3-C10-cycloalkyl, especially cyclopropyl or cyclohexyl, hydroxy-C3-C3-cycloalkyl, such as hydroxy-cyclohexyl, heterocyclyl with 5 or 6 ring atoms and 1 to 3 ring heteroatoms selected from 0, N and S, especially piperidinyl, especially piperidin-1-yl, piperazinyl, especially piperazin-1-yl, morpholinyl, especially morphoIin-1-yl, hydroxy, lov/er alkoxy, for example methoxy, halo-lower alkoxy, especially 2,2,2-trifluoroethoxy, phenyl-lower alkoxy, amho-lower alkoxy, such as 2-eminoethoxy; lower alkanoyloxy, hydroxy-lower alkyl, such as hycroxymethyl or 2-hy-droxyethyi, amino, N-lower alkylamino, N,N-di-lower alkylamino, N-phenyl-Iower alkylamino, N,N-bis(phenyl-Iower alkyl)-amino, lower alkanoylamino, especially acetylamino, benzoyl-amino, carbamoyl-lower alkoxy, N-lower alkylcarbamoyl-lower alkoxy or N.N-di-lower alkyl-carbamoyt-lower alkoxy, amidino, N-hydroxy-amidino, guanidino, amino-lower alkyl, such as aminomethyl or 2-aminoethyl, amidino-lower alkyl, such as 2-amidinoethyl, N-hydroxyami-dino-lower alkyl, such as N-hydroxy-amidino-methyl or —2-ethyl, halogen, for example fluoro, chloro, bromo or iodo, carboxy, lower alkoxycarbonyl, phenyl-, naphthyl- or fluorenyl-lower alkoxycarbonyl, such as benzyloxycarbonyl, lower alkanoyl, sulfo, lower alkanesulfonyl, for example methanesulfonyl (CH3-S(0)2-). phosphono (-P(=0)(0H)2), hydroxy-lower alkoxy phosphoryl or di-lower alkoxyphosphoryl, carbamoyl, mono- or di-lower alkylcarbamoyl, mono- or di-(hydroxy-lower alkyl)-carbamoyl, sulfamoyl, mono- or di-lower alkylaminosulfo-nyl, nitro, cyano-lower alkyl, such as cyanomethyl, and cyano. It goes without saying that substitutents are only at positions where they are chemically possible, the person skilled in the art being able to decide (either experimentally or theoretically) without inappropriate effort which substitutions are possible and which are not. For example, amino or hydroxy groups with free hydrogen may be unstable if bound to carbon atoms with unsaturated (e.g. olefinic) bonds. Alkyl preferably has up to 20, more preferably up to 12 carbon atoms and is linear or branched one or more times; preferred is lower alkyl, especially d-C4-alkylf in particular methyl, ethyl or n-propyl. Alkyi is unsubstituted or substituted, preferably by one or more substituents independently selected from those mentioned above under "Substituted". Unsubstituted alkyl, preferably lower alkyl, is especially preferred as an organic moiety R. Among the moieties corresponding to substituted alkyl, hydroxy-lower alkyl, especially 2-hy-droxyethyl, and/or halo-lower alkyl, especially trifluoromethyl or 2,2,2-trifIuoroethyl, are especially preferred. Aikenyl is preferably a moiety with one or more double bonds and preferably has 2 to 20, more preferably up to 12, carbon atoms; it is linear or branched one or more times (as far as possible in view of the number of carbon atoms). Preferred is C2-C7-alkenyl, especially C3-C4-alkenyl, such as allyl or crotyl. Aikenyl can be unsubstituted or substituted, especially by one or more, more especially up to three, of the substituents mentioned above under substituted". Substituents such as amino or hydroxy (with free dissociable hydrogen) preferably are not bound to carbon atoms that participate at a double bond, and also other subtituents that are not sufficiently stable are preferably excluded. Unsubstituted aikenyl, in particular C2-C7-alkenyl, is preferred. Alkynyl is preferably a moiety with one or more triple bonds and preferably has 2 to 20, more preferably up to 12, carbon atoms; it is linear of branched one or more times (as far as possible in view of the number of carbon atoms). Preferred is C2-C7-alkynyl, especially C3-C4-alkynyl, such as ethinyl or propin-2-yl. Alkynyl can be unsubstituted or substituted, especially by one or more, more especially up to three, of the substituents mentioned above under ..substituted". Substituents such as amino or hydroxy (with free dissociable hydrogen) preferably are not bound to carbon atoms that participate at a triple bond, and also other subtituents that are not sufficiently stable are preferably excluded. Unsubstituted alkynyl, in particular C2-C7-alkynylt is preferred. Aryl preferably has a ring system of not more than 16 carbon atoms, is preferably mono-, bi-or trie-cyclic, and is unsubstituted or substituted preferably as defined above under "Substituted". Preferably, aryl is selected from phenyl, naphthyl, indenyl, azulenyl and anthryl, and is preferably in each case unsubstituted or lower alkyl, especially methyl, ethyl or n-propyl, halo (especially fluoro, chloro, bromo or iodo), halo-lower alkyl (especially trifluoromethyl), hydroxy, lower alkoxy (especially methoxy), halo-lower alkoxy (especially 2,2,2-trifIuoroetho-xy), amino-lower alkoxy (especially 2-amino-ethoxy), lower alkyl (especially methyl or ethyl) carbamoyl, N-(hydroxy-lower alkyl)-carbamoyl (especially N-(2-hydroxyethyI)-carbamoyl) and/or sulfamoyl-substituted aryl, especially a corresponding substituted or unsubstituted phenyl. Heterocyclyl is preferably a heterocyclic radical that is unsaturated, saturated or partially saturated in the bonding ring and is preferably a monocyclic or in a broader aspect of the invention bicyclic or tricyclic ring; has 3 to 24, more preferably 4 to 16 ring atoms; wherein at least in the ring bonding to the radical of the molecule of formula I or I* one or more, preferably one to four, especially one or two carbon ring atoms are replaced by a heteroatom selected from the group consisting of nitrogen, oxygen and sulfur, the bonding ring preferably having 4 to 12, especially 5 to 7 ring atoms; heteroaryl being unsubstituted or substituted by one or more, especially 1 to 3, substitutents independently selected from the group consisting of the substituents defined above under "Substituted"; especially being a heteroaryl radical selected from the group consisting of oxiranyi, azirinyl, 1,2-oxathiolanyl, imidazolyl, thienyl, furyl, tetrahydrofuryl, pyranyl, thiopyranyl, thianthrenyl, isobenzofuranyl, benzofuranyl, chromenyl, 2/7-pyrrolyl, pyrrolyl, pyrrolinyl, pyrrolidinyl, imidazolyl, imidazolidinyi, benzimidazolyl, pyrazoiyl, pyrazinyl, pyrazolidinyl, pyranyol, thiazolyl, isothiazolyl, dithiazolyl, oxazolyl, isoxazolyl, pyridyl, pyrazinyl, pyrimidinyl, piperidyl, especially piperidin-1-yl, piperazinyl, especially piperazin-1-yl, pyridazinyl, morpholinyl, especially morpholino, thiomorpholinyl, especially thiomorpholino, indolizinyl, isoindolyl, 3H-indolyl, in-dolyl, benzimidazolyl, cumaryl, indazolyl, triazolyl, tetrazolyi, purinyl, 4H-quinoIizinyl, isoquinolyl, quinolyi, tetrahydroquinolyl, tetrahydroisoquinolyl, decahydroquinolyl, octahydroisoquinolyi, benzofuranyl, dibenzofuranyl, benzothiophenyl, dibenzothiophenyl, phthalazinyl, naphthyridinyl, quinoxalyl, quinazolinyl, quinazolinyl, cinnolinyl, pteridinyl, carbazolyl, p-carbolinyl, phenanthridinyl, acridinyl, perimidinyl, phenanthrolinyl, furazanyl, phenazinyl, phenothiazinyl, phenoxazinyl, chromenyl, isochromanyl and chromanyl, each of these radicals being unsubstituted or substituted by one to two radicals selected from the group consisting of lower alkyl, especially methyl or tert-butyl, lower alkoxy, especially methoxy, and halo, especially bromo orchloro. Unsubstituted heterocyclyl, especially piperidyl, piperazinyl, thiomorpholino or morpholino, is preferred. Cycloalkyl is preferably C3-Ci0-cycloalkyl, especially cyclopropyl, dimethylcyclopropyl, cyclo-butyl, cyclopentyl, cyclohexyl or cydoheptyl, cycloalkyl being unsubstituted or substituted by one or more, especially 1 to 3, substitutents independently selected from the group consisting of the substituents defined above under "Substituted". Cycioalkeny! is preferably C5-C10-cycloalkenyl, especially cyclopentenyl, cyclohexenyl or cycloheptenyl, cycloalkenyl being unsubstituted or substituted by one or more, especially 1 to 3, substitutents independently selected from the group consisting of the substituents defined above under "Substituted". An inorganic moiety is preferably halogen, hydroxy, amino, or nitro. The bonds represented by dotted (interrupted) lines and binding (CH2)-, are present if p is 2 or 3, or absent if p is zero. An organic moiety is preferably unsubstituted or substituted alkyl, unsubstituted or substituted alkenyl, unsubstituted or substituted alkynyl, unsubstituted or substituted unsubstituted or substituted aryl, unsubstituted or substituted heterocyclyl, unsubstituted or substituted cycloalkyl or unsubstituted or substituted cycloalkenyl, unsubstituted or substituted alkoxy, unsubstituted or substituted alkenyloxy, unsubstituted or substituted alkynyloxy, unsubstituted or substituted aryloxy, unsubstituted or substituted heterocyclyloxy, unsubstituted or substituted cycloalkoxy or unsubstituted or substituted cycloalkenyloxy, or unsubstituted or substituted alkylamino, unsubstituted or substituted alkenylamino, unsubstituted or substituted alkynylamino, unsubstituted or substituted arylamino, unsubstituted or substituted heterocyclylamino, unsubstituted or substituted cycloalkylamino or unsubstituted or substituted cycloalkenylamino. An organic moiety is preferably alkyl, especially lower alkyl, such as methyl, ethyl or propyl, halo-lower alkyl, such as trifluoromethyl, lower alkoxy, such as methoxy, halo-lower alkoxy, such as 2,2,2-trifluoroethoxy, halo, such as chloro or bromo, phenyl, phenylamino, hydroxy-phenyl-amino, such as 4-hydroxyphenylamino, amino-lower alkyl-oxyphenylamino, such as [4-(2-aminoethyl)oxy]-phenyI-amino, carbamoylphenyl-amino, such as 4-sulfamoyl-phenyl-amino, [N-(hydroxy-lower alkyl)-carbamoyl]-phenyl-amino, such as {N-[4-(2-hydroxyethyl)-carbamoyl]-phenyl}-amino, 5- or 6-membered saturated heterocyclyl with 1 or 2 heteroatoms selected from the group consisting of N, O and S, especially piperidyl, such as piperidin-1-yl, piperazinyl, such as piperazin-1-yl, morpholinyl, such as morpholino, or further thiomorpholinyl, such as thiomorpholino. A basic organic moiety is a moiety selected from the definition of an organic moiety as given herein and having basic (alkaline) properties. Preferably a basic organic moiety is piperidyl, especially piperidin-1-yl, piperidyl-lower alkyl, especially piperidin-1 -ylrnethyl, lower alkyl-piperazinyl, especially 4-methyl-piperazin-1-yl or 4-ethyl-piperazin-1-yi. or lower alkyl-piperazinyl-lower alkyl, especially 4-methyl-piperazin-1-ylrnethyl or 4-e:hyl-piperazin-1-yimethyl. If any two of R1( R2 and R3 together form a lower alkylene-dioxy bridge bound via the oxygen atoms said bridge is preferably methylendioxy (0-CH2-0) or ethylendicxy (0-CH2-CH2-0) bound via the oxygen atoms to vicinal carbon atoms, and the remaining one of these moieties is hydrogen or an inorganic or organic moiety as described above. The term "treatment of tyrosine protein kinase dependent diseases" refers to the prophylactic or preferably therapeutic (including palliative and/or curing) treatment of said diseases, especially of the diseases mentioned below. Where subsequently the term "USE" is mentioned, this includes any one or more of the following embodiments of the invention, respectively: the use in the treatment of (especially tyrosine) protein kinase dependent diseases, the use for the manufacture of pharmaceutical compositions for use in the treatment of said diseases, methods of use of diaryl urea derivatives in the treatment of said diseases, pharmaceutical preparations comprising diaryl urea derivatives for the treatment of said diseases, and diaryl urea derivatives for use in the treatment of said diseases, as appropriate and expedient, if not stated otherwise. In particular, diseases to be treated and are thus preferred for USE of a compound of formula I or I* are selected from (especially tyrosine) protein kinase dependent ("dependent" meaning also "supported", not only "solely dependent") diseases mentioned below, especially corresponding proliferative diseases, more especially diseases that depend on ras, Abl, VEGF-receptor tyrosine kinase, Flt3, and/or Bcr-Abl activity, especially the diseases mentioned below under these specific tyrosine protein kinases. Other kinases of interest include PDGF receptor, c-KIT or EphB4 receptor. In the novel diaryl urea derivatives of the formula I or I* in the examples, or salts thereof, or the novel compounds of the formula I or I*, the proviso that if X is NH, each of R4, independently of the others, is a substituent not bound to the rest of formula I or I*, respectively, via a -C(=0)-, -C(NR)- or -S(02)- bridge means that the substituents are such that they do not comprise any of these bridges. Preferred are the substituents given above and below as "organic moieties". The diary! urea derivatives, especially the compounds of formula 1 or T, have valuable pharmacological properties and are useful in the treatment of protein kinase dependent diseases, especially of tyrosine protein kinase dependent for example, as drugs to treat proliferative diseases. The efficacy of the compounds cf the invention as inhibitors of c-Abl protein-tyrosine kinase activity can be demonstrated as follows: An in vitro enzyme assay is performed in 96-well plates as a filter binding assay as described by Geissler et al. in Cancer Res. 1992; 52:4492-4498, with the following modifications. The His-tagged kinase domain of c-Abl is cloned and expressed in the bacu!oyirus/Sf9 system as described by Bhat et al. in J.Biol.Chem. 1997; 272:16170-16175. A protein of 37 kD (c-Abl kinase) is purified by a two-step procedure over a Cobalt metal chelate column followed by an anion exchange column with a yield of 1-2 mg/L of Sf9 cells (Bhat et a/., reference cited). The purity of the c-Abl kinase is >90% as judged by SDS-PAGE after Coomassie blue staining. The assay contains (total volume of 30 pL): c-Abl kinase (50 ng), 20 mM Tris-HCI, pH 7.5, 10 mM MgCI2> 10 pM Na3V04, 1 mM DTT and 0.06 pCi/assay [y33 P]-ATP (5 pM ATP) using 30 pg/mL poly-A!a,Glu,Lys,Tyr-6:2:5:1 (Poly-AEKY, Sigma P1152) in the presence of 1 % DMSO. Reactions are terminated by adding 10 pL of 250 mM EDTA and 30 pL of the reaction mixture is transferred onto Immobilon-PVDF membrane (Millipore, Bedford, MA, USA) previously soaked for 5 min with methanol, rinsed with water, then soaked for 5 min with 0.5 % H3PO4 and mounted on vacuum manifold with disconnected vacuum source. After spotting all samples, vacuum is connected and each well rinsed with 200 pL 0.5 % H3PO4. Membranes are removed and washed on a shaker with 0.5 % H3PO4 (4 times) and once with ethanol. Membranes are counted after drying at ambient temperature, mounting in Packard TopCount 96-well frame, and addition of 10 pL/well of Microscint TM (Packard). Using this test system, compounds of the formula I or I* show IC50 values of inhibition in the range of 0.001 to 100 uM, usually between 0.05 and 5 ^M. The inhibition of VEGF-induced receptor autophosphorylation can be confirmed with a further in vitro experiments in ceils such as transfected CHO cells, which permanently express human VEGF-R2 receptor (KDR), are seeded in complete culture medium (with 10% fetal calf serum = FCS) in 6-well cell-culture plates and incubated at 37QC under 5% C02 until they show about 80% confluency. The compounds to be tested are then diluted in culture medium (without FCS, with 0.1% bovine serum albumin) and added to the cells. (Controls comprise medium without test compounds). After two hours of incubation at 37°C, recombinant VEGF is added; the final VEGF concentration is 20 ng/rnl. After a further five minutes incubation at 37°C, the cells are washed twice with ice-cold PBS (phosphate-buffered saline) and immediately lysed in 100 pi lysis buffer per well. The lysates are then centrifuged to remove the cell nuclei, and the protein concentrations of the supernatants are determined using a commercial protein assay (BIORAD). The lysates can then either be immediately used or, if necessary, stored at -20°C. A sandwich ELISA is carried out to measure the VEGF-R2 phosphorylation: a monoclonal antibody to VEGF-R2 (for example Mab 1495.12.14; prepared by H. Towbin, Novartis or comparable monoclonal antibody) is immobilized on black ELISA plates (OptiPlate™ HTRF-96 from Packard). The plates are then washed and the remaining free protein-binding sites are saturated with 3% TopBlock® (Juro, Cat. # TB232010) in phosphate buffered saline with Tween 20® (polyoxyethylen(20)sorbitane monolaurate, ICI/Uniquema) (PBST). The cell lysates (20 pg protein per well) are then incubated in these plates overnight at 4°C together with an antiphosphotyrosine antibody coupled with alkaline phosphatase (PY20:AP from Zymed). The (plates are washed again and the) binding of the antiphosphotyrosine antibody to the captured phosphorylated receptor is then demonstrated using a luminescent AP substrate (CDP-Star, ready to use, with Emerald II; Applied Biosystems). The luminescence is measured in a Packard Top Count Microplate Scintillation Counter. The difference between the signal of the positive control (stimulated with VEGF) and that of the negative control (not stimulated with VEGF) corresponds to VEGF-induced VEGF-R2 phosphorylation (= 100 %). The activity of the tested substances is calculated as percent inhibition of VEGF-induced VEGF-R2 phosphorylation, wherein the concentration of substance that induces half the maximum inhibition is defined as the IC50 (inhibitory dose for 50% inhibition). Compounds of the formula I or I* here show an IC5Q in the range of 0.0003 to 20 jiM, preferably between 0.001 and10 jiM. In analogy, VEGF-R1 inhibition can be shown as follows: The test is conducted using Flt-1 VEGF receptor tyrosine kinase. The detailed procedure is as follows: 30 jJ kinase solution (10 ng of the kinase domain of Flt-1, Shibuya et al., Oncogene 5, 519-24 (1990)) in 20 mM Tris-HCI pH 7.5, 3 mM manganese dichloride (MnCI2), 3 mM magnesium chloride (MgCI2), 10 mM sodium vanadate, 0.25 mg/ml polyethylenglycol (PEG) 20 000, 1 mM dithiothrettol and 3 ^g/ml poly(Glu, Tyr) 4:1 (Sigma, Buchs, Switzerland), 8 jaM [33P]-ATP (0.2 uCi), 1 % dimethyl sulfoxide, and 0 to 100 nM of the compound of formula I or I* to be tested are incubated together for 10 min at room temperature. The reaction is then terminated by the addition of 10 jJ 0.25 M ethyienediamine tetraacetate (EDTA) pH 7. Using a multichannel dispenser (LAB SYSTEMS, USA), an aliquot of 20 yi\ is applied to a PVDF (= polyvinyl difluoride) Immobilon P membrane (Millipore, USA), through a Millipore microtiter filter manifold and connected to a vacuum. Following complete elimination of the liquid, the membrane is washed 4 times successively in a bath containing 0.5 % phosphoric acid (H3PO4) and once with ethanol, incubated for 10 min each while shaking, then mounted in a Hewlett Packard TopCount Manifold and the radioactivity measured after the addition of 10 j.il Microscint® (p-scinitillation counter liquid). IC50 values are determined by linear regression analysis of the percentages of inhibition of each compound in three conditions (as a rule 0.01, 0.1 and 1 (amol). The IC50 values that can be found with compounds of the formula I or I* are in the range of 0.01 to 100 jiM, preferably in the range from 0.01 to 50 jiM. Flt3 kinase inhibition is determined as follows: The baculovirus donor vector pFbacGOl (GIBCO) is used to generate a recombinant baculovirus expressing the amino acid region amino acids 563-993 of the cytoplasmic kinase domain of human Flt-3. The coding sequence for the cytoplasmic domain of Flt-3 is amplified by PCR from human c-DNA libraries (Clontech). The amplified DNA fragments and the pFbacGOl vector are made compatible for ligation by digestion with BamH1 and Hindlll. Ligation of these DNA fragments results in the baculovirus donor plasmid Flt-3(1.1). The production of the viruses, the expression of proteins in Sf9 cells and the purification of the GST-fused proteins are performed as follows: Production of virus: Transfer vector (pFbacG01-Flt-3) containing the Flt-3 kinase domain is transfected into the DHIOBac cell line (GIBCO) and the transfected cells are plated on selective agar plates. Colonies without insertion of the fusion sequence into the viral genome (carried by the bacteria) are blue. Single white colonies are picked and viral DNA (bacmid) is isolated from the bacteria by standard plasmid purification procedures. Sf9 or Sf21 cells (Ameri- can Type Culture Collection) are then transfected in flasks with the viral DNA using Cellfectin reagent. Determination of small scale protein expression in Sf9 cells: Virus containing media is collected from the transfected cell culture and used for infection to increase its titre. Virus containing media obtained after two rounds of infection is used for large-scale protein expression. For large-scale protein expression 100 cm2 round tissue culture plates are seeded with 5 x 107 cells/plate and infected with 1 mL of virus-containing media (apprcx. 5 MOIs). After 3 days the cells are scraped off the plate and centrifuged at 500 rpm for 5 min. Cell pellets from 10-20, 100 cm2 plates, are resuspended in 50 mL of ice-cold lysis buffer (25 mMTris-HCI, pH 7.5, 2mM EDTA, 1% NP-40, 1 mM DTT, 1 mM PMSF). The cells are stirred on ice for 15 min and then centrifuged at 5000 rpms for 20 min. Purification of GST-tagged proteins: The centrifuged cell lysate is loaded onto a 2 mL gluta-thione-sepharose column (Pharmacia) and washed three times with 10 mL of 25 mM Tris-HCI, pH 7.5, 2 mM EDTA, 1 mM DTT, 200 mM NaCI. The GST-tagged protein is then eluted by 10 applications (1 mL each) of 25 mM Tris-HCI, pH 7.5, 10 mM reduced-glutathione, 100 mM NaCI, 1 mM DTT, 10 % Glycerol and stored at -70°C. Measurement of enzyme activity. Tyrosine protein kinase assays with purified GST-Flt-3 are carried out in a final volume of 30 JIL containing 200-1800 ng of enzyme protein (depending on the specific activity), 20 mM Tris-HCI, pH 7.6, 3 mM MnCI2l 3 mM MgCI2, 1 mM DTT, 10 HM Na3V04, 3 ^g/mL poly(Glu.Tyr) 4:1, 1 % DMSO, 8.0 yM ATP and 0.1 \xC\ [y33 P] ATP). The activity is assayed in the presence or absence of inhibitors, by measuring the incorporation of 33P from [y33P] ATP into the poly(Glu,Tyr) substrate. The assay (30 yL) is carried out in 96-well plates at ambient temperature for 20 min under conditions described below and terminated by the addition of 20 i± of 125 mM EDTA. Subsequently, 40 JIL of the reaction mixture is transferred onto Immobilon-PVDF membrane (Millipore, Bedford, MA, USA) previously soaked for 5 min with methanol, rinsed with water, then soaked for 5 min with 0.5 % H3PO4 and mounted on vacuum manifold with disconnected vacuum source. After spotting all samples, vacuum is connected and each well rinsed with 200 jiL 0.5 % H3P04. Membranes are removed and washed 4 x on a shaker with 1.0 % H3PO4, once with ethanol. Membranes are counted after drying at ambient temperature, mounting in Packard TopCount 96-well frame, and addition of 10 jiLVwell of Microscint TM (Packard). IC5o values are calculated by linear regression analysis of the percentage inhibition of each compound in duplicate, at four concentrations (usually 0.01, 0.1, 1 and 10 JIM). One unit of protein kinase activity is defined as 1 nmole of 33P ATP transferred from [y33P] ATP to the substrate protein per minute per mg of protein at 37 °C. The compounds of the formula I or I* here show IC50 values in the range between 0.005 and 20 jiM, preferably between 0.01 and 10 j.iM. Bcr-Abl inhibition can be determined by a capture ELISA as follows: Tne murine myeloid progenitor cell line 32Dcl3 transfected with the p210 Bcr-Abl expression vector pGDp210Bcr/AbI (32D-bcr/abl) is obtained from J Griffin (Bazzoni et alM J. Clin invest. 98, 521-8 (1996); Zhao et al., Blood 90, 4687-9 (1997)). The cells express the fusion bcr-abl protein with a constitutively active abl kinase and proliferate growth factor-independent. The cells are expanded in RPMI 1640 (AMIMED; cat# 1-41F01), 10 % fetal calf serum, 2 mM glutamine (Gibco) ("complete medium"), and a working stock is prepared by freezing aliquots of 2 x 106 cells per vial in freezing medium (95 % fetal calf serum, 5 % dimethylsulfoxide (SIGMA, D-2650). After thawing, the cells are used during maximally 10-12 passages for the experiments. The antibody anti-abl SH3 domain cat. # 06-466 from Upstate Biotechnology is used for the ELISA. For detection of bcr-abl phosphorylation, the anti-phosphotyrosine antibody Ab PY20, labelled with alkaline phosphatase (PY10(AP)) from ZYMED (cat. # 03-7722) is used. As comparison and reference compound, (N-{5-[4-(4-methyl-piperazino-me-thyl)-benzoylamido]-2-methylpheny!}-4-(3-pyridyl)-2-pyrimidine-amine, in the form of the methane sulfonate (monomesylate) salt (STI571) (marketed as Gleevec® or Glivec®, Novartis), is used. A stock solution of 10 mM is prepared in DMSO and stored at -20 °C. For the cellular assays, the stock solution is diluted in complete medium in two steps (1 : 100 and 1 : 10) to yield a starting concentration of 10 ^M followed by preparation of serial threefold dilutions in complete medium. No solubility problems are encountered using this procedure. The test compounds of formula I or I* are treated analogously. For the assay, 200'000 32D-bcr/abl cells in 50 nl are seeded per well in 96 well round bottom tissue culture plates. 50 jal per well of serial threefold dilutions of the test compoun are added to the cells in triplicates. The final concentration of the test compound range e.g. from 5 |xM down to 0.01 jiM. Untreated cells are used as control. The compound is incubated together with the cells for 90 min at 37 °C, 5 % C02, followed by centrifugation of the tissue culture plates at 1300 rpm (Beckman GPR centrifuge) and removal of the supernatants by careful aspiration taking care not to remove any of the pelleted cells. The cell pellets are lysed by addition of 150 yd lysis buffer (50 mM Tris/HCI, pH 7.4, 150 mM sodium chloride, 5 mM EDTA, 1 mM EGTA, 1 % NP-40 (non-ionic detergent, Roche Diagnostics GmbH, Mannheim, Germany), 2 mM sodium ortho-vanadate, 1 mM phenylmethyl sulfonylfluoride, 50 jig/ml aprotinin and 80 jag/ml teupeptin) and either used immediately for the ELISA or stored frozen at -20 °C until usage. The anti-abl SH3 domain antibody is coated at 200 ng in 50 |J PBS per well to black ELISA plates (Packard HTRF-96 black plates; 6005207) overnight at 4 °C. After washing 3x with 200 jd/well PBS containing 0.05 % Tween 20 (PBST) and 0.5 % TopBlock (Juro, Cat. # TB 232010), residual protein binding sites are blocked with 200 |.i!/wei] PBST, 3 % TopBlock for 4 h at room temperature, followed by incubation with 50 jil lysates of untreated or test compound-treated cells (20 jig total protein per well) for 3-4 h at 4 °C. After 3 x washing, 50 ji!/ well PY20(AP) (Zymed) diluted to 0.5 j.ig/ml in blocking buffer is added and incubated overnight (4 !C). For all incubation steps, the plates are covered with plate sealers (Costar, cat. # 3095). Finally, the plates are washed another three times with washing buffer and once with deionized water before addition of 90 jil/well of the AP substrate CPDStar RTU with Emerald II. The plates now sealed with Packard Top Seal™-A plate sealers (cat. # 6005185) are incubated for 45 min at room temperature in the dark and luminescence is quantified by measuring counts per second (CPS) with a Packard Top Count Microplate Scintillation Counter (Top Count). For the final optimized version of the ELISA, 50 JA! of the lysates of the cells grown, treated and lysed in 96 well tissue culture plates, are transferred directyl from these plates to the ELISA plates that are precoated with 50 ng/well of the rabbit poylclonal ant-abl-SH3 domain AB 06-466 from Upstate. The concentration of the anti-phosphotyrosine AB PY20 (AP) can be reduced to 0.2 jag/ml. Washing, blocking and incubation with the luminescent substrate are as above. The quantification is achieved as follows: The difference between the ELISA readout (CPS) obtained for with the lysates of the untreated 32D-bcr/abI cells and the readout for the assay background (all components, but without cell lysate) is calculated and taken as 100 % reflecting the constitutively phosphorylated bcr-abl protein present in these cells. The activity of the compound in the bcr-abl kinase activity is expressed as percent reduction of the bcr-abl phosphorylation. The values for the IC50 are determined from the dose response curves by graphical inter- or extrapolation. The compounds of the formula I or I* here preferably show IC50 values in the range from 20 nM to 200 jaM. In addition to or instead of inhibiting the above-mentioned protein kinases, the compounds of formula I or I* also inhibit other tyrosine protein kinases that are involved in the signal transmission mediated by trophic factors, for example kinases of the src kinase family, such as especially the c-Src kinase, members of the PDGF receptor tyrosine protein kinase family, for example the PDGF receptor (PDGF-R), c-Kit, VEGF-R and/or FGF-R; all of which play a part in growth regulation and transformation in animal, especially mammal cells, including human cells. An appropriate assay is described in Andrejauskas-Buchdunger et al., Cancer Res. 52, 5353-8(1992). The diaryl urea derivatives useful according to the invention, especially compounds of formula I or r, that inhibit the protein kinase activities mentioned, especially tyrosine protein kinases mentioned above and below, can therefore be used in the treatment of protein kinase dependent diseases. Protein kinase dependent diseases are especially proliferative diseases, preferably benign or especially malignant tumours (for example carcinoma of the kidneys, liver, adrenal glands, bladder, breast, stomach, ovaries, colon, rectum, prostate, pancreas, bngs, vagina or thyroid, sarcoma, glioblastomas and numerous tumours of the neck and head, as well as leukemias). They are able to bring about the regression of tumours and to prevent the formation of tumour metastases and the growth of (also micro)-metastases. In addition they can be used in epidermal hyperproliferation (e.g. psoriasis), in prostate hyperplasia, and in the treatment of neoplasias, especially of epithelial character, for example mammary carcinoma. It is also possible to use the compounds of formula I or I* in the treatment of diseases of the immune system insofar as several or, especially, individual tyrosine protein kinases are involved; furthermore, the compounds of formula I or I* can be used also in the treatment of diseases of the central or peripheral nervous system where signal transmission by at least one tyrosine protein kinase, especially selected from those mentioned specifically, is involved. The p21ras oncogene is a major contributor to the development and progression of human solid cancers and is mutated in 30 % of all human cancers. The endogenous GTPase activity, if alleviated in ras mutated cancer cells, mediates constitutive growth signals to downstream effectors such as raf kinase. Inhibiting the raf kinase signalling pathway can therefore be used for inhibiting the effect of active ras. The diaryl urea derivatives useful according to the present invention, especially the compounds of formula I or I*, as ras inhibitors are thus especially appropriate for the therapy of diseases related to ras overexpression or overactivity. Vascular endothelial growth factor receptor-2 (VEGF-R2; KDR) is selectively expressed on the primary vascular endothelium and is essential for normal vascular development. In order to grow beyond minimal size, tumors must generate new vascular supply. Angiogenesis, or the sprouting of new blood vessels, is a central process in the growth of solid tumors. For many cancers, the extent of vascularization of a tumor is a negative prognostic indicator signifying aggressive disease and increased potential for metastasis. Recent efforts to understand the molecular basis of tumor-associated angiogenesis have identified several potential therapeutic targets, including the receptor tyrosine kinases for the angiogenic factor vascular endothelial growth factor (VEGF) (see Zeng et al., J. Biol. Chem. 276(35), 32714-32719 (2001)). The diary! urea derivatives useful according to the present invention, especially the compounds of formula I or I*, as KDR inhibitors are thus especially appropriate for the therapy of diseases related to VEGF receptor tyrosine kinase overexpression. Among these diseases, especially retinopathies, age-related macula degeneration, psoriasis, haemangioblastoma, haemangioma, arteriosclerosis, inflammatory diseases, such as rheumatoid or rheumatic inflammatory diseases, especially arthritis, such as rheumatoid arthritis, or other chronic inflammatory disorders, such as chronic asthma, arterial or post-transplantational atherosclerosis, endometriosis, and especially neoplastic diseases, for example so-called solid tumors (especially cancers of the gastrointestinal tract, the pancreas, breast, stomach, cervix, bladder, kidney, prostate, ovaries, endometrium, lung, brain, melanoma, Kaposi's sarcoma, squamous cell carcinoma of heand and neck, malignant pleural mesotherioma, lymphoma or multiple myeloma) and liquid tumors (e.g. leukemias) are especially important. Flt3 (FMD-like tyrosine kinase) is especially expressed in hematopoietic progenitor cells and in progenitors of the lymphoid and myeloid series. Aberrant expression of the Flt3 gene has been documented in both adult and childhood leukemias including AML (acute myelogenous leukemia), AML with trilineage myelodysplasia (AMUTMDS), ALL (acute lymphoblastic leukemia), CML (chronic myelogenous leukemia) and myelodysplastic syndrome (MDS), which are therefore the preferred diseases to be treated with compounds of the formula I or l\ Activating mutations in Flt3 have been found in approximately 25 to 30 % of patients with AML. Thus there is accumulating evidence for the role of Flt3 in human leukemias, and the diaryl urea derivatives useful according to the invention, especially the compounds of the formula I or l*f as Flt3 inhibitors are especially of use in the therapy of this type of diseases (see Tse et al., Leukemia 15(7), 1001-1010 (2001); Tomoki et al., Cancer Chemother. Pharmacol. 48 (Suppl. 1), S27-S30 (2001); Birkenkamp et al., Leukemia 15(12), 1923-1921 (2001); Kelly et al., Neoplasia 99(1), 310-318 (2002)). In chronic myelogeous leukemia (CML), a reciprocally balanced chromosomal translocation in hematopoietic stem cells (HSCs) produces the BCR-ABL hybrid gene. The latter encodes the oncogenic Bcr-Abl fusion protein. Whereas ABL encodes a tightly regulated protein tyrosine kinase, which plays a fundamental role in regulating cell proliferation, adherence and apoptosis, the BCR-ABL fusion gene encodes as constitutively activated kinase, which transforms HSCs to produce a phenotype exhibiting deregulated clonal proliferation, reduced capacity to adhere to the bone marrow stroma and a reduces apoptotic response to mutagenic stimuli, which enable it to accumulate progressively more malignant transformations. The resulting granulocytes fail to develop into mature lymphocytes and are released into the circulation, leading to a deficiency in the mature cells and increased susceptibility to infection. ATP-competitive inhibitors of Bcr-Abl have been described which prevent the kinase from activating mitogenic and anti-apoptotic pathways (e.g. P-3 kinase and STAT5), leading to the death of the BCR-ABL phenotype cells and thereby providing an effective therapy against CML. The diary! urea derivatives useful according to the present invention, especially the compounds of the formula I or I*, as Bcr-Abl inhibitors are thus especially appropriate for the therapy of diseases related to its overexpression, especially leukemias, such as leukemias, e.g. CML or ALL. Compounds of the formula I or I*, in view of their activity as PDGF receptor inhibitors, are also especially appropriate in the treatment of prolifeative diseases, especially small lung cancer, atherosclerosis, thrombosis, psoriasis, scleroderma or fibrosis. There are also experiments to demonstrate the antitumor activity of compounds of the formula i or I* in vivo: The in vivo antitumor activity is tested, for example, using breast carcinoma cell lines, such as the the human estrogen dependent breast carcinoma MCF-7 (ATCC: HTB22) or ZR-75-1 (ATCC: CRL1500), or the estrogen-independen breast carcinomas MDA-MB468 (ATCC: HTB132) or MDA-MB231 (ATCC: HTB26); colon carcinoma cell lines, such as the colon-carcinoma Colo 205 (ATCC: CCL222); glioblastoma cell lines, such as the glioblastomas U-87MG (ATCC: HTB14) or U-373MG (ATCC: HTB17); lung carcinoma cell lines, such as the "small cell lung carcinomas" NCI-H69 (ATCC: HTB119) or NCI-H209 (ATCC: HTB172), or the lung carcinoma NCI-H596 (ATCC: HTB178); skin tumor cell lines, such as the melanomas Hs294T (ATCC: HTB140) or A375 (ATCC: CRL1619); tumor cell lines from the genitourinry systems, such as the ovarial carcinoma NlH-Ovcar3 (ATCC: HTB161), as well as the prostate carzinomas DU145 (ATCC: HTB81) or PC-3 (ATCC: CRL1435), or the bladder carcinoma T24 (ATCC: HTB4); epithelial carcinomas, such as the epithelial carcinoma KB31; or (especially with regard to leukemias) K562 cells (American Type Culture Collection, Mannassas, VA) or human CFU-G cells (CFU-G stands for granulocyte colony forming unit, and it represents an early but commited granulocyte forming precursor cell that circulates in the blood stream or bone marrow) each of which is transplanted into female or male Balb/c nude mice. Other cell lines include leukemic cell lines such as K-562, SUPB15, MEG01, Ku812F, MOLM-13, BaF3, CEM/0, JURKAT/0 or U87MG. Tumors are obtained after subcutaneous injection of the respective cells (minimum 2 x 10s cells in 100 ml phosphate buffered physiological saline) into the carrier mice (e.g. 4-8 mice per cell line). The resulting tumors are passed serially through at least three subsequent transplantations before treatment is started. Tumor fragments (about 25 mg each) are injected s.c. into the left flank of the animals using a 13-gauge Trocar needle under Forene narcosis (Abbott, Switzerland) for implantation. Mice transplanted with estrogen-dependent tumor are, in addition, supplied with an estrogen pellet (1.0 cm of a tube with a quality appropriate for medical purposes, Dow Chemicals, with 5 mg estradiole, Sigma). The treatment is started routinely (that is at low or intermediate tumor burden), as soon as the tumor has reached an average size of 100 mm3. Tumor growth is determined once, twice or thrice weekly (depending on tumor growth of the cell line) and 24 h after the last treatment by measurement of the perpendicular diameter. In case of tumors, tumor volumes are determined according to the formula L x D x p/6 (see Evans, B.D., Smith, I.E., Shorthouse, A.J. and Millar, J.J., Brit J. Cancer, 45:466-468, 1982). The antitumor activity is expressed as T/C% (average increase of the tumor volume of treated animals divided by the average increase of tumor volume in control animals multiplied by 100). Tumor regression (%) represents the smallest mean tumor volume compared to the mean tumor volume at the beginning of the treatment. Each animal in which the tumor reaches a diameter of more than 1,5 to 2 cm3 is sacrificed. Leukemia burden is assessed by examining both peripheral white blood count and weight of spleen and thymus in animals tumored with leukemia cell lines. An exemplary (though not limiting) schedule for administration of a diaryl urea derivative, especially of formula I or I*, or a salt thereof, is daily administration, with preferably 1 to 3 daily dosages for a longer time, possibly until the disease is cured or, if only palliateive treatment is achieved, for as long as required; alternatively, treatment e.g. for 5 days, and/or admi- nistration at days 1, 4 and 9, with eventual repetition after a certain tine without treatment is possible. Alternatively, treatment several times a day (e.g. 2 to 5 times) or treatment by continuous administration (e.g. infusion), e.g. at the time points indicated in the last sentence, are possible. Generally, administration is orally or parenterally, preferably orally. The test compounds are preferably diluted in water or in sterile 0.9% saline. All human tumor cell lines are obtained from the American Type Culture Collection (ATCC, Rockville, MD, USA) if not indicated otherwise and are cultivated in the suggested media with the corresponding additives (ATCC culture conditions), if not mentioned otherwise. The c-sis- and v-sis- transformed BALB/c 3T3 cells are obtained from Dr. C, Stiles (Dana Farber Cancer Institute, Boston, MA, USA). They are cultured in "Dulbecco's modified Eagle's medium" (DMEM), that is supplemented with 10 % calf serum and Hygromycin B in a concentration of 0.2 mg/ml or G418 in a concentration of 0.5mg/ml. BALB/c AMuLV A.6R.1 cells (ATCC) are kept in DMEM, supplemented with 10% fetal calf serum. The pharmacological activity of a diaryl urea derivative of the formula i or I* may, for example, be demonstrated in a clinical study or in a test procedure as essentially described hereinafter. Suitable clinical studies are, for example, open label non-randomized, dose escalation studies in patients with one of the tumor diseases mentioned above. The beneficial effects on proliferative diseases can be determined directly through the results of these studies or by changes in the study design which are known as such to a person skilled in the art. The efficacy of the treatment can be determined in such studies, e.g., in case of tumors after 18 or 24 weeks by radiologic evaluation of the tumors every 6 weeks, in case of a leukaemia e.g. by determination of the count of aberrant white blood cells, and by staining mononuclear cells and/or by means of determining minimum residual disease (MRD) e.g. by FACS-LPC MRD or PCR. Alternatively, a placebo-controlled, double blind study can be used in order to prove the benefits of the diaryl urea derivatives useful according to the invention, especially the compounds of the formula I or I*, mentioned herein. The diaryl urea derivatives useful according to the invention, especially the compounds of the formula I, preferably the novel compounds of the formula I, can be prepared according to methods that are known in the art, especially whereby (a) for the synthesis of a compound of the formula I wherein X NR if p is 0, or if p is 2 or 3, X is nitrogen which together with (CH2)P and the bonds represented in dotted (interrupted) lines (including the atoms to which they are bound) forms a ring, and G, Z, A, A', Yu Y2, R, Ri, R2, R3, R*. R5. m, n, p and r have the meanings.given under formula I, an amino compound of the formula II wherein X is as just defined and R4| R5, A, A\ Y1f Y2l m, n, p, r and the bonds represented in dotted (interrupted) lines have the meanings given under formula I, is reacted with an isocyanate of the formula III 0=C=N—G—Z (III) wherein G, Z, R1f R2 and R3 are as defined for compounds of the formula I, or (b) for the synthesis of a compound of the formula I wherein m is 0 (and thus Y2 is missing), n is 1, Y1 is O and G, Z, X, R1f R2, R3, R*, R5, A, A\ p and r are as defined for compounds of the formula I, a hydroxy compound of the formula IV wherein G, Z, X, R1( R2, R3, Rs, P and the bonds represented in dotted (interrupted) lines have the meanings given under formula I, is etherified with a halo compound of the formula V wherein R4 and' r have the meanings as defined for a compound of formula ! and Hal is halo, especially chloro, or (c) for the synthesis of a compound of the formula I wherein p is zero, X is CHK, especially CH2, and G, Z, K, Y1( Y2, Ru R2, R3, R*. R5, A, A', m, n and r have the meanings given for a compound of the formula I, a carboxy! compound of the formula VI wherein K is lower alkyl or preferably hydrogen and A, A\ Y1( Y2, R41 R5. m, n and r have the meanings given for compounds of the formula I, or a reactive derivative thereof, is condensed with an amino compound of the formula VII wherein G, Z, R1f R2 and R3 are as defined for compounds of the formula I, or [d) for the synthesis of a compound of the formula I wherein X is NH, p is zero and G, Z, A, A', Y1( Y2l R1, R2, R3, R4, R5, m, n and r have the meanings given under formula I, an isocyanate of the formula VIII wherein R4, A, A', Y1( Y2, m, n, r and R5 are as defined for compounds of the formula I, is reacted with an amino compound of the formula IX wherein G, Z, R1f R2 and R3 are as defined for compounds of the formula I, and, if desired, after reaction (a), (b), (c) or (d) an obtainable compound of formula I is transformed into a different compound of formula I, a salt of an obtainable compound of formula I is transformed into the free compound or a different salt, or an obtainable free compound of formula I is transformed into a salt; and/or an obtainable mixture of isomers of compounds of formula I is separated into the individual isomers; where for all reactions mentioned functional groups in the starting materials that shall not take part in the reaction are, if required, present in protected form by readily removable protecting groups, and any protecting groups are subsequently removed. The following reaction conditions are preferred, respectively: Within the scope of this text, only a readily removable group that is not a constituent of the particular desired end product of formula I is designated a "protecting group", unless the context indicates otherwise. The protection of functional groups by such protecting groups, the protecting groups themselves, and their cleavage reactions are described for example in standard reference works, such as J. F. W. McOmie, "Protective Groups in Organic Chemistry", Plenum Press, London and New York 1973, in T. W. Greene and P. G. M. Wuts, "Protective Groups in Organic Synthesis", Third edition, Wiley, New York 1999, in "The Peptides"; Volume 3 (editors: E. Gross and J. Meienhofer), Academic Press, London and New York 1981, in "Methoden der organischen Chemie" (Methods of Organic Chemistry), Houben Weyl, 4th edition, Volume 15/1, Georg Thieme Verlag, Stuttgart 1974, in H.-D. Jakubke and H. Jeschkeit, "Aminosauren, Peptide, Proteine" (Amino acids, Peptides, Proteins), Verlag Chemie, Weinheim, Deerfield Beach, and Basel 1982, and in Jochen Lehmann, "Chemie der Kohlenhydrate: Monosaccharide und Derivate" {Chemistry of Carbohydrates: Monosaccharides and Derivatives), Georg Thieme Verlag, Stuttgart 1974. A characteristic of protecting groups is that they can be removed readily (i.e. without the occurrence of undesired secondary reactions) for example by solvolysis, reduction, photolysis or alternatively under physiological conditions (e.g. by enzymatic cleavage). A protecting group for an OH group, namely a tri-lower alkylsilyl group, such as tert-butyl-di-methylsilyl, can, for example, be removed in the presence of fluoride anions, e.g. by reaction with an appropriate ammonium fluoride, such as tert-butylammonium fluoride, or preferably with HF in the presence of a nitrogen base, especially pyridine, in an aprotic solvent, especially an ether, such as tetrahydrofurane, a nitrile, such as acetonitrile, or a mixture thereof, at temperatures between 0 and 50 °C, e.g. at room temperature. Reactions (a) and (d) preferably take place in an appropriate solvent, e.g. an ether, such as tetrahydrofurane (other solvents, such as toluene, may also be present, especially in low amounts), preferably at temperatures in the range from 0 to 50 °C, e.g. at room temperature. Reaction (b), that is, the formation of ethers, preferably takes place in the presence of a metal alcoholate, especially an alkali metal alcoholate, such as potassium tert-butylate, in an appropriate solvent, such as N,N'-dimethypropyIeneura or a di-Iower alkyl-lower alkanoyl-amide, such as dimethylformamide, or mixtures thereof, at preferred temperatures between 50 °C and the reflux temperature of the reaction mixture, for example at 100 °C. The ether formation can also take place under the conditions of the Hartwig-Buchwald type etherification reactions (see e.g. Mann et a!., J. Am. Chem. Soc. 121(13), 3224-5 (1999), or Aranyos et al., J. Am. Chem. Soc. 121, 4369-78 (1999)). Reaction (c), that is, the formation of amide bonds, preferably takes place under standard conditions for the formation of peptide bonds (condensation reaction). In a reactive derivative of a compound of the formula I, the carboxyl group is either functionalized as activated ester (reactive form). The reactive carboxyl groups are, however, preferably synthesized in situ (for example making use of reagents customary in peptide chemistry, e.g. for the preparation of 1-hydroxybenzotriazoie, succinimide- or N-hydroxysuccinimide esters, or in situ deriva-tisation with condensing agents, e.g. with carbodiimides, such as dicyclohexylcarbodiimide, with carbonylimidazole, with N-[(dimethylamino)-1H-1f2,3-triazolo[4,5-b]pyridin-1-ylmethy-lene]-N-methylmethanaminiumhexafluorophosphate-N-oxide (HATU); with 2-(1H-benzo-triazol-1-yl)-1 J,3(3-tetramethyluroniumtetrafluoroborat (HBTU), with 2-(pyridon-1-yl)-1,1,3,3-tetrame^.hyluroniumtetrafluoroborate (TPTU); or benzotriazol-l-yl-oxy-tris(dimethylamino)-phosphoniumhexafluorophosphafe (BOP), or similar reagents). The condensation reaction preferably takes place in the presence of a condensing agent, especially HBTU, in an aprotic polar solvent, preferably a N,N-di-(lower alky!)-lower alkanoylamide, such as dimethylform-amide, at preferred temperatures in the range from 0 to 50 °C, e.g. at room temperature. Compounds of formula I can be transformed into different compounds of formula I. Especially, the following transformations are of interest: In compounds of the formula I wherein A and/or A' is N, a N may be oxidised to an N-»0 by oxidation in the presence of a peroxide, especially a peroxybenzoic acid derivative, such as 3-chioroperoxybenzoic acid, in the presence of a base, e.g. an alkali metal carbonate, such as sodium carbonate, and in an appropriate solvent, e.g. a halogenated hydrocarbon, such as chloroform or methylene chloride. In compounds of the formula I where a lower alkoxy, especially methoxy, substituent R* is present, this substituent may be transformed into the corresponding hydroxy substituent R4, for example in an alcohol, such as ethanol, in the presence of an acid, such as HCI, preferably at elevated temperatures, e.g. under reflux, or in the presence of a tri-lower alkylsilane-iodide, especially Me3Si-l, in an appropriate solvent, e.g. a chlorinated hydrocarbon, such as chloroform or methylene chloride, at elevated temperatures, for example at 40 to 60 °C. The corresponding hydroxy group may then, by way of tautomerism transferring the hydrogen to an adjacent carbon atom with a double bond, form an oxo group, thus leading, if only one of A and A' is N, to a pyridin-on-yl moeity, if both are N, to a pyrimidin-on-yl moiety. Salts of compounds of formula I having at least one salt-forming group may be prepared in a manner known perse. For example, salts of compounds of formula I having acid groups may be formed, for example, by treating the compounds with metal compounds, such as alkali metal salts of suitable organic carboxylic acids, e.g. the sodium salt of 2-ethylhexanoic acid, with organic alkali metal or alkaline earth metal compounds, such as the corresponding hydroxides, carbonates or hydrogen carbonates, such as sodium or potassium hydroxide, carbonate or hydrogen carbonate, with corresponding calcium compounds or with ammonia or a suitable organic amine, stoichiometric amounts or only a small excess of the salt-forming agent preferably being used. Acid addition salts of compounds of formula I are obtained in customary manner, e.g. by treating the compounds with an acid or a suitable anion exchange reagent. Internal salts of compounds of formula I containing acid and basic salt-forming groups, e.g. a free carboxy group and a free amino group, may be formed, e.g. by the neutralisation of salts, such as acid addition salts, to the isoelectric point, e.g. with weak bases, or by treatment with ion exchangers. Salts can be converted in customary manner into the free compounds; metal and ammonium salts can be converted, for example, by treatment with suitable acids, and acid addition salts, for example, by treatment with a suitable basic agent. Mixtures of isomers obtainable according to the invention can be separated in a manner known per se into the individual isomers; diastereoisomers can be separated, for example, by partitioning between polyphasic solvent mixtures, recrystallisation and/or chromatographic separation, for example over silica gel or by e.g. medium pressure liquid chromatography over a reversed phase column, and racemates can be separated, for example, by the formation of salts with optically pure salt-forming reagents and separation of the mixture of diastereoisomers so obtainable, for example by means of fractional crystallisation, or by chromatography over optically active column materials. Intermediates and final products can be worked up and/or purified according to standard methods, e.g. using chromatographic methods, distribution methods, (re-)crystallization, and the like. Starting materials Within the following description of the synthesis of starting materials G, Z, X, Y1? Y2, Ri, R2, R3, R4, R5, A, A\ m, n, p and r have the meanings indicated for compounds of the formula I, if not indicated otherwise. The starting materials of the formulae II - IX are known, commerciai'y avaiable and/or can be prepared according to methods known in the art; in particular, :hey can be prepared using processes as described in the Examples. In the subsequent description of some preferred synthesis methods for preferred starting materials, functional groups that shall not take part in the respective reactions can be present in protected form and the protective croups can be removed at appropriate stages; for protecting groups, there introduction and removal, reference is made to the standard textbooks and methods already mentioned above. A compound of the formula II, for example, wherein Yi is 0 and Y2 is absent or CH2( n is 1 and m is 0 or 1, X is NH and p is zero is preferably prepared by reacting a hydroxy compound of the formula X wherein A, A', R4 and r have the meanings indicated for formula I, preferably only one of A and A' is N, the other CH, and the OH is in para-position to the N, is reacted with a compound of the formula XI h 1 /-wherein R5 is as defined for formula I, Z1 is halo, especially bromo or iodo, and Y2 is absent (m = 0) or CH2 (m = 1), in the presence of a base, especially an alkali metal carbonate, such as potassium carbonate, and of CuBr or Cul, if required in a solvent, resulting in a compound of the formula XII, wherein A, A', R4, R5, Y1( Y2) n, m and r have the meaning given under formulae X and XI, which is then reduced with hydogen in the presence of an appropriate catalyst, especially Raney-Co or more preferably Raney-Ni, in an appropriate solvent, e.g. an alcohol, such as methanol, to yield the corresponding amino compound (X is NH, p is zero) of the formula II. Alternatively, for the synthesis of a compound of the formula II wherein all moieties have the meanings given under formulae X, XI and XII, except that in addition X is NR wherein R has the meanings given for compounds of the formula I, a compound of the formula XIII wherein R4 and r have the meanings indicated for formula 1, Z2 is halo, especially chloro, A is N or CH, A' is N and Z2 is preferably in p-position to N as A or A', is reacted with a compound of the formula XIV wherein R has the meanings indicated for formula I, Y2 and m as well as R5 are as defined under formula XI (preferably, Y2 is absent, m = 0), in the presence of an alkali metal alcoholate, such as potassium tert-butylate, in an appropriate solvent, e.g. a N,N-di-lower alkyl-lower alkanoyiamide, such as dimethylformamide, and/or N,N'-dimethylpropy!eneurea, to yield the corresponding compound of the formula II. Still alternatively, a compound of the formula II wherein each of A and A' is nitrogen, X is NH and the remaining moieties are as defined for compounds of the formula II resulting from a compound of the formula XII, can be obtained by reacting a compound of the formula XIII wherein A and A' are N and R*, r and Z2 are as defined under formula XIII, is reacted with a compound of the formula XV wherein Y2, m and R5 have the meanings given for compounds of the formula XIV, in the presence of a base, especially an alkali metal hydroxide, such as sodium hydroxide, in an aqueous solvent, e.g. water in mixture with a ketone, such as acetone, resulting in a compound of the formula XII wherein A is N, A' is N, Y^ is O, n is 1, Y2 is CH2 (m = 1) or absent (m = 0), which is then reduced as described for a compound of the formula XII to the corresponding amino compound of the formula II. Compounds of the formula II wherein X is nitrogen and p is 2 or 3, Y, is O (n = 1) and Y2 is absent (m = 0) or CH2 (m = 1), while A, A', R,, R5 and r have the meanings given under formula I, is preferably- prepared by reacting a compound of the formula XVI wherein D is CH2 or CH=CH and Y2, m and R5 are as just defined, with a compound of the formula XIII as defined above in the presence of an alkali metal alcoholate, such as potassium tert-butylate, in an appropriate solvent, e.g. a N,N-di-tower alkyl-lower alkanoylamide, such as dimethyiformamide, and/or N.N'-dimethylpropyleneurea, to yield the corresponding compound of the formula XVII wherein A, A\ R4, R5, r, Y2f m and D are as just defined. The double bond(s) in the ring with D are then reduced, preferably with an appropriate complex hydride, especially with sodium cyanoborhhydride (NaBH3CN) in an organic acid, especially acetic acid, to the corresponding compound of the formula II. Alternatively, first reduction of the double bond(s) in the ring with D and then the reaction with a compound of the formula XIII can lead to the compound of formula 1L A compound of the formula III or VIII can, for example, be synthesized from the corresponding amine compound (with -NH2 instead of the -N=C=0), e.g. by reaction with phosgene or triphosgene in an appropriate tertiary nitrogen base, such as pyridine. Compounds of the formula IV are known in the art or can be prepared according to methods that are known in the art; for example, compounds of the formula IV in which X is CHK, wherein K is lower alkyl or hydrogen, and p is zero can be obtained by condensation of a compound of the formula XVIII v wherein p and X are as just defined, or a reactive derivative thereof, with a compound of the formula VII as defined above; the reactive derivatives and the reaction conditions correspond to those~mentioned above for the reaction of a compound of the formula VI with a compound of the formula VII. The result is the corresponding compound of the formula IV. Compounds of the formula V, VI and VII are known, can be prepared according to methods that are known in the art or analogous to those described above and/or are commercially available. Other starting materials are either known in the art, can be prepared according to methods that are known in the art, e.g. analogously to the methods described hereinabove or in the examples, and/or are commercially available. Starting materials are also available according to or analogously to methods described in WO 00/42012, WO 00/41698, WO 99/32436 and WO 99/32463. The present invention relates also to novel starting materials and/or intermediates and to processes for their preparation. The starting materials used and the reaction conditions selected are preferably those that result in the compounds described as being preferred. General process conditions The following applies in general to all processes mentioned hereinbefore and hereinafter, while reaction conditions specifically mentioned above or below are preferred: All the above-mentioned process steps can be carried out under reaction conditions that are known QBT se, preferably those mentioned specifically, in the absence or, customarily, in the presence of solvents or diluents, preferably solvents or diluents that are inert towards the reagents used and dissolve them, in the absence or presence of catalysts, condensation or neutralising agents, for example ion exchangers, such as cation exchangers, e.g. in the H+ form, depending on the nature of the reaction and/or of the reactants at reduced, normal or elevated temperature, for example in a temperature range of from about -100°C to about 190°C, preferably from approximately -80°C to approximately 150°C, for example at from -80 to -60°C, at room temperature, at from -20 to 40CC or at reflux temperature, under atmospheric pressure or in a closed vessel, where appropriate under pressure, and/or in an inert atmosphere, for example under an argon or nitrogen atmosphere. At all stages of the reactions, mixtures of isomers that are formed can be separated into the individual isomers, for example diastereoisomers or enantiomers, or into any desired mixtures of isomers, for example racemates or mixtures of diastereoisomers, for example analogously to the methods described under "Additional process steps*. The solvents from which those solvents that are suitable for any particular reaction may be selected include those mentioned specifically or, for example, water, esters, such as lower alkyl-lower alkanoates, for example ethyl acetate, ethers, such as aliphatic ethers, for example diethyl ether, or cyclic ethers, for example tetrahydrofurane or dioxane, liquid aromatic hydrocarbons, such as benzene or toluene, alcohols, such as methanol, ethanol or 1- or 2-propanol, nitriles, such as acetonitrile, halogenated hydrocarbons, such as methylene chloride or chloroform, acid amides, such as dimethylformamide or dimethyl acetamide, bases, such as heterocyclic nitrogen bases, for example pyridine or N-methylpyrrolidin-2-one, carboxylic acid anhydrides, such as lower alkanoic acid anhydrides, for example acetic anhydride, cyclic, linear or branched hydrocarbons, such as cyclohexane, hexane or isopen-tane, or mixtures of those solvents, for example aqueous solutions, unless otherwise indicated in the description of the processes. Such solvent mixtures may also be used in working up, for example by chromatography or partitioning. The compounds, including their salts, may also be obtained in the form of hydrates, or their crystals may, for example, include the solvent used for crystallization. Different crystalline forms may be present. The invention relates also to those forms of the process in which a compound obtainable as intermediate at any stage of the process is used as starting material and the remaining process steps are carried out, or in which a starting material is formed under the reaction conditions or is used in the form of a derivative, for example in protected form or in the form of a salt, or a compound obtainable by the process according to the invention is produced under the process conditions and processed further in situ. In the process of the present invention those starting materials are preferably used which result in new compounds of formula I described at the beginning as being especially valuable. Special preference is given to reaction conditions that are identical or analogous to those mentioned in the Examples. Preferred embodiments according to the invention: In the following preferred embodiments, general expression can be replaced by the cor-responding more specific definitions provided above and below, thus yielding stronger preferred embodiments of the invention. Preferred is the USE of compounds of the formula I or I*, tautomers thereof or pharmaceutical^ acceptable salts thereof, where the tyrosine protein kinase dependent disease to be treated is a proliferative disease depending on any one or more of of the following tyrosine protein kinases: ras, Abl, VEGF receptor tyrosine kinase, Flt3f and/or Bcr-Abl activity. Preferred is further the USE of a compound of the formula I or a tautomer thereof, or pharmaceutical^ acceptable salts thereof, where, in the compound of the formula I G is either not present, lower alkylene, especially methylene or ethylene, or C3- C5cydoalkylene, especially cyclopropylene, and Z is a radical of the formula la, or G is not present and Z is a radical of the formula lb; A is CH or N and A1 is N or N->0; n is 1; m isOor 1; p is 0, 2 or 3; • risOorl; X is NR if p is 0, wherein R is hydrogen or lower alkyl, or if p is 2 or 3, X is nitrogen which together with (CH2)P and the bonds represented in dotted (interrupted) lines (including the atoms to which they are bound) forms a ring, or X is CHK wherein K is hydrogen and p is zero, with the proviso that the bonds represented in dotted lines, if p is zero, are absent; YT isO, SorCH2; Y2 is O; with the proviso that (Y1)n-(Y2)m does not include O-O, or S-0 groups; each of Ru R2 and R3l independently of the others, is hydrogen, lower alkyl, especially methyl, ethyl, n-propyl, isopropyl or tert-butyl, lower alkenyl, especially isopropenyl, hydroxy-lower alkyl, especially hydroxy-propyl, lower alkoxy, especially methoxy, halo, especially chloro or bromo, halo-lower alkyl, especially trifluoromethyl, halo-lower alkoxy, especially trifluoromethoxy or trifluoroethoxy, amino-lower alkyl, especially am-nomethyl, amino-lower alkoxy, especially aminoethoxy, di-loweralkyl-amino, especially diethylamino, hydroxy-lower alkyl-amino, especially hydroxy-propylamino, bis-(Iower alkoxy-lower alkyl)-amino, especially bis-(2-methoxy-ethyl)-amino, di-lower alkyl-amino-lower alkyl, especially dimethylaminomethyl, phenyl, morpholinyl, especially morpholin-4-yl, piperidyl, especially piperidin-1-yl, piperidyl-Iower alkyl, especially piperidin-1-ylmethyl, lower alkyl-piperazinyl, especially 4-methyl-piperazin-1 -yl or 4-ethyl-piperazin-1 -yl, lower alkyl-piperazinyl-lower alkyl, especially 4-methyl-piperazin-1-ylmethyl or 4-ethyl-piperazin-l-ylmethyl, pyridyl, especially pyridin-2-yl, or lower alkyl-imidazolyl, especially 2- or 4-methyl-imidazol-1-yI; if r is 1, R4 is lower alkyl, especially methyl, ethyl or ispropyl, hydroxy, aminocarbonyl, lower alkyl-carbonyl, especially methylcarbonyl, cyclohexyl, halo, especially chloro orfluoro, halo-lower alkyl, especially trifluoromethyl, lower alkoxy, especially methoxy, amino, lower alkyl-amino, especially methylamino, ethylamino, isopropylamino or tert-butylamino, di-lower alkyl-amino, especially dimethylamino, lower alkenyl-amino, especially prop-2-enylamino or but-3-enylamino, lower aikyl-carbonyl-amino, especially methylcarbonylamino, cyano, azido, hydroxy-phenyl-amino, especially 3- or 4-hydroxy-phenyl-amino, mono or tri-lower alkoxy-phenyl-amino, especially methoxy-phenyl-amino or trimethoxy-phenyl-amino, lower alkoxy-halo-phenyl-amino, especially methoxy-fluoro-phenyl-amino, phenyl-Iower alkylamino, especially benzylamino, (mono or di-lower alkoxy)-phenyl-lower alkylamino, especially methoxy-benzylamino or dimethoxy-benzylamino, aminosulfonyl-phenyl-lower alkylamino, especially aminosulfonyl-benzylamino, amino-lower alkoxy-phenyl-amino, especially aminoethoxy-phenyl-amino, lower alkyl-amino-sulfonyl-lower alkyl-phenylamino, especially methylamino-sulfonylmethyl-phenylamino, lower alkyl-piperazinyl-lower alkylamino, especially 4-methylpiperazin-1-yI-propylamino, morpholinyl-Iower alkylamino, especially morpholin-4-yl-propylamino, lower alkyl-piperidyl-amino, especially 1-methyI-piperidin-4-ylamino, tetrazolyl, especially 1 H-tetrazol-5-yl, lower alkyl-tetrazolyl, especially lower alkyl-tetrazol-5-yl such as 1-methyl-1H-tetrazol-5-yl or 2-methyi-2H-tetrazol-5-yl, or (di-lower alkyl)-amino-lower alkyl-tetrazolyl, especially (di-lower alkyl)-amino-lower a I ky I-te trazo l-5-yl such as 2-(3-dimethylaminopropyl)-2H-tetrazol-5-yl; and R5 is most preferably hydrogen, or lower alkyl, especially methyl, or halo, especially chloro. Especially preferred is the USE of a compound of the formula I or a tautomer thereof, or pharmaceutical^ acceptable salts thereof, where, in the compound of the formula I A and A' are both N, n is 1, m is 0, p is 0 or 2, r is 1, X is NH if p is 0. or if p is 2, X is nitrogen which together with (CH2)2 and the bonds represented in dotted (interrupted) lines (including the atoms to which they are bound) forms a ring, YT is O, G is not present, Z is a radical of the formula la, at least one of Ru R2 and R3 is a basic organic moiety, PM is amino or lower alkylamino and R5 is hydrogen. Preferred is further also the USE of a compound of the formula I* or a tautomer thereof, or pharmaceutical^ acceptable salts thereof, where, in the compound of the formula I* A is CH, N or N~>0 and A' is N or N->0, with the proviso that not more than one of A and A' can be N->0; n is 1; m is 0; p isO, 2 or 3; risO, 1 or 2; X is NR if p is 0, wherein R is hydrogen or lower alkyl, or if p is 2 or 3, X is nitrogen which together with (CH2)P and the bonds represented in dotted (interrupted) lines (including the atoms to which they are bound) forms a ring, or X is CH2 and p is zero, with the proviso that the bonds represented in dotted lines, if p is zero, are absent; Yi is O or CH2; each of Rlf R2 and R3 independently of the others, is hydrogen, lower alkyl, halo, especially bromo or chloro, halo-lower alkyl, especially trifluoromethyl, lower alkoxy, especially metho- xy, halo-lower alkoxy, especially 2,2,2-trifIuoroethoxy, phenyl, piperidyl, especially piperidin- 1-yl, piperazinyl, especially piperazin-1-yl, morpholinyl, especially morpholine, thiomorpho- linyl, especially thiomorpholino, or any two of them together form a lower alkylene-dioxy bridge bound via the oxygen atoms, and the remaining one of these moieties is hydrogen or one of the moieties mentioned; if r is not zero, R4 is lower alkyl, especially methyl or ethyl, lower alkoxy, especially methoxy, lower alkanoylamino, especially acetylamino, hydroxyphenylamino, especially p- hydroxyphenylamino, amino-iower alkyl-oxyphenyl-amino, especially 4-[(2-aminoethyl)- oxyphenyl]-amino, sulfamoylphenylamino, especially 4-sulfamoylphenylamino, carbamo- ylphenylamino, especially 4-carbamoyiphenyIamino, [N-(hydroxy-lov/er alkyl)-carbamoyl]-phenylamino, especially [N-(2-hydroxyethyl)-carbamoyl]-phenylamino, halo, especially chloro, or hydroxyl; and R5 is hydrogen, lower alkyl or halo, especially hydrogen. Preferred among the novel compounds of the formula I are those wherein G is either not present, lower alkylene, especially methylene or ethylene, or C3-Cscycloalkylene, especially cyclopropylene, and Z is a radical of the formula la, or G is not present and Z is a radical of the formula lb; A is CH or N and A' is N or N->0; n is 1; m is 0 or 1; pisO, 2 or 3; r is 1; X is NR if p is 0, wherein R is hydrogen or lower alkyl, or if p is 2 or 3, X is nitrogen, which together v/ith (CH2)P and the bonds represented in dotted (interrupted) lines (including the atoms to which they are bound) forms a ring, or X is CHK wherein K is hydrogen and p is zero, with the proviso that the bonds represented in dotted lines, if p is zero, are absent; Yi isO, SorCH2; Y2 is O; with the proviso that (Yi)n-(Y2)m does not include O-O, or S-0 groups; each of Ri, R2 and R3, independently of the others, is hydrogen, lower alkyl, especially methyl, ethyl, n-propyl, isopropyl or tert-butyl, lower alkenyl, especially isopropenyl, hydroxy-lower alkyl, especially hydroxy-propyl, lower alkoxy, especially methoxy, halo, especially chloro or bromo, halo-lower alkyl, especially trifluoromethyl, halo-lower alkoxy, especially trifluoromethoxy or trifluoroethoxy, amino-lower alkyl, especially aminomethyl, amino-lower alkoxy, especially aminoethoxy, di-lower alkyl-amino, especially diethyiamino, hydroxy-lower alkyl-amino, especially hydroxy-propylamino, bis-(lower alkoxy-lower alkyl)-amino, especially bis-(2-methoxy-ethyl)-amino, di-lov/er alkyl-amino-lower alkyl, especially dimethylaminomethyl, phenyl, morpholinyl, especially morpholin-4-yl, piperidyl, especially piperidin-1-yi, piperidyl-lower alkyl, especially piperidin-1 -ylmethyl, lower alkyl-piperazinyl, especially 4-methyl-piperazin-1-yl or 4-ethyl-piperazin-1-yl, lower alkyl-piperazinyl-lower alkyl, especially 4-methyl-piperazin-1-ylmethyl or 4-ethyl-piperazin-1-ylmethyl, pyridyl, especially pyridin-2-yI, or lower alkyl-imidazolyl, especially 2- or 4-methyl-imidszoM-yl, with the proviso that if G is not present and Z is a radical of the formula la, R1( R2 and R3 cannot all be hydrogen and with the further proviso that if one of R«, R2 and R3 is halo, the other two cannot both be hydrogen; R4 is lower alkyl, especially methyl, ethyl or ispropyl, hydroxy, aminocarbonyl, lower aikyl-carbonyl, especially methylcarbonyl, cyclohexyl, halo, especially chloro or fluoro, halo-lower alkyl, especially trifluoromethyl, lower alkoxy, especially methoxy, amino, lower alkyl-amino, especially methylamino, ethylamino, isopropylamino or tert-butyiamlno, di-lower alkyl-amino, especially dimethylamino, lower alkenyl-amino, especially prop-2-enylamino or but-3-enylamino, lower aikyl-carbonyl-amino, especially methylcarbonylamino, cyano, azido, hydroxy-phenyl-amino, especially 3- or4-hydroxy-phenyl-amino, mono or tri-lower alkoxy-phenyl-amino, especially methoxy-phenyl-amino or trimethoxy-phenyl-amino, lower alkoxy-halo-phenyl-amino, especially methoxy-fluoro-phenyl-amino, phenyl-lower alkylamino, especially benzylamino, (mono or di-lower alkoxy)-phenyl-lower alkylamino, especially methoxy-benzylamino or dimethoxy-benzylamino, aminosulfonyl-phenyl-lower alkylamino, especially aminosulfonyl-benzylamino, amino-lower alkoxy-phenyl-amino, especially aminoethoxy-phenyl-amino, lower alkyl-amino-sulfonyl-lower alkyl-phenylamino, especially methylamino-sulfonylmethyl-phenylamino, lower alkyl-piperazinyl-lower alkylamino, especially 4-methylpiperazin-1-yl-propylamino, morpholinyl-lower alkylamino, especially morpholin-4-yl-propylamino, lower alkyl-piperidyl-amino, especially 1-methyl-piperidin~4-ylamino, tetrazolyl, especially 1H-tetrazol-5-yl, lower alkyl-tetrazolyl, especially lower alkyl-tetrazol-5-yl such as 1-methyl-1H-tetrazol-5-yl or 2-methyl-2H-tetrazol-5-yl, or (di-lower alkyl)-amino-lower alkyl-tetrazolyl, especially (di-lower alkyl)-amino-lower alkyl-tetrazoI-5-yl such as 2-(3-dimethylaminopropyl)-2H-tetrazol-5-ylI with the proviso that if X is NH, R* is not aminocarbonyl or lower alkyl-carbonyl and with the further proviso that if n is 1, m is 0, p is 0, r is 1, X is NH, Yi is 0, G is not present and Z is a radical of the formula la, R,, together with the benzene ring containing A and A\ does not form methylpyridinyl, 2-hydroxy-pyridin-4-yI or 1 -H-2-oxo-1,2-dihydropyridin-4-yl; R5 is most preferably hydrogen, or lower alkyl, especially methyl, or halo, especially chloro; or a tautomer thereof; or pharmaceutically acceptable salts thereof. Very preferred among the novel compounds of the formula I are those wherein A and A' are both N, n is 1, m is 0, p is 0 or 2, r is 1, X is NH if p is 0, or if p is 2, X is nitrogen which together with (CH2)2 and the bonds represented in dotted (interrupted) lines (including the atoms to which they are bound) forms a ring, Y^ is O. G is not present, Z is a radical of the formula la, at least one of R1( R2 and R3 is a basic organic moiety, R4 is amino or lower alkylamino and R5 is hydrogen, or a tautonner thereof, or pharmaceutical^ acceptable salts thereof. Preferred among the novel compounds of the formula I* are those wherein A, A\ n, m, p, Y1, Y2, R1, R2, R3 and R4 have the meanings given under formula I* above, and r is 1 to 5, X is NR if p is 0, wherein R is hydrogen or an organic moiety, or if p is 2 or 3, X is nitrogen which together with (CH2)P and the bonds represented in dotted (interrupted) lines (including the atoms to which they are bound) forms a ring, or X is CH2 and p is zero, and, if p is zero, the bonds represented in dotted lines are absent; with the proviso that if X is NH, each of R4, independently of the others, if present, is a moiety as defined under formula I* above but not bound to the rest of formula I* via a -C(=0)-, -C(NR)- or -S(02)- bridge, and the substituents R1t R2 and R3 are selected from the following moieties, whereby positions (0 = ortho, m = meta, p = para) are indicated with regard to the position where the ring is bound to the rest of the molecule in formula I* (via the NH-C(=0)-X-moiety): if only R1 is other than hydrogen: ■ Ri = p-lower alkyl, especially p-methyl, p-ethyl, p-n-propyl; m-halo-lower alkyl, especially m-trifluoromethyi; of phenyl, p-piperidin-1-yl or p-piperazin-1-yl; if both R1 and R2 are other than hydrogen: Ri = m-halo-lower alkyl, especially m-trifluoromethyl, and R2 = p-halo, especially p- bromo; Ri = m-halo-lower alkyl, especially m-trifluoromethyl, and R2 = p-halo-lower alkoxy, especially p-(2,2,2-trifluoroethoxy); Ri = m-halo-lower alkyl, especially m-trifluoromethyl, and R2 = m-lower alkoxy, especially m-methoxy; R1 = m-halo-lower alkyl, especially m-trifluoromethyl, and R2 = p-phenyl; Ri = m-halo-lower alkyl, especially m-trifluoromethyl, and R2 = p-piperidin-1-yl or p- piperazin-1-yl; Ri = m-halo-lower alkyl, especially m-trifluoromethyl, and R2 = p-N-morpholino or p-N- thiomorpholino; Rt = m-Iower alkoxy, especially m-methoxy, and R2 = p-halo, especially p-bromo (less preferred); Rt = m-lower alkoxy, especially m-methoxy, and R2 = p-halo-lower alkoxy, especially p-2,2,2-trifluoroethoxy; Ri = m-lower alkoxy, especially m-methoxy, and R2 = p-phenyl; or Ri = m-lower alkoxy, especially m-methoxy, and R2 = p-piperidin-1-yl or p-piperazin-1- yi; or, if R1( R2 and R3are other than hydrogen: Ri = m-lower alkoxy, especially m-methoxy; R2 = m-lower alkoxy, especially m-methoxy; and R3 = p-lower alkoxy, especially p-methoxy; or Ri = lower alkoxy, especially methoxy, and R2 and R3 together form a lower-alkylene-dioxy, especially -0-CH2-CH2-0-, bridge; and R5 is hydrogen, lower alkyl or halo, especially hydrogen; with the proviso that if n is 1, m is 0, p is 0, r is 1, X is NH and Yt is O, R4, together with the benzene ring containing A and A', does not form methylpyridinyl, 2-hydroxy-pyridin-4-yl or 1-H-2-oxo-1,2-dihydropyridin-4-yl; or a tautomer thereof; or pharmaceutical^ acceptable salts thereof. Further preferred among the novel compounds of the formula I* are those wherein A is CH, N or N-»0 and A' is N or N->0, with the proviso that not more than one of A and A' can be N->0; n is 1; m is 0; p is 0, 2 or 3; r is 1 or 2; X is NR if p is 0, wherein R is hydrogen or lower alkyl, or if p is 2 or 3, X is nitrogen which together with (CH2)P and the bonds represented in dotted (interrupted) lines (including the atoms to which they are bound) forms a ring, or X is CH2 and p is zero, with the proviso that the bonds represented in dotted lines, if p is zero, are absent; Yn is O or CH2; R1( R2 and R3 are selected from the following moieties, whereby positions (o = ortho, m = meta, p = para) are indicated with regard to the position where the ring is bound to the rest of the molecule in formula I* (via the NH-C(=0)-X-moiety): if only Ri is other than hydrogen: Rt = p-lower alkyl, especially p-methyl, p-ethyl, p-n-propyl; m-halo-lower alkyl, especially m-trifluoromethyl; or phenyl, p-piperidin-1-yl or p-piperazin-1-yl; if both Rj and R2 are other than hydrogen: Ri = m-halo-lower alkyl, especially m-trifluoromethyl, and R2 = p-halo, especially p- bromo; Ri = m-halo-lower alkyl, especially m-trifluoromethyl, and R2 = p-halo-lower alkoxy, especially p-(2,2,2-trifiuoroethoxy); Ri = m-halo-lower alkyl, especially m-trifluoromethyl, and R2 = m-lower alkoxy, especially m-methoxy; Ri = m-halo-lower alkyl, especially m-trifluoromethyl, and R2 = p-phenyl; Ri = m-halo-lower alkyl, especially m-trifluoromethyl, and R2 = p-piperidin-1-yl or p- piperazin-1-yl; Ri = m-halo-lower alkyl, especially m-trifluoromethyl, and R2 = p-N-morpholino or p-N- thiomorpholino; Ri = m-lower alkoxy, especially m-methoxy, and R2 = p-halo, especially p-bromo (less preferred); Ri = m-lower alkoxy, especially m-methoxy, and R2 = p-halo-Iower alkoxy, especially p-2,2,2-trifIuoroethoxy; Ri = m-lower alkoxy, especially m-methoxy, and R2 = p-phenyl; or Ri = m-lower alkoxy, especially m-methoxy, and R2 = p-piperidin-1-yl or p-piperazin-1- yi; or, if R1( R2 and R3 are other than hydrogen: Ri = m-lower alkoxy, especially m-methoxy; R2 = m-lower alkoxy, especially m-methoxy; and R3 = p-lower alkoxy, especially p-methoxy; or Ri = lower alkoxy, especially methoxy, and R2 and R3 together form a lower-alkylene-dioxy, especially -0-CH2-CHrO-, bridge; and, if r is not zero, R4 is lower alkoxy, especially methoxy, lower alkanoylamino, especially acetylamino, hydroxyphenylamino, especially p-hydroxyphenylamino, amino-Iower alkyl-oxyphenyl-amino, especially 4-[(2-aminoethyl)-oxyphenyl]-amino, sulfamoylphenylamino, especially 4-sulfamoylphenylamino, carbamoylphenylamino, especially 4- carbamoyiphenylamino, [N-(hydroxy-Iower alkyl)-carbamoyl]-phenyIamino, especially [N-(2- hydroxyethyl)-carbamoyI]-phenylamino, or halo, especially chloro; and R5 is halo, especially chloro, lower alkyl, especially methyl, or preferably hydrogen; or a tautomer thereof; or pharmaceutically acceptable salts thereof. Very preferred is a novel compound of the formula I or I*, as well as their USE, provided in the Examples, or a pharmaceutically acceptable salt thereof. Very preferred is also the method of synthesis for these compounds analogously to the methods described in the Examples. Pharmaceutical Compositions: The invention relates also especially to pharmaceutical compositions comprising a novel compound of the formula I or I*, to the use of a compound of the formula I or I* in the therapeutic (in a broader aspect of the invention also prophylactic) treatment or a method of treatment of a (especially tyrosin) protein kinase dependent disease, especially the preferred diseases mentioned above, to the compounds of formula I or I* for said use and to the preparation of pharmaceutical preparations, especially for said uses. The pharmacologically acceptable compounds of the present invention may be used, for example, for the preparation of pharmaceutical compositions that comprise a pharmaceutically effective amount of a compound of the formula I or l*f or a pharmaceutically acceptable salt thereof, as active ingredient together or in admixture with a significant amount of one or more inorganic or organic, solid or liquid, pharmaceutically acceptable carriers. The invention relates also to a pharmaceutical composition that is suitable for administration to a warm-blooded animal, especially a human (or to cells or cell lines derived from a warmblooded animal, especially a human, e.g. lymphocytes), for the treatment or, in a broader aspect of the invention, prevention of (= prophylaxis against) a disease that responds to inhibition of tyrosin protein kinase activity, especially one of the diseases mentioned above as being preferred for USE of a compound of formula I or I*, comprising an amount of a novel compound of formula I or I*, or a pharmaceutically acceptable salt thereof, which is effective for said inhibition, together with at least one pharmaceutically acceptable carrier. The pharmaceutical compositions according to the inyention are those for enteral, such as nasal, rectal or oral, or parenteral, such as intramuscular or intravenous, administration to warm-blooded animals (especially a human), that comprise an effective dose of the pharmacologically active ingredient, alone or together with a significant amount of a pharmaceutical^ acceptable carrier. The dose of the active ingredient depends on the species of warmblooded animal, the body weight, the age.and the individual condition, individual pharmacokinetic data, the disease to be treated and the mode of administration. The invention relates also to a method of treatment for a disease that responds to inhibition of an (especially tyrosine) protein kinase, especially one of the diseases mentioned above as being preferred for USE of a compound of formula I or I*; which comprises administering an (against the mentioned disease) prophylactically or especially therapeutically effective amount of a compound of formula I or I* according to the invention, especially to a warmblooded animal, for example a human, that, on account of one of the mentioned diseases, requires such treatment. The dose of a compound of the formula I or I*, or a pharmaceutically acceeptable salt thereof to be administered to warm-blooded animals, for example humans of approximately 70 kg body weight, is preferably from approximately 3mg to approximately 30 g, more preferably from approximately 10 mg to approximately 1.5 g, most preferably from about 100 mg to about 1000 mg per person per day, divided preferably into 1 to 3 single doses which may, for example, be of the same size. Usually, children receive half of the adult dose. The pharmaceutical compositions comprise from approximately 1 % to approximately 95%, preferably from approximately 20 % to approximately 90%, active ingredient. Pharmaceutical compositions according to the invention may be, for example, in unit dose form, such as in the form of ampoules, vials, suppositories, dragees, tablets or capsules. The pharmaceutical compositions of the present invention are prepared in a manner known perse, for example by means of conventional dissolving, lyophilising, mixing, granulating or confectioning processes. Solutions of the active ingredient, and also suspensions, and especially isotonic aqueous solutions or suspensions, are one preferred form used, it being possible, for example in the case of lyophilised compositions that comprise the active ingredient alone or together with a carrier, for example mannitol, for such solutions or suspensions to be produced prior to use. The pharmaceutical compositions may be sterilised and/or may comprise excipients, for example preservatives, stabilisers, wetting and/or emulsifying agents, solubilisers, salts for regulating the osmotic pressure and/or buffers, and are prepared in a manner known per se, for example by means of conventional dissolving or lyophilising processes. The said solutions or suspensions may comprise viscosity-increasing substances, such as sodium car-boxymethylcellulose, carboxymethylcellulose, dextran, polyvinylpyrrolidone or gelatin. Suspensions in oil comprise as the oil component the vegetable, synthetic or semi-synthetic oils customary for injection purposes. There may be mentioned as such especially liquid fatty acid esters that contain as the acid component a long-chained fatty acid having from 8 to 22, especially from 12 to 22, carbon atoms, for example lauric acid, tridecylic acid, myristic acid, pentadecylic acid, palmitic acid, margaric acid, stearic acid, arachidic acid, behenic acid or corresponding unsaturated acids, for example oleic acid, elaidic acid, erucic acid, brasidic acid or linoleic acid, if desired with the addition of antioxidants, for example vitamin E, p-ca-rotene or 3,5-di-tert-butyl-4-hydroxytoluene. The alcohol component of those fatty acid esters has a maximum of 6 carbon atoms and is a mono- or poly-hydroxy, for example a mono-, di- or tri-hydroxy, alcohol, for example methanol, ethanol, propanol, butanol or pentanol or the isomers thereof, but especially glycol and glycerol. The following examples of fatty acid esters are therefore to be mentioned; ethyl oleate, isopropyl myristate, isopropyl palmitate, "Labrafil M 2375" (polyoxyethylene glycerol trioleate, Gattefosse, Paris), "Miglyoi 812" (triglyceride of saturated fatty acids with a chain length of C8 to C12, Huls AG, Germany), but especially vegetable oils, such as cottonseed oil, almond oil, olive oil, castor oil, sesame oil, soybean oil and more especially groundnut oil. Injection compositions are prepared in customary manner under sterile conditions; the same applies also to introducing the compositions into ampoules or vials and sealing the containers. Pharmaceutical compositions for oral administration can be obtained by combining the active ingredient with solid carriers, if desired granulating a resulting mixture, and processing the mixture, if desired or necessary, after the addition of appropriate excipients, into tablets, dragee cores or capsules. It is also possible for them to be incorporated into plastics carriers that allow the active ingredients to diffuse or be released in measured amounts. Suitable carriers are especially fillers, such as sugars, for example lactose, saccharose, mannitol or sorbitol, cellulose preparations and/or calcium phosphates, for example trical-cium phosphate or calcium hydrogen phosphate, and binders, such as starch pastes using for example corn, wheat, rice or potato starch, gelatin, tragacanth, methylcellulose, hydro-xypropylmethylcellulose, sodium carboxymethylceilulose and/or polyvinylpyrrolidone, and/or, if desired, disintegrators, such as the above-mentioned starches, and/or carboxymethyl starch, crosslinked polyvinylpyrrolidone, agar, alginic acid or a salt thereof, such as sodium alginate. Excipients are especially flow conditioners and lubricants, for example silicic acid, talc, stearic acid or salts thereof, such as magnesium or calcium stearate, and/or polyethylene glycol. Dragee cores are provided with suitable, optionally enteric, coatings, there being used, inter alia, concentrated sugar solutions which may comprise gum arabic, talc, polyvinylpyrrolidone, polyethylene glycol and/or titanium dioxide, or coating solutions in suitable organic solvents, or, for the preparation of enteric coatings, solutions of suitable cellulose preparations, such as ethylcellulose phthalate or hydroxypropylmethylceliulose phthaiate. Capsules are dry-filled capsules made of gelatin and soft sealed capsules made of gelatin and a plasticiser, such as glycerol or sorbitol. The dry-filled capsules may comprise the active ingredient in the form of granules, for example with fillers, such as lactose, binders, such as starches, and/or glidants, such as talc or magnesium stearate, and if desired with stabilisers. In soft capsules the active ingredient is preferably dissolved or suspended in suitable oily excipients, such as fatty oils, paraffin oil or liquid polyethylene glycols, it being possible also for stabilisers and/or antibacterial agents to be added. Dyes or pigments may be added to the tablets ,or dragee coatings or the capsule casings, for example for identification purposes or to indicate different doses of active ingredient. A compound of the formula I or I* may also be used to advantage in combination with other antiproliferative agents. Such antiproliferative agents include, but are not limited to aromatase inhibitors, antiestrogens, topoisomerase I inhibitors, topoisomerase II inhibitors, microtubule active agents, alkylating agents, histone deacetylase inhibitors, farnesyl transferase inhibitors, COX-2 inhibitors, MMP inhibitors, mTOR inhibitors, antineoplastic antimetabolites, platin compounds, compounds decreasing the protein kinase activity and further anti-angiogenic compounds, gonadorelin agonists, anti-androgens, bengamides, bisphosphonates, antiproliferative antibodies and temozolomide (TEMODAL®). The term "aromatase inhibitors" as used herein relates to compounds which inhibit the estrogen production, i.e. the conversion of the substrates androstenedione and testosterone to estrone and estradiol, respectively. The term includes, but is not limited to steroids, especially exemestane and formestane and, in particular, non-steroids, especially aminoglutethimide, vorozole, fadrozole, anastrozole and, very especially, letrozole. Exemestane can be administered, e.g., in the form as it is marketed, e.g. under the trademark AROMASIN™. Formestane can be administered, e.g., in the form as it is marketed, e.g. under the trademark LENTARON™. Fadrozole can be administered, e.g., in the form as it is marketed, e.g. under the trademark AFEMA™. Anastrozole can be administered, e.g., in the form as it is marketed, e.g. under the trademark ARIMIDEX™. Letrozole can be administered, e.g., in the form as it is marketed, e.g. under the trademark FEMARA™ or FEMAR™. Aminoglutethimide can be administered, e.g., in the form as it is marketed, e.g. under the trademark ORIMETEN™. A combination of the invention comprising an antineoplastic agent which is an aromatase inhibitor is particularly useful for the treatment of hormone receptor positive breast tumors. The term "antiestrogens" as used herein relates to compounds which antagonize the effect of estrogens at the estrogen receptor level. The term includes, but is not limited to tamoxifen, fulvestrant, raloxifene and raloxifene hydrochloride. Tamoxifen can be administered, e.g., in the form as it is marketed, e.g. under the trademark NOLVADEX™. Raloxifene hydrochloride can be administered, e.g., in the form as it is marketed, e.g. under the trademark EVISTA™. Fulvestrant can be formulated as disclosed in US 4,659,516 or it can be administered, e.g., in the form as it is marketed, e.g. under the trademark FASLODEX™. The term "topoisomerase I inhibitors" as used herein includes, but is not limited to topotecan, irinotecan, 9-nitrocamptothecin and the macromolecular camptothecin conjugate PNU-166148 (compound A1 in WO99/17804). Irinotecan can be administered, e.g., in the form as it is marketed, e.g. under the trademark CAMPTOSAR™. Topotecan can be administered, e.g., in the form as it is marketed, e.g. under the trademark HYCAMTIN™. The term "topoisomerase II inhibitors" as used herein includes, but is not limited to the antracyclines doxorubicin (including liposomal formulation, e.g. CAELYX™), epirubicin, idarubicin and nemorubicin, the anthraquinones mitoxantrone and losoxantrone, and the podophiHotoxines etoposide and teniposide. Etoposide can be administered, e.g., in the form as it is marketed, e.g. under the trademark ETOPOPHOS™. Teniposide can be administered, e.g., in the form as it is marketed, e.g. under the trademark VM 26-BRISTOL ™. Doxorubicin can be administered, e.g., in the form as it is marketed, e.g. under the trademark ADRIBU\STIN™. Epirubicin can be administered, e.g., in the form as it is marketed, e.g. under the trademark FARMORUBICIN™. Idarubicin can be administered, e.g., in the form as it is marketed, e.g. under the trademark ZAVEDOS™. Mitoxantrone can be administered, e.g., in the form as it is marketed, e.g. under the trademark NOVANTRON™. The term "microtubule active agents" relates to microtubule stabilizing and microtubule destabilizing agents including, but not limited to the taxanes paclitaxel and docetaxel, the vinca alkaloids, e.g., vinblastine, especially vinblastine sulfate, vincristine especially vincristine sulfate, and vinorelbine, discodermolide and epothilones, such as epothilone B and D. Docetaxel can be administered, e.g., in the form as it is marketed, e.g. under the trademark TAXOTERE™. Vinblastine sulfate can be administered, e.g., in the form as it is marketed, e.g. under the trademark VINBLASTIN R.P.™. Vincristine sulfate can be administered, e.g., in the form as it is marketed, e.g. under the trademark FARMISTIN™. Discodermolide can be obtained, e.g., as disclosed in US 5,010,099. The term "alkylating agents" as used herein includes, but is not limited to cyclophosphamide, ifosfamide and melphalan. Cyclophosphamide can be administered, e.g., in the form as it is marketed, e.g. under the trademark CYCLOSTIN™. Ifosfamide can be administered, e.g., in the form as it is marketed, e.g. under the trademark HOLOXAN™. The term "histone deacetylase inhibitors" relates to compounds which inhibit the histone deacetylase and which possess antiproliferative activity. The term "farnesyl transferase inhibitors" relates to compounds which inhibit the farnesyl transferase and which possess antiproliferative activity. The term "COX-2 inhibitors" relates to compounds which inhibit the cyclooxygenase type 2 enyzme (COX-2) and which possess antiproliferative activity such as celecoxib (Celebrex©), rofecoxib (Vioxx®) and lumiracoxib (COX189), The term "MMP inhibitors" relates to compounds which inhibit the matrix metalloproteinase (MMP) and which possess antiproliferative activity. The term "mTOR inhibitors" relates to compounds which inhibit the mammalian target of rapamycin (mTOR) and which possess antiproliferative activity such as sirolimus (Rapamune®), everolimus (Certican™), CCI-779 and ABT578. The term "antineoplastic antimetabolites" includes, but is not limited to 5-fIuorouracil, tegafur, capecitabine, cladribine, cytarabine, fiudarabine phosphate, fluorouridine, gemcitabine, 6-mercaptopurine, hydroxyurea, methotrexate, edatrexate and salts of such compounds, and furthermore ZD 1694 (RALTITREXED™), LY231514 (ALIMTA™), LY264618 (LOMOTREXOL™) and OGT719. The term "platin compounds" as used herein includes, but is not limited to carboplatin, cis-platin and oxaliplatin. Carboplatin can be administered, e.g., in the form as it is marketed, e.g. under the trademark CARBOPLAT™. Oxaliplatin can be administered, e.g., in the form as it is marketed, e.g. under the trademark ELOXATIN™. The term "compounds decreasing the protein kinase activity and further anti-angiogenic compounds" as used herein includes, but is not limited to compounds which decrease the activity of e.g. the Vascular Endothelial Growth Factor (VEGF), the Epidermal Growth Factor (EGF), c-Srcf protein kinase C, the Platelet-derived Growth Factor (PDGF), Bcr-Abl, c-Kit, Flt-3, the Insulin-like Growth Factor I Receptor (IGF-IR) and the Cyclin-dependent kinases (CDKs), and anti-angiogenic compounds having another mechanism of action than decreasing the protein kinase activity. Compounds which decrease the activity of VEGF are especially compounds which inhibit the VEGF receptor, especially the tyrosine kinase activity of the VEGF receptor, and compounds binding to VEGF, and are in particular those compounds, proteins and monoclonal antibodies generically and specifically disclosed in WO 98/35958 (describing compounds of formula I), WO 00/09495, WO 00/27820, WO 00/59509, WO 98/11223, WO 00/27819, WO 01/55114, WO 01/58899 and EP 0 769 947; those as described by M. Prewett et al in Cancer Research 59 (1999) 5209-5218, by F. Yuan et al in Proc. Natl. Acad. Sci. USA, vol. 93, pp. 14765-14770, December 1996, by Z. Zhu et al in Cancer Res. 58, 1998, 3209-3214, and by J. Mordenti et al in Toxicologic Pathology, vol. 27, no. 1, pp 14-21, 1999; in WO 00/37502 and WO 94/10202; Angiostatin™, described by M. S. O'Reilly et al, Cell 79, 1994, 315-328; and Endostatin™, described by M. S. O'Reilly et al, Cell 88, 1997, 277-285; compounds which decrease the activity of EGF are especially compounds which inhibit the EGF receptor, especially the tyrosine kinase activity of the EGF receptor, and compounds binding to EGF, and are in particular those compounds generically and specifically disclosed in WO 97/02266 (describing compounds of formula IV), EP 0 564 409, WO 99/03854, EP 0520722, EP 0 566 226, EP 0 787 722, EP 0 837 063, WO 98/10767, WO 97/30034, WO 97/49688, WO 97/38983 and, especially, WO 96/33980; compounds which decrease the activity of c-Src include, but are not limited to, compounds inhibiting the c-Src protein tyrosine kinase activity as defined below and to SH2 interaction inhibitors such as those disclosed in WO97/07131 and WO97/08193; compounds inhibiting the c-Src protein tyrosine kinase activity include, but are not limited to, compounds belonging to the structure classes of pyrrolopyrimidines, especially pyrrolo[2,3-djpyrimidines, purines, pyrazopyrimidines, especially pyrazo[3,4-d]pyrimidines, pyrazopyrimidines, especially pyrazo[3,4-d]pyrimidines and pyridopyrimidines, especially pyrido[2,3-d]pyrimidines. Preferably, the term relates to those compounds disclosed in WO 96/10028, WO 97/28161, W097/32879 and WO97/49706; compounds which decreases the activity of the protein kinase C are especially those staurosporine derivatives disclosed in EP 0 296 110 (pharmaceutical preparation described in WO 00/48571) which compounds are protein kinase C inhibitors; further specific compounds that decrease protein kinase activity and which may also be used in combination with the compounds of the present invention are Imatinib (GleevecO/Glivec®), PKC412, Iressa™ (ZD1839), PKI166, PTK787, ZD6474, GW2016, CHIR-200131, CEP-7055/CEP-5214, CP-547632, KRN-633 and SU5416; anti-angiogenic compounds having another mechanism of action than decreasing the protein kinase activity include, but are not limited to e.g. thalidomide (THALOMID), ceiecoxib (Celebrex) and ZD6126. The term "gonadorelin agonist" as used herein includes, but is not limited to abareiix, goserelin and goserelin acetate. Goserelin is disclosed in US 4,100,274 and can be administered, e.g., in the form as it is marketed, e.g. under the trademark ZOLADEX™. Abareiix can be formulated, e.g. as disclosed in US 5,843,901. The term "anti-androgens" as used herein includes, but is not limited to bicalutamide (CASODEX™), which can be formulated, e.g. as disclosed in US 4,636,505. The term "bengamides" relates to bengamides and derivatives thereof having aniproliferative properties. The term "bisphosphonates" as used herein includes, but is not limited to etridonic acid, dodronic acid, tiludronic acid, pamidronic acid, aiendronic acid, ibandronic acid, risedronic acid and zoledronic acid. "Etridonic acid" can be administered, e.g., in the form as it is marketed, e.g. under the trademark DIDRONEL™. "Clodronic acid" can be administered, e.g., in the form as it is marketed, e.g. under the trademark BONEFOS™. "Tiludronic acid" can be administered, e.g., in the form as it is marketed, e.g. under the trademark SKELID™. "Pamidronic acid" can be administered, e.g., in the form as it is marketed, e.g. under the trademark AREDIA™. "Aiendronic acid" can be administered, e.g., in the form as it is marketed, e.g. under the trademark FOSAMAX™. "Ibandronic acid" can be administered, e.g., in the form as it is marketed, e.g. under the trademark BONDRANAT™. "Risedronic acid" can be administered, e.g., in the form as it is marketed, e.g. under the trademark ACTONEL™. "Zoledronic acid" can be administered, e.g., in the form as it is marketed, e.g. under the trademark ZOMETA™. The term "antiproliferative antibodies" as used herein includes, but is not limited to trastuzumab (Herceptin™), Trastuzumab-DM1, eriotinib (Tarceva™), bevacizumab (Avastin ™), rituximab (Rituxan®), PR064553 (anti-CD40) and 2C4 Antibody. For the treatment of acute myeloid leukemia (AML), compounds of formula I or I* can be used in combination with standard leukemia therapies, especially in combination with therapies used for the treatment of AML. In particular, compounds of formula I or I* can be administered in combination with e.g. famesyltransferase inhibitors and/or other drugs useful for the treatment of AML, such as Daunorubicin, Adriamycin, Ara-C, VP-16, Teniposide, Mitoxantrone, Idarubicin, Carboplatinum and PKC412. The structure of the active agents identified by code nos., generic or trade names may be taken from the actual edition of the standard compendium "The Merck Index" or from databases, e.g. Patents International (e.g. IMS World Publications). The above-mentioned compounds, which can be used in combination with a compound of the formula I or I*, can be prepared and administered as described in the art such as in the documents cited above. Examples The following Examples serve to illustrate the invention without limiting the scope thereof. Abbreviations * • abs. absolute AcOEt ethyl acetate AcOH acetic acid Anal. elemental analysis (for indicated atoms, difference between calculated measured value brine saturated solution of NaCI in water cat. catalyst cone. concentrated d day(s) decomp. decomposition DIBAH diisobutyi-aluminium-hydride DIEA diisopropyl-ethyl-amine DMF dimethyl formamide DMPU 1,3-dimethyl-3,4,5,6-tetrahydro-2-(1 H)pyrimidinone DMEU 1,3-dimethyl-2-imidazolidinone DMSO dimethylsulfoxide DMSO-d6 per-deuterated dimethylsulfoxide ether diethylether EtOH ethanol equiv Ex. h HPLC L Me min m.p. MPLC NEt3 NMM NMR Rf rt TBS TBTU THF TFA TLC TPTU tR triphosgene Tween 80 equivalent(s) Example hour(s) high pressure liquid chromatography litre(s) methyl minute(s) melting point medium pressure liquid chromatography (Combi Flash system) triethylamine N-methylmorpholine Nuclear Magnetic Resonance ratio of fronts (thin layer chromatography) room temperature tert-butyl-dimethylsilyl 0-(benzotriazol-1-yl)-N,N,N,IN'-tetramethyluronium tetrafluoroborate tetrahydrofuran (distilled from Na/benzophenone) trifluoroacetic acid thin layer chromatography 0-(2-oxo-1(2H)-pyridyl)-N)NJN,,N'-tetramethyluronium tetrafluoroborate retention time (HPLC) bis(trichloromethyl) carbonate polyoxyethylen(20)sorbitane monooleate (trademark of ICI, Uniquema) HPLC Conditions: System 1: HPLC is performed on an Agilent HP 1100 using a Nucieosil 100-3 C18 HD 125 x 4.0 mm column (1 ml/min; Linear gradient 20-100% CH3CN (0.1% TFA) and H20 (0.1% TFA) in 7 min). System 2: Linear gradient 2-100% CH3CN (0.1% TFA) and H20 (0.1% TFA) in 10 min + 2 min 100% CH3CN (0.1% TFA); detection at 215 nm, flow rate 0.7 ml/min at 25 or 30 °C. Column: Nucieosil 120-3 C18 (125 x 3.0 mm). System 3: Linear gradient 20-100% CH3CN (0.1% TFA) and H20 (0.1% TFA) in 13 min + 5 min 100% CH3CN (0.1% TFA); detection at 215 nm. flow rate 1 ml/min at 25 or 30 °C. Column: Nucleosil 120-3 C18 (125 x 3.0 mm). Example 1: N-(4-pyridin-4-vl-oxy-phenvl)-N'-(4-ethyl-phenvl)-urea A solution of pyridine (3.46 ml, 43 mmol), 4-ethyl aniline (0.69 ml, 5.37 mmol) and phosgene (11.1 mi, 20 % in toluene; 21.5 mmol) in CH2CI2 (66 mL) is stirred at 0 °C overnight. After concentrating under reduced pressure, the reaction mixture is taken in THF (26 ml), filtrated, and added to a solution of 4-(pyridin-4-yl-oxy)-phenylamine (Stage 1.1; 0.5 g, 2.69 mmol) and pyridine (0.43 ml, 0.43 mmol) in THF (3.3 ml) and stirred at rt for 24 h. The reaction solution is filtered over silica gel (30 g), taken up in AcOEt (100 ml), washed with H20 (20 ml), NaHC03 (5 %, 20 ml), and brine (20 ml, 2x)t dried over Na2S04) concentrated under reduced pressure, and flash chromatographed (silica gel, 2x18 cm; AcOEt/hexane = 2:1 -> 4:1) giving compound of Example 1 as a colorless solid; M+H = 334, 1H-NMR (400 MHz, DMSO-d6): 8.70 (s, 1H, NH), 8.60 (s, 1H, NH), 8.44 (d, Hz, 6.5 Hz, 2H, pyridinyl), 7.54 (d, 9.5 Hz, 2H, 4-ethyl-p/?e/7y/), 7.37 (d, 9.5 Hz, 2H, oxo-pfteny/-amine), 7.11 (d/d, 9.5 Hz, 4H, oxo-phenyZ-amine/ 4-ethyl-p/7e/?y/), 6.89 (d, 6.5 Hz, 2H, pyridinyl), 2.55 (qu, 7.5 Hz, 2H, CH2), 1.16 (t, 7.5 hz, 3H( CH3); Rf (AcOEt/hexane = 2:1): 0.16; m.p. = 166.5-168 °C. The starting material is prepared as follows: Stage 1,1: (4-(pyridin-4-vl-oxv>phenvl-amine) A solution of 4-aminophenol (15 g, 0.135 mol), 4-chloropyridine hydrochloride (22.5 gf 0.148 mol), and KOtBu (45.8 g, 0.404 mol) in DMPU (208 ml) and DMF (52 ml) is stirred at 100 °C for 24 h, cooled to rt, poured into H20 (0.6 L), and extracted with AcOEt (150 ml, 6x). The combined organic phases are washed with H20 (100 ml, 2x), brine (100 ml, 2x), dried (Na2S04), concentrated under reduced pressure, and flash chromatographed (silica gel, 4.5 x 25 cm; AcOEt/hexane = 1:9 -> 3:7) to give the title compound of Stage 1.1 as a colorless solid: M+H = 187.2; 1H-NMR (400 MHz, DMSO-d6): 8.37 (d, 6.5 Hz, 2H, pyridinyl), 6.79 (d, 9.5 Hz, 2H, phenyl), 6.78 (d, 9.5 Hz, 2H, pyridinyl) 5.12 (s, 2H, NH2); Rf (AcOEt/CH2CI2 = 3:7): 0.23; m.p. = 165.8-166.6 °C. Compounds of Examples 2-15 are synthesized analogously to the preparation of the compound of Example 1 via urea formation of the corresponding aryl isocyanates and 4-(pyridin-4-yl-oxy)-phenylamine, methyI-[4-(pyridin-4-yi-oxy)-phenyl]amine, 4-(pyridin-4-ylmethyl)-phe-nylamine or methyl-[4-(pyridin-4-ylmethyl)-phenyl]arnine, respectively. Structures and analytical data are given below (Table 1). Starting materials: Methyl-[4-(pyridin-4-yl-oxy)-phenyl]amine for the synthesis of compounds of Examples 5-8 is prepared according to the procedure of the preparation of the compound of Stage 1.1. After flash chromatography, the product is further purified by Kugelrohr distillation (110 °C, 0.3 mbar) and crystallized from AcOEt/hexane: M+H = 201.1; 1H-NMR (400 MHz, DMSO-d6): 8.37 (d, 6.5 Hz, 2H, pyridinyl), 6.78 (d, 9.5 Hz, 2H. pyridinyl), 6.56 (d, 9.5 Hz, 2H, phenyl), 5.71 (s/broad, 1H, NH), 2.65 (d, 2.5 Hz, 3H, CH3-N); Rf (acetone/CH2CI2 = 3:7): 0.23. Table 1: Structures and analytical data of compounds of Examples 2-15 1 I Aryl ether formation of 4-chIoropyridine and N-(4-ethyI-phenyl)-2-(4-hydroxy-phenyI)-acet-amide (Stage 16.1) is performed according to the procedure of the synthesis of Stage 1.1: M+H = 333.1; 1H-NMR (400 MHz, DMSO-d6): 10.10 (s, 1H, NH), 8.42 (d, Hz, 6.5 Hz, 2H, pyridinyl), 7.48/7.41 (d/d, 9.5 Hz, 4H, phenyl), 6.81 (d, 6.5 Hz, 2H, pyridinyl), 7.10 (d/d, 9.5 Hz, 4H, phenyl), 3.62 (s, 2H, aryl-CH2-aryl), 2.52 (qu, 7.5 Hz, 2H, CH2), 1.12 (t, 7.5 Hz, 3H, CH3); Rf (AcOEt/hexane = 2:1): 0.35; oil. The starting material is prepared as follows: Stage 16.1: N-(4'Ethvl-phenvl)-2-(4-hvdroxv-phenyl)-acetamide 4-Hydroxyphenyl acetic acid (1.55 g, 10.2 mmol), 4-ethyl-phenylamine (1.28 ml, 10.3 mmol), TBTU (4.82 g, 15 mmol), and NMM (8.79 ml, 80 mmol) are stirred in DMF (30 ml) at rt for 5 h. The reaction mixture is taken up in AcOEt (0.2 L), washed with H20 (40 ml, 2x) and brine (40 ml, 2x), dried (Na2S04), concentrated under reduced pressure, and flash chromatogra-phed (silica gel, 3.5 x 25 cm, AcOEt/hexane = 1:2 ->2:3) giving the title compound of Stage 16.1 as a colorless solid (1.68g( 6.59 mmol; 66 %): M+H = 256.1; 1H-NMR (400 MHz, DMSO-de): 10.0/9.24 (s/s, 1H, NH/OH), 7.46 (d, 8.5 Hz, 2H, phenyl), 7.09 (d, 8.5 Hz, 4H, phenyl), 6.66 (d, 8.5 Hz, 2H, phenyl), 3.47 (s, 2H, aryl-CH2), 2.53 (qu, 7.5 Hz, 2H, CH2), 1.13 (t, 7.5 Hz, 3H, CH3); Rf (AcOEt/hexane = 1:1): 0.66; m.p. =146-148 °C. Compounds of Examples 17 and 18 are synthesized analogously to the preparation of the compound of Example 16 (data are enlisted on Table 2). After stirring a solution of 3-(trifuoromethyl)-phenyl isocyanate (0.348 ml, 2.45 mmol), 5-(pyri-din-4-yl-oxy)-2,3-dihydroindole (Stage 19.1; 0.13 g, 0.613 mmol), pyridine (0.104 ml, 1.29 mmol) in THF (4 ml) is stirred at rt for 4 d. The reaction mixture is concentrated under reduced pressure and flash chromatographed (silica gel, 2.5 x 18 cm, acetone/CH2CI2 = 1:3) to give compound of Example 19 as a beige solid: M+H = 400.1; 1H-NMR (400 MHz, DMSO-d6): 8.87 (s, 1H, NH), 8.41 (d, Hz, 6.5 Hz, 2H, pyridinyl), 8.02 (s, 1H, 3-CF3-p/7eny/), 7.93 (d, 9.5 Hz, H, indoline), 7.86 (d, 8.0 Hz, H, -CF2-phenyf), 7.53 (t, 8.0 Hz, 1H, 3-CFrphenyl), 7.36 (d, 8.0 Hz, H, CFrphenyl)f 7.07 (d, 3.5 Hz, 1H, indoline), 6.94 (dd, 9.5 Hz, 3.5 Hz, 1H, indoline), 6.84 (d, 6.5 Hz, 2H, pyridinyl, 4.19 (t, 8.0 Hz, 2H, CH2), 3.19 (t, 8.0 Hz, 2H, CH2); Rr (acetone/H2CI2 = 1:3): 0.22; m.p. = 171-172.5 °C. The starting materials are prepared as follows: Stage 19.1: 5'(PYridin-4-yNoxvV2,3-dihvdroindole During 5 min, NaBH3CN (315 mg, 4.76 mmol) is added to a solution of 5-pyridin-4-yI-oxy-indoline (Stage 19.2; 0.2 g, 0.95 mmol) in AcOH (4.75 ml) at 0 °C. After stirring for 4 h at rt, ice (10 g) is added and the AcOH is evaporated under reduced pressure. The resulting oil is adjusted to pH = 11 by adding 1 N NaOH, extracted with ether (20 ml, 3 x). The combined ether phases are washed with 1N NaOH (10 ml), H20 (10 ml, 2x), and brine (10 ml, 2x), dried (MgS04), concentrated under reduced pressure, and flash chromatographed (silica gel, 2.5 x 18 cm; acetone/CH2CI2 = 1:3) to give the title compound of Stage 19.1 as a pale solid: M+H = 213.1; 1H-NMR (400 MHz, DMSO-d6): 8.37 (d, Hz, 6.5 Hz,~2H, pyridinyl), 6.82 (d, 3.5 Hz. 1H. indoline). 6.80 (d. 6.5 Hz. 2H. ovridinvIV 6.67 (dd. 9.5 Hz. 3.5 Hz, 1H. indoline). 6.50 (d, 9.5 Hz, H, indoline), 5.54 (s/broad, 1H, NH), 3.44 (t, 8.0 Hz, 2H, CH2), 2,92 (t, 8.0 Hz, 2H, CH2); Rf (acetone/H2CI2 = 1:3): 0.22; m.p. = 115.5-117.5 °C. Stage 19.2: 5-pyridin-4-yl-oxvindoline The title compound of Stage 19.2 is synthesized according to the procedure of the preparation of the compound of Stage 1.1: M+H = 211.0; 1H-NMR(400 MHz, DMSO-d5): 8.37 (d, Hz, 6.5 Hz, 2H, pyridinyl), 7.47 (d, 9.5 Hz, 1H, indo!e-H7), 7.44 (d, 2.0 Hz, 1H, indole-H2), 7.34 (d, 2.0 Hz, 1H, indole-H5), 6.84 (d, 9.5 Hz, H, indo!e-H8), 6.83 (d, Hz, 6.5 Hz, 2H, pyridinyl), 6.42 (d, 2.0 Hz, 1H, indole-H3); R, (acetone/H2CI2 = 1:3): 0.38; m.p. = 176-177.5 eC. Example 20: 5-(4-pyridvl-oxy)-N-(3-trifluoromethyl-Dhenyl)amino-carbonyl-1,2,3.4-tetrahy-droquinoline The title compound of Example 20 is prepared analogously to the synthesis of the compound of Example 19 via urea formation with 6-(pyridin-4-yl-oxy)-1,2,3,4-tetrahydroquinoline (Stage 20.1): M+H = 414.0; 1H-NMR (400 MHz, DMSO-d6): 9.19 (s, 1H, NH), 8.42 (d, Hz, 6.5 Hz, 2H, pyridinyl), 7.94 (s, 1H, 3-CFrphenyl), 7.73 (d, 9.5 Hz, H, indoline), 7.45 (t, 8.0 Hz, 1H, 3-CFTphenyl), 7.43 (s, 1H, 1H, dihydroquinole-H8), 7.29 (d, 8.0 Hz, H, CFrphenyl), 6.98 (d, 3.5 Hz, 1H, dihydroquinole-H5), 6.93 (dd, 9.5 Hz, 3.5 Hz, 1H, dihydroquinole-H7), 6.89 (d, 6.5 Hz, 2H, pyridinyl), 3.75 (t, 8.0 Hz, 2H, CH2), 2.75 (t, 8.0 Hz, 2H, CH2), 1.90 (sext, 8.0 Hz, 2H, CH2); R, (acetone/CH2CI2 = 1:3): 0.33; m.p. = 185.5-188 °C. The starting materials are prepared as follows: Stage 20.1: 6-(pvridin-4-vl-oxv)-1.2.3,4-tetrahvdroquinoline The title compound is prepared via reduction of the corresponding quinoline (Stage 20.2) analogously to the synthesis of the compound of Example 19.1: M+H = 227.1; 1H-NMR (400 MHz, DMSO-dg): 8.37 (d, Hz, 6.5 Hz, 2H, pyridinyl), 6.78 (d, 6.5 Hz, 2H, pyridinyl), 6.66 (m, 2H, tetrahydroquinoline), 6.46 (d, 9.5 Hz, 3.5 Hz, 1H, tetrahydroquinoline), 5.74 (s/broad, 1H, NH), 3.17 (t, 8.0 Hz, 2H, CH2), 2,65 (t, 8.0 Hz, 2H, CH2) 1.74 (sext, 8.0 Hz, 2H, CH2); R, (acetone/H2CI2 = 1:3): 0.26; m.p. = 117-121.5 °C. Stage 20.2: 6-(pvridin-4-yl-oxv)-quino!ine The compound of Stage 20.2 is synthesized according to the procedure of the preparation of the compound of Stage 19.2: M+H = 211.0; 1H-NMR (400 MHz, DMSO-d6): 8.87 (dd, 3.5 Hz, 2.0 Hz, 1H, quinoline-H1), 8.48 (d, 6.5 Hz, 2H, pyridinyl), 8.35 (dd, 7.7 Hz, 2.0 Hz, 1H, quinoline-H3), 8.11 (d, 9.0 Hz, 1H, quinoline-HS), 7.75 (d, 3.0 Hz. 1H, quino!ine-H5), 7.59 (dd, 9.0 Hz, 3.0 Hz, H, quinoline-H7), 7.54 (dd, 7.7 Hz, 3.5 Hz, 1H, quinoline-H2), 7.03 (d, Hz, 6.5 Hz, 2H, pyridinyl); R, (acetone/H2CI2 = 1:3): 0.26. Example 21: N-(4-(6-Chloropyrimidin-4-vD-oxyphenvl)-N'-(3-trifluoromethylphenyl)-urea After stirring 3-trifluoromethyl-phenyl isocyanate (412 mg , 2.2 mmol), 4-(6-chloro-pyrimidin-4-yl-oxy)-aniline (Stage 21.1; 0.25 g, 1.1 mmol), and pyridine (0.18 ml), dissolved in THF (3 ml) overnight, the reaction solution is concentrated under reduced pressure and flash chromatographed (silica gel, 2.5 x 17 cm; acetone/CH2CI2 = 5:95 -> 1:9) to give compound of Example 21 as a colorless solid: M+H = 408.9/410.9; 1H-NMR (400 MHz, DMSO-d6): 9.07 (s, 1H, NH), 8.89 (s, 1H, NH), 8.63 (d, 2.0 Hz, 1H, pyridinyl), 8.01 (s, 1H, 3-CFrphenyl), 7.57 (d/broad, 8.0 Hz, 1H, CF3-p/ieny/), 7.52 (d, 9.5 Hz, 2H, oxo-p/ieny/-amine), 7.50 (m, 1H, 3-CF3-pheny!), 7.32 (d, 2.0 Hz, 1H, pyridinyl), 7.29 (d/broad, 8.0 Hz, 1H, -CF3-phenyf), 7.15 (d, 9.5 Hz, 2H, oxo-p/?eny/-amine), (d, 6.5 Hz, 2H, pyridinyl); Rf (acetone/CH2CI2 = 1:9): 0.54; m.p. = 187.4-189.7 °C. The starting materials are prepared as follows: Stage 21.1: 4-(6-Chloro-Dvrimidin-4-vl-oxvVaniline 4-Chloro-6-(4-nitro-phenoxy)-pyrimidine (Stage 21.2; 3.6 g, 14.3 mmol) dissolved in MeOH (250 ml) is hydrogenated in the presence of Raney-Ni (3 g) at 40 °C for 3 d. The reaction solution is filtered, concentrated under reduced pressure and crystallized from AcOEt/hexane to give the title compound of Stage 21.1: M+H = 222/224; 1H-NMR (400 MHz, DMSO-d6): 8.62 (s, 1H), 7.13 (s, 1H), 6.83 (d, 9 Hz, 2H, phenyl), 6.56 (d, 9Hz, 2H, phenyl), 5.12 (s, 2H, NH2);m.p. = 135.5-138.1 °C. Stage 21.2: 4-Chloro-6-(4-nitro-phenoxv)-pyrimidine 4-Nitrophenol (2.8 g, 20.1 mmol), 2,4-dichIoro-pyrimidine (3 g, 20.1 mmol), NaOH (0.8 g, 20.1 mmol) dissolved in H20/acetone (80 ml; 1:1) are stirred at 60-65 °C for 1 h. The reaction solution is concentrated under reduced pressure and flash chromatographed (silica gel, 4.5 x 22 cm, AcOEt/hexane = 1:4) to give the title compound of Stage 21.2 as a colorless solid: M+H = 252/254; 1H-NMR (400 MHz, DMSO-d5): 8.67 (s, 1H, pyrimidinyl), 8.34 (d, 9 Hz, 2H, phenyl), 7.58 (d, 9Hz, 2H, phenyl), 7.53 (s, 1H. pyrimidinyl); Rf (AcOEt/hexane = 1:1): 0.16; m.p. = 125.4-126.6 °C. Example 22: N-(4-(4-(4-hvdroxvDhenvlamino)-Dvrimidin-6-vl)-oxvDhenyl)-N'-(3-trifluoromethylphenvD-urea 1-(4-{6-[4-(tert-Butyl-dimethyl-silyloy!oxy)-phenylamino]-pyrimidin-4-yl-oxy}-phenyl)-3-(3-trifIuoromethyl-phenyl)urea (Stage 22.1; 0.7 g, 1.17 mmol) is dissolved in HF/pyridine (70 %, 1 ml) and MeCN/THF (4 ml/2 ml) at 0° C. After stirring for 3 h at rt, the reaction mixture is neutralized by adding phosphate buffer (pH = 7, 10 ml_) and the product is taken up in AcOEt (10 ml, 2x)f dried (MgS04), flash chromatographed (silica gel, 2.5 x 17 cm, MeOH/CH2CI2 = 1:9) to give the title compound of Example 22 as a colorless solid: M+H = 481.9; 1H-NMR (400 MHz, DMSO-d6): 9.23/9.21 (s/s, 2H, NH, OH), 9.10/8.91 (s/s, 2H, NH-urea,), 8.23 (s, 1H, pyrimidinyl), 8.01 (s, 1H, CFZ-phenyl), 7.58 (d, 8.8 Hz, 1H( CFZ-phenyl), 7.51 (m, 3H, phenyl-ureaiCFZ-phenyl), 7.26 (m, 3H, phenyl-OH{CF3-pheny[), 7.10 (d, 8.8 Hz, 2H, phenyl-uvea), 6.71 (d, 8.8 Hz, 2H, phenyi-OH)% 5.90 (s, 1H, pyrimidinyl); Rf (MeOH/CH2CI2 =1:9) = 0.29 (silica gel); m.p. = 142 °C (decomp.). The starting materials are prepared as follows: Stage 22.1: 1 -(4-{6-f4-(tert-Butvl-dimethvl-silvlovloxv)-phenvlamino1-pyrimidin-4-vl-oxvV phenvlV3-(3-trifluoromethyl-phenv0urea After stirring [6-(4-amino-phenoxy)-pyrimidin-4-yl][4-(tert-butyl-dimethyl-silyloxy)-phenyl]- amine (Stage 22.2; 1 g, 2.45 mmol), 3-trifluoromethyl-phenyI-isocyanate (916 mg, 4.9 mmol), NEt3 (0.682 ml, 4.9 mmol) dissolved in DMF (6 ml) for 1h, the reaction mixture is concentrated under reduced pressure and flash chromatographed (silica gel, 2.5 x 19 cm, AcOEt/hexane = 1:2 -> 2:1) to give the title compound of Stage 22,1 as a colorless solid: M+H = 595.9; 1H-NMR (400 MHz, DMSO-d6): 9.36/9.07/8.85 (s/s's, 3H, NH-urea, NH), 8.24 (s, 1H, pyrimidinyl), 8.02 (s, 1H, CFrPhenyf), 7.57 (d, 8.8 Hz, 1H, C?z-pheny!)1 7.50 (m, 3H, phenyI-urea/CF3-phenyi), 7.39 (m, 3H, phenyl-OTBSlCFz-phenyi), 7.10 (d, 8.8 Hz, 2H, pfteny/-urea), 6.78 (d, 8.8 Hz, 2H, phenyl-OlQS), 5.92 (s, 1H, pyrimidinyl), 0.90 (s, 9H, TBS), 0.18 (s, 6H, TBS). Stage 22.2: [6-(4-Amino-phenoxv)-pvrimidin^-vl1[4-(tert-butvl-dirr1ethvl-silvloxy)-phenvn-amine [4-(tert-Butyl-dimethy!-silyloxy)-phenyl]-[6-(4-nitro-phenoxy)-pyrimidin-4-yl]-amine (Stage 22.3; 1.8 g, 4.1 mmol) is reduced by means of Raney-Ni (0.4 g) in EtOH/HTHF (35/15 ml) during 3 h and purified by flash chromatography (silica gel, 3.0 x 18 cm, AcOEt/hexane = 1:1 -> 4:1) to give compound of Stage 22.2 as a colorless solid: M+H = 409.1; 1H-NMR(400 MHz, DMSO-de): 9.22 (s, 1H, NH), 8.20 (s, 1H, pyrimidinyl), 7.37 (d, 8.8 Hz, 2H, phenyl-OTBS), 6.77 (d, 8.8 Hz, 2H, phenyI-NH2), 6.70 (d, 8.8 Hzr 2H, phenyt-OTBS), 6.55 (8.8 Hz, 2H, p/?eny/-NH2)p 5.79 (s, 1H, pyrimidinyl), 5.02 (s, 2H, NH2), 0.90 (s, 9H, TBS), 0.12 (s, 6H, TBS); Rf (AcOEt/hexane = 2:1): 0.22. Stage 22.3: f4-(tert-Butvl-dimethvl-silvloxv)-phenvn-[6-(4-nitro-DhenoxvVpyrimidin-4-vl1-amine 4-[6-(4-Nitro-phenoxy)-pyrimidin-4-ylamino]-phenol (Stage 22.4; 1.5 g, 4.63 mmol), tert-butyl-dimetylsilyl chloride (1.39 g, 9.26 mmol), NEt3 (1.29 ml, 9.26 mmol) dissolved in DMF (20 ml) are stirred for 3.5 h. After concentrating the reaction mixture under reduced pressure and dissolving in phosphate buffer (50 ml, pH = 7), the product is extracted by means of AcOEt (10 ml) and purified by flash chromatography (silica gel, 3.0 x 17 cm, AcOEt/hexane = 1:1 -> 4:1) to give the title compound compound of Stage 22.3 as a colorless solid; M+H = 439.0; 1H-NMR (400 MHz, DMSO-d6): 9.56 (s, 1H, NH), 8.28 (m, 3H, pyrimidinyl, p/)eny/-N02), 7.40 (m, 4H, p/)eny/-OTBS, p/>eny/-N02), 6.81 (d, 8.8 Hz, 2H, phenyl-OTBS, 6.20 (s, 1H, pyrimidinyl), 0.93 (s, 9H, TBS), 0.18 (s, 6H, TBS). Stage 22.4: 4-[6-(4-Nitro-phenoxv)-pvrimidin-4-ylamino1-phenol 4-Chloro-6-(4-nitro-phenoxy)~pyrimidine (Stage 22.5; 3 g, 11.9 mmol), 4-nitrophenoI (1.95 g, 17.9 mmol), and diisopropyiethytamine (DIPEA) (3.04 ml, 17 9 mmol) dissolved in 2-propanol (50 ml) are stirred at 85° C for 18 h. After concentrating the reaction mixture under reduced pressure, the product precipitates as a colorless fins solid: M+H = 245.0; 1H-NMR (400 MHz, DMSO-d6): 9.40/9.25 (s/s, 2H, NH/OH), 8.28 (d, 7.5 Hz, 2H, phenyl-N02), 8.26 (s, 1H, pyri-midinyl). 7.40 (d, 7.5 Hz, 2H, phenyl-HOz), 7.24 (d, 8.0 Hz, 2H, phenyl-OH), 6.77 (d, 8.0 Hz, 2H, phenyl-OH), 6.15 (s, 1H, pyrimidinyl); R, (AcOEt/hexane = 2:1): 0.48. Stage 22.5: 4-Chloro-6-(4-nitro-phenoxv)-pvrimidirie 4,6-Dichioropyrimidine (3 g, 20 mmol), 4-nitrophenol (2.8 g, 20 rr.mol), NaOH (0.8 g, 20 mmol) dissolved in H20/acetone (25/25 ml) are stirred at 45° C for 22 h. The precipitated product is isolated by filtration: M+H = 252.0/254.0; 1H-NMR (400 MHz, DMSO-ds): 9.67 (s, 1H, pyrimidinyl), 9.32 (d, 8.2 Hz, 2H, phenyl), 7.58 (s, 1H, pyrimidinyl), 7.56 (d, 8.2 Hz, 2H, phenyl); R, (AcOEt/hexane = 1:1): 0.20. In accordance with the methods described hereinbefore, the following compounds, with the substituents given in Table 4, are prepared: Example 23: M+H = 450.0; 1H-NMR (400 MHz, DMSO-d6): 9.15 (s, 1H, NH), 8.95 (s, 1H, NH), 8.44 (d, 6.5 Hz, 2H, pyridinyl), 8.09 (s, 1H, CFj/phenyi-p/ieny/), 7.67 (d, 6.5 Hz, 1H, CFs/phenyl-pfceny/), 7.57 (d, 8.5 Hz, 2H, oxo-p/?eny/-amine), 7.41 (M, 3H, phenyl), 7.31 (t, 7.5 Hz, 2H, phenyl),7.15 (d, 8.5 Hz, 2H, oxo-pfteny'-amine), 6.90 (m, 4H, pyridinyl/ piperidinyl-pheny/), 2.99 (t, 6.5 Hz, 4H, CH2, piperidinyl), 1.60 (t/broad, 4H, CH2, piperidinyl), 1.47 (m/broad, 1H, piperidinyl); Rf (acetone/CH2CI2 = 1:3): 0.22; m.p: 120 °C (decomp.). Example 24: M+H = 458.9; 1H-NMR (400 MHz, DMSO-d6): 8.97 (s, 1H, NH), 8.85 (s, 1H, NH), 8.43 (d, Hz, 6.5 Hz, 2H, pyridinyl), 7.89 (s, 1H, 3-CF3-pheny/), 7.59 (d, 9.5 Hz, 1H, 3-CF3-phenyl), 7.54 (d, 8.0 Hz, 2H, oxo-phenyl), 7.49 (t, 8.0 Hz, 1H, 3-CF3-phenyf), 7.11 (d, 8.0 Hz, 2H, oxo-phenyl), 6.84 (d, 6.5 Hz, 2H, pyridinyl), 3.68 (s/broad, 4H, morphoiinyl), 2.78 (s/broad, 4H, morpholinyl); Rf (MeOH/CH2CI2 = 1:19): 0.11; m.p. > 120 °C (decomp.). Example 25: M+H = 396.0; 1H-NMR (400 MHz, DMSO-d6): 8.73 (s, 1H, NH), 8.62 (s, 1H, NH), 8.42 (d/broad, 6.5 Hz, 2H, pyridinyl), 7.56 (d, 9.5 Hz, 2H, oxo-p/7eny/-amine), 7.10 (d, 9.5 Hz, 2H, oxo-p/?eny/-amine), 6.84 (d, 6.5 Hz, 2H, pyridinyl), 6.77 (s, 2H, trimethoxy-pfreny/), 3.73 (s, 6H, CH3) 3.32 (s, 3H, CH3); R, (acetone/CH2CI2 = 1:3): 0.26; m.p: 179 °C (decomp.). Example 26: Is synthesized according to the synthesis of compound of Example 1 starting from 2-methoxy-biphenyl-4-ylamine (Stage 26.1): M+H = 412.0; 1H-NMR (400 MHz, DMSO-d6): 8.81/8.79 (s/s, 2H, NH), 8.41 (d, 6.5 Hz, 2H, pyridinyl), 7.56 (d, 9.5 Hz, 2H, oxo-phenyl-amine), 7.44 (d, 7.0 Hz, 2H, phenyl), 7.36 (Vs. 7.0 Hz, 3H, phenyl/p/7eny/-OMe), 7.24 (t, 7.0 Hz, 1H, phenyl), 7.18 (d, 8.5 Hz, 1H, p/?enyl-OMe), 7.09 (d, 9.5 Hz, 2H, oxo-p/)eny/-amine), 7.01 (d, 8.5 Hz, 1H, phenyl-OMe), 6.84 (d, 6.5 Hz, 2H, pyridinyl), 3.73 (s, 6H, CH3) 3.73 (s, 3H, CH3); Rf MeOH/CH2CI2 = 5:95): 0.31. Stage 26.1: 2-Methoxy-4-nitro-biphenyl (Stage 26.2) (867 mg, 3.78 mmol) dissolved in THF/EtOH (1:5, 20 mL) is hydrogenated in the presence of Pd/C (100 mg) at rt for 30 min. After filtering off the catalyst and washing with EtOH (5 mL), the reaction solution is evaporated under reduced pressure to give compound of Stage 26.1 as colorless oil: M+H = 200.0; 1H-NMR (400 MHz, DMSO-d6): 7.37 (d, 7.0 Hz, 2H, phenyl), 7.31 (t, 7.0 Hz, 2H, phenyl), 7.17 (t, 7.0 Hz, 1H. phenyl), 6.83 (d, 8.5 Hz, 1H, pheny\-OMe), 6.30 (s, 1H, pheny\-OMe), 5.21 (s, 2H, NH2), 3.64 (s, 3H OMe); HPLC (System 1): 3.92 min. Stage 26.2: To 1-bromo-2-methoxy-4-nitro-benzene (1.0 g, 4.3 mmol) dissolved in DMF (37 ml_), under Ar-atmosphere, phenyl-boronic acid (578 mg, 4.74 mmol), (AcO):Pd (48 mg, 0.215 mmol), tri-o-tolyl-phosphane (131 mg, 0.431 mmol), and K:C03 (1M, 11 ml_, 10.77 mmol) are added. After stirring at 120 °C for 1 h, the reaction solution is fitered over Hyflo, concentrated under reduced pressure, partitioned between AcOEt and H20 (100mU100 ml_), and extracted with AcOEt (50 ml_, 2*). The combined organic phases are washed with H20 (50 mL), dried (Na2S04), concentrated under reduced pressure, and flash chromatographed (silica gel, 4.5 * 22 cm, hexane/AcOEt = 9:1) to give compound of Stage 26.2 as colorless oil: M+H = 231.0; 1H-NMR (400 MHz, DMSO-d6): 7.92 (d, 7.0 Hz, 1H), 7.88 (s, 1H), 7.57 (d, 7.0 Hz, 1H), 7.54 (d, 7.0 Hz, 1H), 7.49 (t, 7.0 Hz, 3H), 7.42 (d, 7.0 Hz, 1H), 3.92 (s, 3H OMe); HPLC (System 1): 7.06 min. Example 27: M+H = 434.0; 1H-NMR (400 MHz, DMSO-d6): 8.74 (s, 1H, NH), 8.62 (s, 1H, NH), 8.41 (d, Hz, 6.5 Hz, 2H, pyridinyl), 7.52 (d, 8.5 Hz, 2H, oxo-p/7eny/-amino), 7.29 (s, 1H, WleO-phenyl), 7.09 (d, 8.0 Hz, 2H, oxo-p/7eny/-amino), 6.97 (d, 8.5 Hz, 1H, MeO-phenyl), 6.94 (d, 6.5 Hz, 2H, pyridinyl), 3.77 (s, 3H, MeO); R, (MeOH/CH2CI2 = 5:95): 0.27. Example 28: Is synthesized according to the synthesis of compound of Example 1 starting from 3-methoxy-4-piperidin-1-yt-phenylamine (Stage 28.1): M+H = 419.1; 1H-NMR (400 MHz, DMSO-d6): 8.68/8.51 (s/s, 2H, NH), 8.39 (d, 6.5 Hz, 2H, pyridinyl), 7.52 (d, 9.5 Hz, 2H, oxo-p/7e/?y/-amine), 7.17 (s, 1H, phenyl-OMe), 7.09 (d, 9.5 Hz, 2H, oxo-p/7er)y/-amine), 6.85 (d, 6.5 Hz, 2H, pyridinyl), 6.83/6.78 (d/d, 8.0 Hz, 4H, prieny/-OMe), 3.74 (s, 6H, 0-CH3) 2.80/1.60 (m/m, 4H/4H, CH2-piperidinyl), 1.48 (m, 2H, CH2-piperidinyl); R, MeOH/CH2CI2 = 1:9): 0.42. Stage 28.1: 1-(2-Methoxy-4-nitro-phenyl)-piperidine (Stage 28.2) (3.9 g, 16.5 mmol) dissolved in EtOH (20 mL) is hydrogenated in the presence of Pd/C (100 mg) at rt for 3 h. After filtering off the catalyst and washing with EtOH (5 mL), the reaction solution is evaporated under reduced pressure to give compound of Stage 28.1 as colorless oil: M+H = 207.1; 1H-NMR (400 MHz, DMSO-de): 6.58 (d, 8.0 Hz, 1H, phenyl), 6.19 (s, 1H, phenyl), 6.03 (d, 8.0 Hz, 1H, phenyl), 4.64 (s. 2H, NH2), 3.66 (s, 6H, 0-CH3) 2.91/1.57 (m/m, 4H/4H, CH2-piperidinyl), 1.42 (m, 2H, CHrpiperidinyl); HPLC (System 1): 4.36 min. Stage 28.2: 1-Bromo-2-methoxy-4-nitro-benzene (5 g, 21.5 mmol) and piperidine (8.5 mL, 86.2 mmol) are stirred under reflux for 4 h. After taking up in H20 (80 mL), the reaction solution is extracted with CH2CI2 (80 mL, 2*). The combined organic phases are dried (Na2S04), concentrated under reduced pressure, and flash chromatographed (silica gel, 5.5 * 22 cm, hexane/AcOEt = 9:1) to give compound of Stage 28.2 as colorless solid: M+H = 237-1; 1H-NMR (400 MHz, DMSO-d6): 7.80 (d, 8.0 Hz, 1H, phenyl), 7.63 (s, 1H, phenyl), 6.97 (d, 8.0 Hz, 1H, phenyl), 4.64 (s, 2H, NH2), 3.88 (s, 6H, 0-CH3), 3.16/1.61 (m/m, 4H/4H, CH2-piperidinyl), 1.58 (m, 2H, CH2-piperidinyl); HPLC (System 1): 4.90 min. Example 29: M+H = 389.2; 1H-NMR (400 MHz, DMSO-d6): 8.64 (s, 1H, NH), 8.21 (d, 6.5 Hz, 2H, pyridinyl), 8.38 (s, 1H, NH), 7.51 (d, 9.5 Hz, 2H, oxo-pfteny/-amine), 7.23 (s, 1H, phenyl-piperidinyl), 7.07 (d, 9.5 Hz, 2H, oxo-p/7eny/-amine), 6.86 (m, 4H, pyridinyl/p/7eny/-pyridinyl), 2.99/1.60 (m/m, 4H/4H, CH2-piperidinyl), 1.48 (m, 2H, CH2-piperidinyI); R, (acetone/CH2Cl2 = 3:7): 0.14. Example 30: M+H = 387.9; 1H-NMR (400 MHz, DMSO-d6): 9.07 (s, 1H, NH), 8.85 (s, 1H, NH), 8.29 (d, Hz, 6.5 Hz, 1H, pyridinyl), 8.01 (s, 1H, 3-CF3-p/?e/?y/), 7.58 (d, 9.5 Hz, 2H, oxo-p/?er?y/-amine), 7.50 (d, 8Hz, 1H, oxo-phenyl), 7.53 (t, 8.0 Hz, 1H, 3-CF^-phenyl), 7.30 (d, 8.0 Hz, 1H, 3-CF3-phenyl), 7.04 (d, 9.5 Hz, 2H, oxo-phenyl), 6.73 (d, 3.5 Hz, 1H, pyridinyl), 6.69 (dd, 3.5 Hz, 6.5 Hz, 1H, pyridinyl), 2.18 (s, 3H, CH3); R, (acetone/CH2CI2 = 1:3): 0.19; m.p. = 160-163 °C (decomp.). Example 31: Is synthesized in analogy to the preparation of compound of Example 22: M+H = 482.4; 1H-NMR (400 MHz, DMSO-d6): 10.25/9.98 (s/s, 2H, NH/OH), 9.27/8.99 (s/s, 2H, NH-urea,), 8.26 (d, 6.5 Hz, 1H, pyrimidinyl), 7.96 (s, 1H, CF2-phenyl), 7.70 (m, 2H, CF3- phenyl), 7.53 (d, 8 Hz,, 2H, oxo-phenyl-urea), 7.44 (d, 7.0 Hz, 1H, CF3-phenyl), 7.30 (d, 8.0 Hz, 2H, hydroxy-p/7er?y/-amino), 7.18 (d, 8.0 Hz. 2H, oxo-p/?e,oy/-urea), 6.58 (d, 8-0 Hz, 2H, hydroxy-pr?eny/-amino), 6.30 (d, 6.5 Hz, 1H, pyrimidinyl); HPLC (System 1): 6.55 min. Example 32: Is synthesized in analogy to the preparation of compound of Example 22: M+H = 579.8; 1H-NMR (400 MHz, DMSO-d6): 9.25/9.23 (s/s, 2H, NH, OH), 8.94/8.88 (s/s, 2H, NH-urea,), 8.23 (s, 1H, pyrimidinyl), 7.94 (d, 2 Hz, 1H, CF3-CH2-0-/CF3-p/7eny/), 7.65 (dd, 8.5 Hz, 2 Hz, 1H, CF3-CH2-0-/CF3-p/?er7y/), 7.55 (d, 9.0 Hz, 2H, oxo-p/?eny/-amino), 7.36 (d, 8.5 Hz, 1H, CF3-CH2-0-/CF3-p/)eny/), 7.29 (d, 9.0 Hz, 2H, oxo-phenyl-urea), 7.10 (d, 8.8 Hz, 2H, oxo-p/?eny/-urea), 6.75 (d, 9.0 Hz, 2H, oxo-p/?eny/-amino), 5.93 (s, 1H, pyrimidinyl), 4.38 (q, 8.4 Hz, 2H, CH2); R, (NHj/MeOH/CH^ = 0.01:1:9): 0.27. Example 33: Compound of Example 2 (29 mg, 0.078 mmol) and m-chloro-perbenzoic acid (28.9 mg, 0.17 mmol) are stirred in CH2CI2/CHCI3 (1:1; 3 ml_) for 3 h at 45 °C. Separation is performed by preparative TLC (2 plates, 20 x 20 cm, MeOH/CH2CI2 = 1:4): M+H = 390.0; 'H-NMR (400 MHz, DMSO-d6): 9.39 (s, 1H, NH), 9.21 (s, 1H, NH), 8.11 (d, 9.0 Hz, 2H, pyridinyl), 8.01 (s, 1H, CF3-phenyl), 7.59 (d, 8.5 Hz, 1H CF3-phenyl), 7.54 (d, 10.0 Hz, 2H, oxo-phenyl), 7.49 (t, 8.5 Hz, 1H, CF3-phenyl), 7.28 (d, 8.5 Hz, 1H, CFs-phenyl), 7.09 (d, 10.0 Hz, 2H, oxo-phenyl), 6.93 (d, 9.0 Hz, 1H, pyridinyl); R, (MeOH/CH2CI2 = 1:9): 0.19. Example 34: Is preapared according to the procedure of the synthesis of compound of Example 22: M+H = 525.7; 1H-NMR (400 MHz, DMSO-d6): 9.13/8.90 (s/s, 2H, NH-urea), 8.22 (s, 1H, pyrimidinyl), 7.98 (s, 1H, CF3-phenyl), 7.56 (d, 7.5 Hz, 1H, CF3-phenyl), 7.47 (t, 7.5 Hz, 1H, CF3-p/?er?y1), 7.42 (d, 8.3 Hz, 2H, oxo-p/?eny-urea), 7.29 (d, 7.5 Hz, 1H, CF3-phenyl), 7.13 (d, 8.8 Hz, 2H, oxo-p/?eny/-amino), 6.96 (d, 8.3 Hz, 2H, oxo-phenyl-urea), 5.87 (s, 1H, pyrimidinyl), 5.42 (s, 1H, NH), 3.91/2.83 (t/t/broad, 4H, CH2). Example 35: N-r4-(pvridin-4-vl-oxvV3-chloro-phenvn-N'-(3-trifluoromethvl*phenyl)-urea Triphosgene (91 mg, 0.30 mmol) dissolved in CH2CI2 (9 mL) is added to a solution of 3-chloro-4-(pyridin-4-y!oxy)-phenylamine (Stage 35.1) (0.2 g, 0.906 mmol) and NEt3 (0.11 mL, 1.5 mmol) in CH2CI2(4.5 mL) during 4 min at 0 °C. After stirring the reaction solution for 10 min at rt, a solution of 3-trifluoromethyl-phenylamine (0.114 mL, 0.906 mmol) and NEt3 (0.11 mL, 1.5 mmol) in CH2CI2 (4.5 mL) is added. After stirring for 4.5 h, the rection solution is poured onto concentrated NaHC03 solution, and extracted with CH2CI2 (25 mL, 5*). The combined organic phases are washed with brine (20 mL), died (MgS04), concentrated under reduced pressure, and fklash chromatographed (silica gel, 3.5 * 35 cm; AcOEt/hexane = 2:1 -> 3:1) to give compound of Example 35 as slightly yellowish solid (301 mg, 0.74 mmol; 81 %), M+H = 408.0; 1H-NMR (400 MHz, DMSO-d6): 9.20/9.11 (s/s, 2H, NH), 8.45 (d, 6.5 Hz, 2H, pyrimidinyl), 8.01 (s, 1H, CFrphenyf), 7.90 (s, 1H, Cl-phenyl), 7.60 (d, 7.5 Hz, 1H, CF3-phenyl), 7.53 (t, 7.5 Hz, 1H, CFrpheny\), 7.41 (d, 8.5 Hz, 1H, Cl-phenyl), 7.33 (m, 2H, phenyl-C\/CF3-phenyl), 6.88 (s, 2H, pyrimidinyl); HPLC (System 1): 5.43 min. Stage 35.1: Is prepared according to the synthesis of compound of Stage 1.1: M+H = 221.0; 1H-NMR (400 MHz, DMSO-dg): 8.38 (d, 6.5 Hz, 2H, pyrimidinyl), 6.98 (d, 8.5 Hz, 1H Cl-phenyl), 6.77 (d, 7.0 Hz, 2H, Cl-phenyl), 6.73 (s, 1H, Cl-phenyl), 6.53 (s, 2H, pyrimidinyl), 5.44 (s, 2H, NH2); HPLC (System 1): 5.43 min. Example 36: N-f4-(pvridin-4-Yl-oxv)-3-methvl-phenvll-N'-(3-trifluoromethvl-phenyl)-urea The title compound is synthesized according to the preparation of compound of Example 35 starting from Stage 36.1: M+H = 388.2; 1H-NMR (400 MHz, DMSO-d6): 9.03/8.90 (s/s, 2H, NH), 8.39 (d, 6.5 Hz, 2H, pyrimidinyl), 8.01 (s, 1H, CF3-phenyl), 7.53 (d, 7.5 Hz, 1H, CFr phenyl), 7.46 (m, 2H, CH3-pheny\), 7.35 (d, 8.5 Hz, 1H, CF3-phenyl), 7.29 (d, 7.5 Hz, 1H, CFz-phenyl), 7.00 (d, 7.5 Hz, 1H, CH3-phenyl), 6.76 (d, 6.5 Hz, 2H, pyrimidinyl), 3.30 (s, 3H, CH3); HPLC (System 1): 5.26 min. Stage 36.1: The compound is synthesized according to the preparation of compound of Stage 35.1: slightly brownish solid: M+H = 201.1; 1H-NMR (400 MHz, DMSO-d6): 8.36 (d, 6.5 Hz, 2H, pyrimidinyl), 6.73 (m, 3H, pyrimidinyl/p/7er7y/-CH3), 6.49 (s, 1H, phenyl-CF\3), 6.44 (m, 2H, phenyl-CH3), 5.06 (s, 2H, NH2), 1.S6 (s, 3H, CH3); Rf (hexane/AcOEt = 1:2): 0.14. Example 37: 1-(3-Methoxv-5-trifluoromethyl-phenvn-3-[4-(pyridin-4-yloxy)-phenvl1-urea The tit's comound is synthesized analogously to the described procedures: M+H = 404.1; 1H-NMR (400 MHz, DMSO-d6): 9.07 (s, 1H, NH), 8.87 (s, 1H, NH), 8.40 (d, Hz, 6.5 Hz, 2H, pyridinyl), 7.55 (d, 9.5 Hz, 2H, oxo-p/ieny/-amine), 7.48 (s, 1H, CHT0-IC?3-phenyl), 7.24 (s, 1H, O-CHz/CFrphenyl), 7.09 (d, 9.5 Hz, 2H, oxo-p/7eny/-amine), 6.84 (d, 6.5 Hz, 2H, pyridinyl), 6.80 (s, 1H, CH3-0-/CF3-phenyl), 3.79 (s, 3H, CH3-0); R, (MeOH/CH2C!2 = 1:3): 0.19; m.p. = 162.5-164.5 °C. Example 38: 1 -(4-[Bis-(2-methoxy-ethvl)-aminol-3-trifluoromethvl-phenyl)-3-f4-(pyridin-4-yloxy)-phenyll-urea The title compound is synthesized according to the preparation of compound of Example 1 starting from N*1*,N*r-bis-(2-methoxy-ethyl)-2-trifluoromethyl-benzene-1,4-diamine (Stage 38.1): M+H = 505.0; 1H-NMR (400 MHz, DMSO-d6): 8.97 (s, 1H, NH), 8.86 (s, 1H, NH), 8.40 (d, 6.5 Hz, 2H, pyridinyl), 7.88 (s, 1H, CF3-CH2-0-/CF3-p/7e/7y/), 7.55 (m, 4H, oxo-phenyl-amine, CF3-CH2-0-/CF3-p/7eny/), 7.11 (d, 9.5 Hz, 2H, oxo-pheny/-amine), 6.84 (d, 6.5 Hz, 2H, pyridinyl), 3.27 (t, 8 Hz, 4H, CH2), 3.16 (s, 6H, CH3-0), 3.08 (t, 8 Hz, 4H, CH2); Rf (acetone/CH2CI2 = 1:3): 0.20. Stage 38.1: The compound is synthesized by nucleophilic substitution reaction from 1-bromo-4-nitro-2-trifluoromethyl-benzene with bis-(2-methoxy-ethyl)-amine (140 °C, 4 h) and further hydrogenolytic reduction of the nitro-function to the amine by means of Raney Nickel: M+H = 293.0; 1H-NMR (400 MHz, DMSO-d6): 7.24 (d, 9 Hz, 1H), 6.77 (m, 2H), 5.37 (s/broad, 2H, NH2), 3.26 (t, 8 Hz, 4H, CH2), 3.16 (s, 6H, CH3-0), 2.98 (t, 8 Hz, 4H, CH2); R, (acetone/CH2CI2 = 1:3): 0.50; m.p. = 64.5 - 65 °C. Example 39: 1 -(4-Diethvlamino-3-trifluoromethvl-phenvl)-3-f4-(pyridin-4-vloxv)-Dhenvn-urea The title compound is synthesized according to the preparation of compound of Example 1 starting from N*1*,N*1*-diethyl-2-trifluoromethyl-benzene-1,4-dia.Tiine (Stage 39.1): M+H = 445.0; 1H-NMR (400 MHz, DMSO-d6): 8.94 (s, 1H, NH), 8.86 (s, 1H, NH), 8.42 (d/broad, 6.5 Hz, 2H, pyridinyl), 7.89 (s, 1H, NEt2-/CF3-pfieny/), 7.59 (d/broad, 9.5 Hz, 1H, NEt2-/CF3-phenyl), 7.56 (d, 9.5 Hz, 2H, oxo-p/7eny/-amine), 7.43 (d, 9.5 Hz, 1H, NEt2-/CF3-pfteny/), 7.11 (d, 9.5 Hz, 2H, oxo-p/?eny/-amine), 6.84 (d, 6.5 Hz, 2H, pyridinyl), 2.84 (qu, 7.5 Hz, 4H, CH2), 0.90 (t, 7.5 Hz, 6H, CH3); Rf (acetone/CH2CI2 = 1:3): 0.21; m.p.: 60 °C (decomp.). Stage 39.1: The compound is synthesized according to the preparation of Stage 38.1: M+H = 293.0; 1H- NMR (400 MHz, DMSO-d6): 7.24 (d, 9 Hz, 1H), 6.77 (m, 2H), 5.37 (s/broad, 2H, NH2), 3.26 (t, 8 Hz, 4H, CH2), 3.16 (s, 6H, CH3-0), 2.98 (t, 8 Hz, 4H, CH2); R, (acetone/CH2CI2 = 1:3): 0.50. Example 40: N-Methyl-C-[4-(6-(4-r3-(3-trifluoromethyl-phenvl)-ureido1-phenoxv}-pyrimidin-4-vlamino)-phenyn-methanesulfonamide The title compound is synthesized in analogy to the preparation of compound of Example 22: M+H = 572.8; 1H-NMR (400 MHz, DMSO-d6): 9.61 (s, 1H, NH), 9.01/8.87 (s/s, 2H, NH-urea), 8.36 (s, 1H, pyrimidinyl), 8.02 (s, 1H, CF3-phenyl), 7.58 (m, 3H, am\no-phenyl/CFrphenyl), 7.50 (m, 3H, oxo-p/?eny/-urea/CF3-phenyt), 7.12 (d, 8.0 Hz, 2H, oxo-p/7e/?y-urea), 6.85 (q, 5.0 Hz, 1H, NH-S02), 6.04 (s, 1H, pyrimidinyl), 4.22 (s, 2H, CH2), 2.57 (d, 5.0 Hz, 3H, CH3); HPLC (System 1): 5.80 min. Examples 41: 1-f4-(4-Methyl-piperazin-1-yO-3-trifl^ phenyll-urea The title compound is synthesized according to the preparation of Example 1 starting from 4-(4-methyl-piperazin-1-yl)-3-trifluoromethyl-phenylamine (Stage 41.1): M+H = 472.0; 1H-NMR (400 MHz, DMSO-d6): 9.18 (s, 1H, NH), 9.08 (s, 1H, NH), 8.43 (d, Hz, 6.5 Hz, 2H, pyridinyl), 7.90 (s, 1H, 3-CF^-phenyl), 7.59 (d, 9.5 Hz, 1H, 3-CF3-pr?eny/), 7.54 (d, 8.0 Hz, 2H, oxo-phenyl), 7.49 (t, 8.0 Hz, 1H, 3-CF3-phenyl), 7.13 (d, 8.0 Hz, 2H, oxo-phenyl), 6.89 (d, 6.5 Hz, 2H, pyridinyl), 2.85 (s/broad, 4H, piperidinyl), 2.56 (s/broad, 4H, piperidinyl), 2.32 (s/broad, 3H, NMe); R, (MeOH/CH2CI2 = 1:9): 0.10; m.p. > 100 °C (decomp.). Stage 41.1: The compound is synthesized according to the preparation of Stage 39.1: M+H = 260.1; 1H-NMR (400 MHz, DMSO-d6): 7.21 (d, 9 Hz, 1H), 6.74 (m, 2H), 5.35 (s/broad, 2H, NH2), 2.70 (m/broad, 4H, CH2), 2.36 (s/broad, 4H, CH2), 2.18 (s, 3H, CH3); Rf (MeOH/CH2CI2 = 1:5): 0.17; m.p. = 121-123 °C. Example 42: 1 -f4-(2-Hydroxv-propvlamino)-3-trifluoromethvl-phenyn-3-r4-(pvridin-4-vloxv)-pherwH-urea The title compound is synthesized according to the preparation of Example 22 starting from 4-(4-methyl-piperazin-1-yl)-3-trifluoromethyl-phenylamine (Stage 42.1): M+H =447.0; 1H-NMR (400 MHz, DMSO-d6): 8.70 (s, 1H, NH), 8.48 (s, 1H, NH), 8.39 (d/broad, 6.5 Hz, 2H, pyridinyl), 7.62 (s, 1H, HO-propyl-NH-/CF3-p/?eny/), 7.53 (d, 11 Hz, 2H, oxo-p/?eny/-amine), 7.37 (d/broad, 9.5 Hz, 1H, HO-propyl-NH-/CF3-p/7eny/), 7.09 (d, 11 Hz, 2H, oxo-phenyl-amine), 6.84 (d, 6.5 Hz, 2H, pyridinyl), 6.78 (d, 9.5 Hz, 1H, HO-propyl-NH-/CF3-p/7eny/), 4.90 (t/broad, 1H, NH), 4.84 (d, 6.5 Hz, 1H, OH), 3.81 (sept/broad, 1H, CH), 3.11/2.90 (m/m, 2H, CH2), 1.10 (d, 6.5 Hz, 3H, CH3); Rf (acetone/CH2CI2 = 1:3): 0.11; m.p.: 140 °C (decomp.). Stage 42.1: The compound is synthesized according to the preparation of Stage 39.1: M+H = 236.2; 1H-NMR (400 MHz, DMSO-d6): 6.74 (s, 1H) 6.72 (d, 9 Hz, 1H), 6.60 (d, 9.0 Hz, 1H), 4.80 (s/broad, 1H, NH), 4.67 (2, 2H NH2), 4.37 (m/broad, 1H, OH), 3.80 (m/broad, 1H, CH), 3.02 (m/broad, 1H, CH2), 2.79 (m/broad, 1H, CH2), 1.07 (s, 3H, CH3); Rf (hexane/AcOEt = 1:1): 0.13; m.p. = 91 -93°C. Example 43: 1 -(4-Methvl-3-trifluoromethvl-phenvl)-3-[4-(pvridin-4-vloxv)-phenvn-urea The comound is synthesized analogously to the described procedures: M+H = 388.2; 1H-NMR (400 MHz, DMSO-d6): 8.96 (s, 1H, NH), 8.84 (s, 1H, NH), 8.42 (d/broad, 6.5 Hz, 2H, pyridinyl), 7.93 (s, 1H, CF JMe-phenyf), 7.56 (d, 9.5 Hz, 2H, oxo-p/7eny/-amine), 7.52 (d, 9.0 Hz, 1H, CFJMe-phenyl), 7.33 (d, 9.0 Hz, 1H, CF^/Me-phenyl), 7.10 (d, 9.5 Hz, 2H, oxo-pheny/-amine), 6.84 (d, 6.5 Hz, 2H, pyridinyl), 2.36 (s, 3H, CH3); Rf (acetone/CH2Cl2 = 1:3): 0.25; m.p.: 149 °C (decomp.). i Example 44: 5-(Pyridin-4-yloxv)-2,3-dihydro-indole-1-carboxylic acid r4-'(2,2,2,-trifluoro-ethoxyV3-trifluoromethyl-phenvn-amide Is prepared in analogy to the synthesis of compound of Example 20: M+H = 497.9; 1H-NMR (400 MHz, DMSO-d6): 8.73 (s, 1H, NH), 8.40 (d, Hz, 6.5 Hz, 2H, pyridinyl), 7.92 (m, 2H, indolinyl/3-CF3-p/?eny/), 7.82 (d, 8.0 Hz, H, 3-CFz-phenyl), 7.36 (t, 8.0 Hz, 1H, 3-CFTphenyl), 7.04 (s, 1H, indoline), 6.95 (dd, 9.5 Hz, 3.5 Hz, 1H, indoline), 6.84 (d, 6.5 Hz, 2H, pyridinyl), 4.89 (q, 9.0 Hz, 2H, CF3-CH2), 4.26 (t, 7.5 Hz, 2H, CH2-indolinyi), 3.17 (t, 7.5 Hz, 2H, CH2-indolinyl); Rf (acetone/CH2CI2 = 1:3): 0.20. Example 45: 1 -(4-r6-(4-Hydroxv-phenvlaminoV^ 3-trifluoromethyl-phenvl)-urea The title compound is synthesized according to the synthesis of compound of Example 22: M+H = 564.8; 1H-NMR (400 MHz, DMSO-d6): 9.23 (s, 2H, NH, OH), 8.96/8.78 (s/s, 2H, NH-urea), 8.21 (s, 1H, pyrimidinyl), 7.92 (s, 1H, morpholinyl-pfteny/), 7.53 (m, 3 H, morpholinyl-phenyl/oxo-phenyl-am\no)t 7.24 (d, 8.5 Hz, 1H, morpholinyi-prteny/), 7.08 (d, 9.0 Hz, 2H, oxo-p/7eny/-urea), 6.69 (d, 9.0 Hz, 2H, oxo-p/)e/7y/-amino), 5.87 (s, 1H, pyrimidinyl), 3.65 (m, 4H, CH2), 2.79 (m, 4H, CH2); Rf (NH3/MeOH/CH2CI2 = 0.01:1:9): 0.33. Example 46: C-[4-(6-(4-r3-(4-Ethyl-phenyl)-ureido]-phenoxy)-pyrimidin-4-ylamino)-phenyl1-N-methyl-methanesulfonamide 1-Ethyl-4-isocyanato-benzene (25.7 mg, 0.175 mmol) is slowly added to C-{4-[6-(4-amino-phenoxy)-pyrimidin-4-ylamino]-phenyl}-N-methyl-methanesulfonamide (45 mg, 0.117 mmol) and pyridine (18.9 mL, 0.234 mmol) dissolved in THF/DMF (2:1, 3 mL) at 0 °C. After stirring at rt for 4 h, the solvent is evaporated under reduced pressure, and the product is isolated by preparative thin layer chromatography (4 plates of 20 x 20 cm, acetone/CH2CI2 = 3.7) giving the compound of Example 46 as a white solid: M+H = 532.5; 1H-NMR (400 MHz, DMSO-d6): 8.70/8.57(s/s, 2H( NH-urea), 8.33 (s, 1H, pyrimidinyl), 7.59 (d, 9.5 Hz, 2H, p/?eny/-CH2), 7.55 (d, 9.5 Hz, 2H, amino-pfteny/), 7.36 (d, 9.5 Hz, 2H, ethyl-p/7e/7yl), 7.25 (d, 9.5 Hz, 2H, pheny-CH2), 7.10 (d, 9.5 Hz, 4H, ethyl-p/7eny//amino-p/?eny/), 6.83 (m, 2H, NH-sulfonamide), 6.05 (s, 1H, pyrimidinyl), 4.22 (s, 2H, CH2), 2.57 (m, 5H, C^ethyl/NH-Ctf3), 1.16 (t, 7.5 Hz, 3H, CH^ethyl); Rf (acetone/CH2CI2 = 3:7): 0.32. Example 47: 1-(4-[6-(4-Methoxv-phenvlamino)-pyrimidin-4-vloxy1-phenvlV3-(4-morpholin-4-vl-3-trifluoromethyl-phenylVurea [6-(4-AJTiino-phenoxy)-pyrimidin^-yl]-(4-methoxy-phenyl)-amine (Stage 47.1; 200 mg, 0.648 mmol) and triethylamine (0.075 ml, 0,54 mmol) dissolved in CH2Cl2 (6 mL) is slowly added to a solution of triphosgene (64 mg, 0.213 mmol) in CH2CI2 (10 mL) at 4 °C. After stirring at rt ■ for 15 min, a solution of 4-morpholin-4-yl-3-trifluoromethyI-pheny1amine (160 mg, 0.648 mmol) and triethylamine (0.075 mi, 0.54 mmol) in CH2CI2 (6 mL) is added and the reaction mixture is stirred for 2 h. After adding concentrated NaHC03 solution (20 mL), the product is extracted with CH2CI2 (20 ml, 2 x). The combined organic phases are washed with water (20 mL), dried (Na2S04), and concentrated under reduced pressure. The product is purified by flash chromatography (silica gel, 2.5 x 20 cm, MeOH/CH2CI2 = 5:95) giving a white solid: M+H = 580.9; 1H-NMR (400 MHz, DMSO-d6): 9.32 (s, 1H, NH), 9.35/8.78 (s/s, 2H, NH-urea), 8.23 (s, 1H, pyrimidine), 7.89 (s, p/?eny/-CF3), 7.58 (d, 8.5 Hz, 1H, p/7eny/-CF3), 7.53 (d, 8.5 Hz, 1H, pfteny/-CF3), 7.49/7.40/7.08/6.86 (d/d/d/d, 9.0 Hz, 8H, phenyl-oxo/phenyl-OMe), 5.91 (s, 1H, pyrimidinyl), 3.70 (s, 3H, CHT0), 3.66/2.79 (m/m, 4H/4H, morpholinyl); R( (MeOH/CH2CI2 = 5:95): 0.16; HPLC (System 1): 6.31 min. Stage 47.1: [6-(4-Amino-phenoxvVpyrimidin-4-vn-(4-methoxY-phenvlVamine (4-Methoxy-phenyI)-[6-(4-nitro-phenoxy)-pyrimidin-4-yl]-amine (Stage 47.2; 1.06 g, 3.13 mmol) dissolved in THF/EtOH (1:2; 27 mL) is hydrogenated in the presence of Raney-Ni (0.2 g) during '36 h. After filtering off the catalyst and washing with EtOH (20 mL), the solvent is evaporated under reduced pressure and flash chromatographed (silica gel, 4.5 x 26 cm, MeOH/CH2CI2 = 5:95) giving a white solid: M+H = 309.1; 1H-NMR (400 MHz, DMSO-d6): 9.23 (s, 1H. NH-pyrimidinyl), 8.22 (s, 1H, pyrimidine), 7.40/6.85/6.79/6.57 (d/d/d/d, 9.0 Hz, 8H, phenyl-oxoIphenyl-OMe)f 5.81 (s," 1H, pyrimidinyl), 5.07 (s, 2H, NH2), 3.72 (s, 3H, CHrO); Rf (MeOH/CH2CI2 = 1:9): 0.44; HPLC (System 1): 3.45 min. Stage 47.2: f4-Methoxy-phenvl)-r6'(4'nitro-phenoxy)-pyrimidin-4-vn-amine 4-Chloro-6-(4-nitro-phenoxy)-pyrimidine (1 g, 3.97 mmol), p-anisidine (514 mg, 4.178 mmol), and diisopropylethylamine (0.715 mL, 4.178 mmol) dissolved in 2-propanol (27 mL) are stirred under reflux under Ar. After 16h, p-anisidine (245 mg, 1.99 mmol) is added and the reaction mixture is stirred for additional 20 h. After cooling the reaction mixture down to rt, compound of Stage 47.2 precipitates as white crystals: M+H = 339.1; 1H-NMR (400 MHz, DMSO-d6): 9.49 (s, 1H, NH-pyrimidinyl), 8.25 (s, 1H, pyrimidine), 8.23/7.40/6.90 (d/d/d/, 9.0 Hz, 2H/4H/2H, phenyl-oxo/phenyl-OMe), 6.18 (s, 1H, pyrimidinyl), 3.72 (s, 3H, CHrO); Rf (MeOH;CH2CI2 = 1:9): 0.44; HPLC (System 1): 6.15 min. Example 48: N-Methvl-C-f4-(6-(4-[3-(4-morpholin-4-vl-3-trifluoromethvl-phenyl)-ureido1-phenoxv)-pyrimidin-4-vlamino)-ohenyl1-methanesulfonamide 4-Morpholin-4-yI-3-trifluoromethyl-phenylamine (28.8 mg, 0.117 mmol), triethylamine (0.05 mL, 0.36 mmol), and triphosgene (35 mg, 0.117 mmol) are dissolved in CHCI3 (2 ml_) at 0 °C. After stirring at rt for 15 min, C-{4-[6-(4-amino-phenoxy)-pyrimidin-4-ylamino]-phenyl}-N-methyl-methanesulfonamide (45 mg, 0.117 mmol) and triethylamine (0.05 mL) dissolved in DMF/DMSO (4:1; 5 mL) are added and strirring is continued for 16 h. After evaporating the solvent under reduced pressure, the product is isolated by preparative thin layer chromatography (four 20 x 20 cm plates, acetone/CH2CI2 = 3.7) giving the compound of Example 48 as a white solid: M+H = 658.1; 1H-NMR (400 MHz, DMSO-d6): 9.57 (s, 1H, phenyl-yVH-phenyl), 8.97/8.81 (s/s, 2H, NH-urea), 8.34 (s, 1H, pyrimidinyl), 7.89 (s, 1H, phenyl-CF3)t 7.58 (d, 9.0 Hz, 3H, phenyl-CFzlphenyl-CH2)t 7.50 (d, 9.0 Hz, 3H, phenyl-CFz/oxo-phenyl), 7.24 (d, 9.0 Hz, 2H, phenyI-CH2), (d, 9.0 Hz, 2H, oxo-phenyf)t 6.83 (d, 4.0 Hz, 1H, NH-sulfonamide), 6.06 (s, 1H, pyrimidinyl), 4.23 (s, 2H( CH2), 3.64/2.78 (m/m, 4H/4H, morpholinyl), 2.52 (d, 4.0 Hz, CH3-N); Rf (acetone/CH2CI2 = 3:7): 0.40. Example 49:1 -{4-r6-f3-Hvdroxv-phenvlamino)-pvrimidin-4-vloxv1-phenylV3-(4-morpholin-4'Vl-3-trifluoromethvl-phenvn-urea To a solution of 1-(4-{6-[3-(tert-butyl-dimethyl-silanyloxy)-phenylamino]-pyrimidin-4-yloxy}-phenyl)-3-(4-morpholin-4-yl-3-trifluoromethyl-phenyl)-urea (Stage 49.1) (283 mg, 0.415 mmol) in MeCN/THF (1.9 mL/0.95 mL), HF (30 % in pyridine; 0.5 mL) is added at 4 °C. After stirring at rt for 2 h, phosphate buffer (pH = 7, 10 mL) is added and the product is extracted with AcOEt (2 x, 20 mL). The combined organic layers are washed with H20 (20 mL), dried (MgSCs), concentrated under reduced pressure, and flash chromatographed (silica gel, 3.0 x 20 cm, MeOH/CH2CI2 = 5:95) giving a white solid: M+H = 566.9; 1H-NMR (400 MHz, DMSO-d6): 9.40/9.35 (s/s, 2H, NH-urea), 9.05/8.87 (s/s, 2H, OH/NH), 8.33 (s, 1H, pyridinyl), 7.92 (s, 1H, phenyl-CF2), 7.62 (d, 8.5 Hz, 1H, phenyl-OH), 7.52 (d, 9.0 Hz, 3H, phenyl-oxoi'phenyl-CF3), 7.15 (s, 1H, phenyl-OH), 7.13 (d, 9.0 Hz, 2H, phenyl-oxo), 7.06 (t, 9.0 Hz, 1H, phenyl-OH), 6.97 (d, 9.0 Hz, 1H, phenyl-OH), 6.41 (d, 8.5 Hz, 1H, phenyl-CF3), 6.06 (s, 1H, pyrimidinyl), 3.69/2.81 (m/m, 4H/4H, morpholinyl); Rf(MeOH/CH:CI2 = 1:9): 0.31; HPLC (System 1): 5.80 min. Stage 49.1: 1-(4-(6-[3-(tert-Butvl-dimethvl-silanyloxy)-phenylamino1-pyrimidin-4-yloxv)-phenvl)-3-(4-morpholin-4-vl-3-trifluoromethvl-phenyl)-urea [6-(4-Amino-phenoxy)-pyrimidin-4-yl]-[3-(tert-butyl-dimethyl-silanyloxy)-phenyl]-amine (Stage 49.2; 121 mg, 0.489 mmol) and triethylamine (0.057 mL, 0.83 mmol) dissolved in CH2CI2 (6 mL) are added to a solution of triphosgene (48 mg, 0.161 mmol) in CH2CI2 (10 mL) at 4 °C under Ar. After stirring at rt for 15 min, 4-morpholin-4-yl-3-trifluoromethyl-phenylamine (121 mg, 0.489 mmol) and triethylamine (0.057 mL) dissolved in CH2CI2 (6 mL) are added and the reaction mixture is stirred for 2 h at rt. After adding concentrated NaHC03 (20 mL), the reaction mixture is extracted with CH2CI2 (20 ml, 2 x). The combined organic layers are washed with H20, dried (Na2S04), concentrated under reduced pressure, and flash chromatograped (silica gel, 2.5 x 22 cm, MeOH/CH2CI2 = 2:098) to give the compound of Stage 49.1 as a white solid: M+H = 680.9; 1H-NMR (400 MHz, DMSO-d6): 9.49 (s, 1H, NH-pyrimidinyl), 8.94/8.80 (s/s, 2H, NH-urea), 8.33 (s, 1H, pyrimidinyl), 7.89 (s, 1H, phenyl-CF3), 7.59 (d, 8.5 Hz, 1H, phenyl-CF3), 7.50 (d, 9.0 Hz, 3H, phenyl-OTBSIphenyl-oxo), 7.23 (s/broad, 1H, phenyl-OJBS), 7.16 (t, 8.0 Hz, 1H, phenyl-OTBS), 7.11 (d, 9.0 Hz, 3H, phenyl-OTBS/phenyl-oxo), 6.44 (d/broad, 8.0 Hz, 1H, phenyl-CF3), 6.02 (s, 1H, pyrimidinyl), 3.69/2.80 (m/m, 4H/4H, morpholinyl) 0.92 (s, 9H, terf-butyl-Si), 0.20 (s, 6H, Me-Si); Rf (MeOH/CH2CI2 = 5:95): 0.31; HPLC (System 1): 8.54 min. Stage 49.2: f6-(4-Amino-phenoxv)-pvrimidin-4-vll-[3-(tert-butvl-dimethvl-silanyloxv)-phenvn-amine [3-(tert-Butyl-dimethyl-silanyloxy)-phenyl]-[6-(4-nitro-phenoxy)-pyrimidin-4-ylI-amine (Stage 49.3, 1.01 g, 2.306 mmol) dissolved in EtOH/THF (2:1; 26 mL) are hydrogenated in the presence of Raney-Ni (0.2 g) for 22 h. After filtering off the catalyst and washing with EtOH (20 mL), the reaction solution is evaporated and the crude product is flash chromatographed (silica gel, 4.5 x 28 cm, MeOH/CH2CI2 = 2:98) to give compound of Stage 49.2 as a white solid: M+H = 409.1; 1H-NMR (400 MHz, DMSO-d6): 9.39 (s, 1H, NH-pyrimidinyl), 8.35 (s, 1H, pyrimidinyl), 7,23 (s, 1H, phenyi-OTBS), 7.17 (d, 8.5 Hz, 1H,pheny/-OTBS), 7.11 (t, 8.5 Hz, 1H, phenyl-OTBS), 7.16 (t, 8.0 Hz, 1H, phenyl-OTBS)t 7.11 (d, 9.0 Hz, 1H, phenyl-OTBS), 6.82/6.58 (d/d, 8.5 Hz/8.5 Hz, 4H, phenyl-oxo), 6.44 (d, 8.5 Hz, 1H, phenyl-OTBS), 5.92 (s, 1H, pyrimidinyl), 5.09 (s, 2H, NH2), 0.96 (s, 9H, terf-butyl-Si), 0.19 (s, 6H, Me-Si); Rf (MeOH/CH2CI2 = 5:95): 0.32; HPLC (System 1): 6.31 min. Stage 49.3: f3-(tert-Butvl-dimethvl-silanvioxv)-phenvl1-[6-(4-nitro-phenoxv)-pyrimidin-4-vll-amine 3-[6-(4-Nitro-phenoxy)-pyrimidin-4-ylamino]-phenol (Stage 49.4; 830 mg, 2.56 mmol), tert-butyl-dichlorosilane (579 mg, 3.84 mmol), and triethylamine (0.536 mL, 3.84 mmol) dissolved in DMF (11 mL) are stirred under Ar for 3 at rt. After adding H20 (20 mL), the reaction mixture is extracted with CH2CI2 (20 mL, 2 x). The combined organic phases are washed with H20 (10 mL)f dried (Na2SOj), concentrated under reduced pressure, and flash chromatographed (silica gel, 5.5 x 30 cm, MeOH/CH2Cl2 = 5:95) to give the compound of Stage 49.3 as a white solid: M+H = 439.0; 1H-NMR (400 MHz, DMSO-d6): 9.65 (s, 1H, NH-pyrimidinyl), 8.35 (s, 1H, pyrimidinyl), 7.23 (s, 1H, phenyl-OTBS), 7.17 (m, 2H, phenyl-OTBS), 6.50 (d, 8.0 Hz, 1H, p/7eny/-OTBS), 8.29/7.43 (d/d, 8.5 Hz/8.5 Hz, 4H, phenyl-oxo), 6.28 (s, 1H, pyrimidinyl), 0.96 (s, 9H( /erf-butyl-Si), 0.19 (s, 6H, Me-Si); Rf (MeOH/CH2CI2 = 5:95): 0.34; HPLC (System 1): 8.87 min. Stage 49.4: 3-r6-(4-Nitro-phenoxv)-pyrimidin-4-vlamino1-phenol 4-Chloro-6-(4-nitro-phenoxy)-pyrimidine (1 g, 3.97 mmol), 3-amino-phenoI (456 mg, 4.175 mmol), diisopropylethylamine (0.715 mL, 4.175 mmol) dissolved in 2-propanol (17 mL) are stirred under reflux. After 16 and 22 h, the same amount of 3-amino-phenol and diisopropylethylamine is added to the reaction mixture. After 42 h, the solvent is evaporated under reduced pressure, and the reaction mixture is flash chromatographed (silica gel, 4.5 x 26 cm, MeOH/CH2CI2 = 5:95) to give the compound of Stage 49.4 as a white solid: M+H = 325.1; 1H-NMR (400 MHz, DMSO-d6): 9.59/9.37 (s/s, 2H, NH-pyrimidinyl/OH), 8.35 (s, 1H, by hydrogenation in the presence of Raney-Ni in EtOH at 40 °C during 3 h: M+H = 201.0; Rf (CH2CI2/acetone = 85:15): 0.17. 4-(4-Nitro-phenoxymethyl)-pyridine: 4-hydroxymethyl-pyridine (2.23 g, 20 mmol) is added to a suspension of KOH (1.32 g, 20 mmol) and Aliquat 336 (0.937 ml_). After stirring for 5 nnin at rt, 1-chloro-4-nitro-benzene (2.68 g, 16.7 mmol) is added. The resulting reaction mixture is further stirred at rt for 5 min and then at 80 °C for 2 h. The reaction mixture is filtered over si!:ca gel (15 g), concentrated under reduced pressure, and flash chronatographed (silica gel, 3 x 50 cm, acetone/CH2CI2 = 5:95 -> 15:85) to give the title compound as a yellow solid: M+H =231.0; 1H-NMR (400 MHz, DMSO-d6): 8.58 (d, 6.5 Hz, 2H, pyrimidinyl), 8.22 (d, 8.5 Hz, 2H; phenyl-N02), 7.44 (d, 6.5 Hz, pyrimidinyl), 7.21 (d, 8.5 Hz, 2H, phenyl-N02), 5.34 (s, 2H, CH2); Rf(acetone/CH2CI2 = 15:85): 0.32; HPLC (System 1): 3.40 min. The substituted 3-trifluoromethyl-anilines for the synthesis of compounds of Examples 52 and 53 are prepared from the 1-bromo-3-nitro-5-trifluoromethyl-benzene by nucleophilic substitution of the bromine by the corresponding amine and subsequent hydrogenation of the nitro function to the amine by means of Raney-Ni. Example 55: 1-(4-Aminomethvl-phenvl)-3-r4-(pyridin-4-vloxv)-phenvn-urea 4-{3-[4-(Pyridin-4-yIoxy)-phenyl]-ureido}-benzyl)-carbamic acid benzyl ester (Stage 55.1) (0.1 g, 0.213 mmol) dissolved in EtOH/THF (2:1, 6 mL) is hydrogenated in the presence of Pd/C (Engelhard 4505,100 mg) for 5 h. After filltering of the catalyst, the reaction solution is concentrated under reduced pressure and flash chromatographed (silica gel, 2.5 x 46 cm, CH2CI2/MeOH/ cone. NH3 = 9:1:0.01 -» 85:15:0.1) to give the compound of Example 55 as a white solid: M+H = 335.0; Rf (CH2CI2/MeOH/ cone. NH3 = 85:15:0.1): 0.15; HPLC (System 1): 5.74 min. Stage 55.1: 4-(3-f4-(Pvridin-4-vloxv)-phenvl1-ureido)-benzvl)-carbamic acid benzyl ester The compound is synthesized in analogy to the preparation of compound of Example 1 starting from (4-amino-benzyl)-carbamic acid benzyl ester (Stage 55.2): M+H = 469.1; Rf (CH2CI2/MeOH = 85:15): 0.26; HPLC (System 1): 4.85 min. Stage 55.2: (4-amino-benzyl)-carbamic acid benzyl ester After stirring [4-(benzyloxycarbonylamino-methyl)-phenyl]-carba.Tiic acid tert-butyl ester (Stage 55.3) (1.06 g, 2.97 mmol) in TFA/H20 (95:5, 10 mL), the solvent is evaporated in vacuo. The residue is taken up in NaHC03 (20 mL) and extracted with AcOEt (20 mL). The organic phase is dried (MgS04), concentrated under reduced pressure, and flash chromatographed (silica gel, 4.5 x 52 cm, MeOH/CH2CI2 = 5:95) to give the compound of Stage 55.2 as a colorless solid: M+H = 257.1; Rf (CH2CI2/MeOH = 95:5): 0.67; HPLC (System 1): 3.62 min. Stage 55.3: r4-(benzyloxvcarbonylamino-methyl)-phenvn-carbamic acid tert-butyl ester To a solution of 4-(aminomethyl)-1-N-Boc-aniline (1 g, 4.5 mmol) dissolved in CH2CI2 (10 mL), triethylamine (0.626 mL, 4.5 mmol) and chloro-formic acid benzyl ester (0.698 mL, 4.95 mmol) are added, the reaction solution is stirred at rt for 2 h, taken up in CH2CI2 (10 mL) and washed with concentrated NaHC03 solution (20 mL) and H20 (20 mL). The aqueous phase is washed with CH2CI2 (20 mL). The combined organic phases are dried (Na2S04), concentrated under reduced pressure and flash chromatographed (silica gel, 3.5 x 60 cm, AcOt/hexane = 1:4) to give the compound of Stage 55.3 as a white solid: M+H = 355.1; Rf (AcOEt/hexane = 1:4): 0.15; HPLC (System 1): 6.53 min. Example 56: 1 'r4-f6-Chloro-pvrimidin-4'Vloxv)-phenvl1-3-f3-trifluoromethyl-phenyl)-urea After stirring 3-trifIuoromethyl-phenyl isocyanate (412 mg , 2.2 mmol), 4-(6-chloro-pyrimidin-4-yloxy)-aniline (Stage 56.1; 0.25 g, 1.1 mmol), and pyridine (0.18 mL) overnight, the reaction solution is concentrated under reduced pressure and flash chromatographed (silica gel, 2.5 x 17 cm; acetone/CH2CI2 = 5:95 -> 1:9) to give the compound of Example 56 as a white solid material: M+H = 408.9/410.9; 1H-NMR (400 MHz, DMSO-d6): 9.07 (s, 1H, NH), 8.89 (s, 1H, NH), 8.63 (d, 2.0 Hz, 1H, pyridinyl), 8.01 (s, 1H, 3-CF3-p/?eny/)f 7.57 (d/broad, 8.0 Hz, 1H, CF3-phenyf), 7.52 (d, 9.5 Hz, 2H, oxo-p/7eny/-amine), 7.50 (m, 1H, 3-CF3-phenyl), 7.32 (d, 2.0 Hz, 1H, pyridinyl), 7.29 (d/broad, 8.0 Hz, 1H, -CF3-phenyl), 7.15 (d, 9.5 Hz, 2H, oxo-p/7eny/-amine), (d, 6.5 Hz, 2H, pyridinyl); Rf (acetor.e/CH2CI2 = 1:9): 0.54; m.p. = 187.4-189.7 °C. Stage 56.1: 4-(6-chloro-pyrimidin-4-vloxY)-aniline 4-Chloro-S-(4-nitro-phenoxy)-pyrimidine (Stage 56.2; 3.6 g, 14.3 mmol) dissolved in MeOH (250 ml_) is hydrogenated in the presence of Raney-Ni (3 g) at 40 °C for 3 d. The reaction solution is filtred, concentrated under reduced pressure and crystalized from AcOEt/hexane to give the compound of Stage 56.1: M+H = 222/224; 1H-NMR (400 MHz, DMSO-d6): 8.62 (s, 1H, piperidinyl), 7.13 (s, 1H, piperidinyl), 6.83 (d, 9 Hz, 2H, phenyl), 6.56 (d, 9Hz, 2H, phenyl), 5.12 (s, 2H, NH2); m.p. = 135.5-138.1 °C. Stage 56.2: 4-Chloro-6-(4-nitro-phenoxv)-pyrimidine 4-Nitrophenol (2.8 g, 20.1 mmol), 2,4-dichloro-pyrimidine (3 g, 20.1 mmol), NaOH (0.8 g, 20.1 mmol) dissolved in H20/acetone (80 mL; 1:1) are stirred at 60-65 °C for 1 h. The reaction solution is concentrated under reduced pressure and flash chromatographed (silica gel, 4.5 x 22 cm, AcOEt/hexane = 1:4) to give the compound of Stage 56.2 as a white solid material: M+H = 252/254; 1H-NMR (400 MHz, DMSO-d6): 8.67 (s, 1H, piperidinyl), 8.34 (d, 9 Hz, 2H, phenyl), 7.58 (d, 9Hz, 2H, phenyl), 7.53 (s, 1H, piperidinyl); Rf (AcOEt/hexane = 1:1): 0.16; m.p. = 125.4-126.6 °C. Example 57: 1 -r4-(6-Methvlamino-pvrimidin-4-vloxv)-phenvll-3-(3-trifluoromethyl-phenvl)-urea 1-[4-(6-Chloro-pyrimidin-4-yloxy)-phenyl]-3-(3-trifluoromethyl-phenyl)-urea (Example 56) (42.7 mg, 0.1 mmol) is dissolved in methylamine (30 % in EtOH, 1 mL) in a sealable tube and heated under Ar for 10 min at 50 °C. After evaporating the solvent, the product is purified by preparative TLC (2 20 * 20 cm plates, acetone/CH2CI2 = 3:7) to give the title compound as a white solid: M+H = 404.1; 1H-NMR (400 MHz, CDCI3): 8.22 (s, 1H, pyridinyl), 7.84 (s/broad, 1H, NH), 7.62 (s, 1H, 3-CF3-phenyl), 7.52 (d, 8.0 Hz, 1H, CFTphenyl), 7.35 (t, 8.0 Hz, 1H, 3-CFrphenyl), 7.28 (m, 3H, CFz-phenyl/oxo-phenyl-amme), 6.97 (d, 9.5 Hz, 2H, 9:1): 0.42; 1H-NMR (400 MHz, DMSO-d5): 8.93/8.80 (s/s, 2H, urea), 7.91 (d, 2 Hz, 1H, pyrimidinyl), 7.51 (d, 9.5 Hz, 2H, phenyl), 7.47 (d, 8.0 Hz, 1H, phenyl-CF3), 7.29 (d, 8 Hz, 1H, pherr,]-CF3), 7.27 (s, 1H, phenyl-CF3),7.13 (d, 9.5 Hz, 2H, phenyl), 4.08 (m, 1H, pyrimidinyl), 2.63 (s/broad, 3H, CH3); m.p. = 183.0 - 184.5 °C. Example 77: 1-r4-(6-Amino-pvrimidin-4-yloxy)-phenvn-3-(3-trifluoromethvl-phenyl)-urea Compound of Example 56 (50 mg, 0.122 mmol) is dissolved in 2 mL EtOH and 2 m!_ NH3 (25 % aqueous) and stirred at 80 °C in a sealed tube for 13 h. After evaporating the solvent under reduced pressure, the product is isolated by TLC (two 20 x 20 cm plates, 10 % MeOH in CH2CI2): M+H = 390.0; R, (CH2CI2/MeOH = 9:1): 0.15; 1H-NMR (400 MHz, DMSO-d6): 9.07/8.87 (s/s, 2H, urea), 7.98 (s/broad, 1H, pyrimidinyl), 7.56 (d, 8.0 Hz, H, phenyl-CF3), 7.47 (d, 8.0 Hz, 1H, phenyl-CF3), 7.49 (d, 8.5 Hz, 2H, phenyl), 7.46 (s, 1H, phenyl-CF3), 7.27 (d, 8.0 Hz, 1H, phenyl-CF3),7.04 (d, 8.5 Hz, 2H, phenyl), 6.77 (s/broad, 2H, NH2), 5.64 (s/broad, 1H, pyrimidinyl). Example 78: 1 -f4-(2-Chloro-pvrimidin-4-yloxv)-phenvll-3-(4-ethvl-phenvl)-urea The title compound is synthesized in analogy to the preparation of compound of Example 56: M+H = 369.0/371.0; R, (Hexane/AcOEt = 1:1): 0.31; Anal.: C: 62.20 % (61.88 %), H: 4.85 % (4.65 %), N: 14.73 % (15.19 %). Example 79: 1 -f4-(2-Chloro-pvrimidin-4-vloxy)-phenvn-3-(4-piperidin-1 -yl-3-trifluoromethyl-phenvD-urea The title compound is synthesized in analogy to the preparation of compound of Example 56: M+H = 491.9/493.9; Rf (Hexane/AcOEt = 1:1): 0.38; Anal.: C: 55.67 % (56.16 %), H: 4.32 % (4.30 %), N: 13.62 % (14.24 %). Example 80: N-(4-(6-Chloropvrimidin-4-vl-oxv)-phenyl)-N'-(4-fe^-butvlphenvl)-urea To a solution of 4-(6-chloro-pyrimidin-4-yl-oxy)-aniline (Stage 21.1; 3.77 g, 15 mmol) in THF (55 ml) under ^-atmosphere, 4-terf-butylphenyl isocyanate (5.26 g, 30 mmol) dissolved in THF (5 ml) is added. During stirring for 1 h at rt a suspension is formed. The mixture is then re-dissolved in AcOEt and a solution of NaHC03 in water, the aqueous layer separated off and extracted twice with AcOEt. The organic phases are washed with water and brine, dried (Na2S04) and concentrated in vacuo. Stirring of the resulting solid in Et20 finally yields the title compound: m.p.: 111-112 °C; 1H-NMR (DMSO-d6): 8.75 (s. HN), 8.65 (s, 1H), 8.62 (s, HN), 7.51 (d, 2H), 7.36 (d, 2H), 7.33 (s, 1H), 7.31 (d, 2H), 7.17 (d, 2H), 1.27 (Me3C). Example 81: N-f4-(6-Chloropvrimidin-4-vl-oxv)-phenvn-N,-(4-chlorO"3-trifluoromethyl'PhenvlV urea To a solution of 4-(6-chloro-pyrimidin-4-yl-oxy)-aniline (Stage 21.1; 3.77 g, 15 mmol) in THF (40 ml) under N2-atmosphere, 4-chloro-3-trifluoromethylphenyl isocyanate (4.98 g, 22.5 mmol) dissolved in THF (20 ml) is added. After 1 h at rt the solution is diluted with AcOEt and NaHC03 in water, the aqueous layer separated off and extracted twice with AcOEt. The organic phases are washed with water and brine, dried (Na2S04) and concentrated in vacuo. Stirring of the resulting solid in Et20 finally yields the title compound: m.p.: 180-181 °C; 1H- NMR (DMSO-d6): 9.22 (s, HN), 8.97 (s, HN), 8.65 (s, 1H), 8.11 (s, 1H),7.65(mf 1H), 7.63 (m, 1H), 7.53 (d, 2H), 7.34 (s, 1H), 7.19 (d, 2H); Anal.: CHNCIFO. Example 82: N-(4-(4-Methvlaminopyrimidin-6-vl-oxv)-phenvn-N'-(4-fe/t-butvlDhenyl)-urea Under N2-atmosphere, a solution of N-(4-(4-chloropyrimidin-6-yl-oxy)-phenyl)-N'-(4-te/t-butylphenyl)-urea (319 mg, 0.80 mmol) in methylamine/ethanol (8.03 M; 5 ml) is stirred for 50 min at 40 °C. Then the reaction mixture is concentrated in vacuo, the residue re-dissolved in water and AcOEt, the aqueous layer separated off and extracted twice with AcOEt. The organic phases are washed with water and brine, dried (Na2S04) and concentrated in vacuo after adding 2 g of Si02. The resulting powder is put on top of a Si02-column and eluted with AcOEt/hexane 9:1, yielding the title compound: m.p.: 245-246 °C; 1H-NMR (DMSO-d6): 8.7 (s, HN), 8.6 (s, HN), 8.13 (s, 1H), 7.45 (d, 2H), 7.35 (d, 2H), 7.31 (d, 2H), 7.05 (d, 2H), 6.78 (s, HN), 5.79 (s, 1H), 2.83 (MeN), 1.30 (Me3C). Example 83: N-(4-(4-Benzvlaminopyrimidin-6-vl-oxv)-phenvl)-N,-(4-feAf-butvlphenvl)-urea Under N2-atmosphere, a suspension of N-(4-(4-chloropyrimidin-6-yl-oxy)-phenyl)-N,-(4-teAf-butylphenyl)-urea (397 mg, 1.00 mmol) and benzylamine (327 JIM) in isopropanol (3 ml) is stirred for 21 h at 70 °C. Then the reaction mixture is concentrated in vacuo, the residue re-dissolved in saturated NaHC03 solution and AcOEt, the aqueous layer separated off and extracted twice with AcOEt. The organic phases are washed with water and brine, dried (Na2S04) and concentrated. The crude product is dissolved in CH2CI2 and after addition of Si02 again concentrated. The resulting powder is put on top of a Si02-column and eluted with AcOEt/hexane 3:1, yielding the title compound: m.p.: 118-120 °C; 1H-NMR (DMSO-d6): 8.73 (s, HN), 8.62 (s, HN), 8.13 (s, 1H), 7.84 (s, HN), 7.46 (d, 2H), 7.35 (d, 2H), 7.30 (m, 4H). 7.28 (m, 2H), 7.24 (m, 1H), 7.03 (d, 2H), 5.78 (s, 1H), 4.49 (s, 2H), 1.26 (Me3C). Example 84: N-(4-(4-Aminopvrimidin-6-vl-oxyVphenvl)-N'-(4-chloro-3-trifluoromethvl-phenvl)-urea In a sealed tube under N2-atmosphere, N-(4-(4-chloropyrimidin-6-yl-oxy)-phenyl)-N'-(4-chloro-3-trifluoromethyl-phenyl)-urea (443 mg, 1.00 mmol) and 25 % aqueous NH3 (2 ml) in ethanol (2 ml) is stirred for 22 h at 80 °C. Then the reaction mixture is diluted with water and AcOEt, the aqueous layer separated off and extracted 3 times with AcOEt. The organic phases are washed with 3 portions of water and brine, dried (Na2S04) and concentrated. Column chromatography (Si02; CH2CI2/MeOH 9:1) yields the title compound: m.p.: 197-198 °C; 1H-NMR (DMSO-d6): 9.20 (s, HN), 8.93 (s, HN), 8.12 (m, 1H), 8.08 (s, 1H), 7.63 (m, 2H), 7.51 (d, 2H), 7.08 (d, 2H), 6.82 (s, H2N), 5.67 (s, 1H). Example 85: N-(4-(4-Chloropyrimidin-6-yl-oxy)-phenvl)-N'-(3-methoxv-4-piperidin-1 -yl-phenyQ-urea A solution of triphosgene (1.4 g, 4.7 mmol) in CH2CI2 (95 ml) under N2-atmosphere is cooled by an ice bath. 3-Methoxy-4-piperidin-1-yl-phenylamine (Stage 85.1; 2.95 g, 14.3 mmol) and NEt3 (2.0 ml; 14.3 mmol) in CH2CI2 (48 ml) is then added dropwise and the resulting suspension stirred for 20 min at rt. Then a solution of 4-(6-chIoro-pyrimidin-4-yl-oxy)-aniline (Stage 21.1; 3.17 gt 14.3 mmol) and NEt3 (2.0 ml; 14.3 mmol) in CH2CI2 (48 ml) is added dropwise, whereby a brown solution is formed, which is stirred for 4.5 h at rt. The reaction mixture is added to saturated NaHC03 solution (0.3 L) and extracted with CH2CI2. The organic phase is washed with water and brine, dried (Na2S04) and concentrated. The crude product is dissolved in AcOEt/methanol, Si02 is then added and the solvent evaporate off//? vacuo. The resulting powder is put on top of a chromatography column (Si02; AcOEt/hexane 4:1) and the title compound eluted with AcOEt/hexane 4:1: m.p.: 175 °C; 1H-NMR (DMSO-d6): 8.68 (s, 1H), 8.62 (s, 1H), 8.50 (s, 1H), 7.50 (d, 2H), 7.30 (s, 1H), 7.13 (m, 3H), 6.85 (d, 1H), 6.77 (d, 1H). 3.75 (s, 3H), 2.82 (m, 4H), 1.60 (m, 4H), 1.49 (m, 2H). The starting materials are prepared as follows: Stage 85.1: 3-Methoxv-4-piperidin-1-vl-phenylamine 1-(2-Methoxy-4-nitro-phenyI)-piperidine (Stage 85.2; 4.0 g, 17 mmol) in ethanol/THF 5:1 (90 ml) is hydrogenated in the presence of Pd/C 10 % ("Engelhard 4505"; 0.4 g). Then the catalyst is filtered off and the filtrate is concentrated yielding the title compound: 1H-NMR (DMSO-d6): 6.58 (d, 1H), 6.19 (d, 1H), 6.04 (dd, 1H), 4.66 (s, H2N), 3.65 (s, H3CO), 2.70 (m, 4H), 1.56 (m,4H), 1.43 (m, 2H). Stage 85.2: 1-(2-Methoxv-4-nitro-phenyl)-piperidine 2-Bromo-5-nitroanisole (5.0 g, 21.5 mmol) and piperidine (8.5 ml) is stirred for 5 h at 105 °C under N2-atmosphere. Water (80 ml) is added and the mixture is extracted twice with CH2CI2 (2 x 80 ml). The organic phases are washed with water and brine, dried (Na2S04) and concentrated. The crude product is dissolved in AcOEt, Si02 is then added and the solvent evaporate off in vacuo. The resulting powder is put on top of a chromatography column (Si02; AcOEt/hexane 9:1) and the title compound eluted with hexane/AcOEt 9:1 ->4:1: MS: [M+1f=237; Rf = 0.2 (AcOEt/hexane 9:1). Example 86: N-(4-(6-Chloropvrimidin-4-vl-oxv)-phenv0-N'-(4-(4-ethyl-piperazin-1 -yl)-3-methoxy-phenyQ-urea The title compound is prepared from 4-(4-ethyl-piperazin-1-yl)-3-methoxy-phenylamine (Stage 86.1; 3.99 g, 16.5 mmol) and 4-(6-chloro-pyrimidin-4-y!-oxy)-aniline (Stage 21.1; 3.67 g, 16.5 mmol) analogously to Example 85: m.p.: 170-171 °C; 1H-NMR (DMSO-d6): 8.67 (s, 1H), 8.61 (s, 1H), 8.52 (s, 1H), 7.48 (d, 2H), 7.28 (s, 1H), 7.15 (d, 1H), 7,12 (d, 2H), 6.84 (d, 1H), 6.77 (d, 1H), 3.74 (s, 3H), 2.86 (m, 4H), 2.44 (m, 4H), 2.33 (q, 2H), 0.98 (t, H3C); Anal.: CHNCI. The starting materials are prepared as follows: Stage 86.1: 4-(4-Ethyl-piperazin-1-yl)-3-methoxv-phenylamine 1-Ethy!-4-(2-methoxy-4-nitro-phenyi)-piperazine (Stage 86.2; 2.89 g, 11 mmol) in ethanol/THF 5:1 (70 ml) is hydrogenated in the presence of Pc/C 10 % ("Engelhard 4505"; 0.3 g). Then the catalyst is filtered off and the filtrate is concentrated yielding the title compound: 1H-NMR (CD3OD): 6.79 (d, 1H), 6.44 (d, 1H), 6.29 (dd, 1H), 3.80 (s, H3CO), 2.97 (m, 4H), 2.65 (m, 4H), 2.52 (q. 2H), 1.14 (t, H3C). Stage 86.2: 1-Ethvl-4-(2-methoxy-4-nitro-phenyl)-piperazine 2-Bromo-5-nitroanisoIe (4.7 g, 20 mmol) and N-ethyl-piperazin (10.3 ml) is stirred for 13 h at 110 °C under N2-atmosphere. Water (80 ml) is added and the mixture extracted twice with CH2CI2 (2 x 80 ml). The organic phases are washed with water and brine, dried (Na2S04) and concentrated. Column chromatography (Si02; CH2CI2/MeOH 19:1 -> 9:1) gives the title compound: m.p.: 84-85 °C. Example 87: N-(4-(4-Chloropvrimidin-6-vl-oxv)-phenyl)-N,-(3-methoxy-4-(piperidin-1-ylmethyl)-phenyl)-urea The title compound is prepared from 3-methoxy-4-(piperidin-1-ylmethyl)-phenylamine (Stage 87.1) and 4-(6-chloro-pyrimidin-4-yI-oxy)-aniline (Stage 21.1) analogously to Example 85: MS: [M+1]+=468. The starting materials are prepared as follows: Stage 87.1: 3-Methoxv^(piperidin-1-ylmethvl)-phenvlamine Hydrogenation of 1-(2-methoxy-4-nitro-benzyl)-piperidine (Stage 87.2) in THF with Raney Nickel as catalyst affords the title compound: MS: [M+1]+=221. Stage 87.2: 1-(2-Methoxy-4-nitro-benzylVpiperidine (2-Methoxy-4-nitro-phenyl)-piperidin-1-yl-methanone (Stage 87.3; 200 mg, 0.76 mmol) is dissolved in THF (8 ml) at -20 °C. DIBAH (1 M in THF: 2.3 ml) then is added. After 90 min at -20 °C, another portion of DIBAH (0.8 ml) is added and stirring continued for 2 h. Then the reaction mixture is hydrolysed by water (30 ml) and a saturated solution of sodium potassium tartrate (25 ml) and extracted 3 times with AcOEt. The organic phases are washed with brine, dried (Na2S04) and concentrated. The crude product is dissolved in AcOEt, Si02 is then added and the solvent evaporate off in vacuo. The resulting powder is put on top of a chromatography column (Si02; AcOEt) and the title compound eluated with AcOEt: 1H-NMR (DMSO-d6): 7.83 (dd, 1H), 7.73 (d, 1H), 7.60 (d, 1H), 3.91 (s, H3CO), 3.49 (s, 2H), 2.36 (m, 4H), 1.52(m, 4H), 1.39 (m,2H). Stage 87.3: (2-Methoxv^-nitro-phenYl)-piperidin-1-yl-methanone To an ice-cooled suspension of 2-methoxy-4-nitro-benzoic acid (5.915 g, 30 mmol) in acetonitrile (50 ml) and CH2CI2 (40 ml) under N2-atmosphere, TPTU (8.912 g, 30 mmol) and NEt3 (8.36 ml, 60 mmol) is added. After stirring for 40 min, piperidine (3.26 ml, 33 mmol) is added and the reaction mixture is slowly warmed up to rt. After 16 h, AcOEt (0.5 L), water (0.4 L) and saturated NaHC03 solution (0.2 L) is added, the aqueous phase separated off and extracted 3 x with AcOEt. The organic layers are washed with 10 % citric acid solution, water and brine, dried (Na2S04) and concentrated. Crystallization from AcOEt/hexane yields the title compound: m.p.: 104 °C; 1H-NMR (DMSO-d6): 7.88 (dd. 1H), 7.84 (d, 1H), 7.47 (d, 1H), 3.93 (s, H3C), 3.7-3,5 (m, 2H), 3.07 (m, 2H), 1.64-1.5 (m, 4H), 1.42 (m, 2H). Example 88: The following compounds can be prepared analogously to the described procedures (Table 7): To a solution of 4-(4-ethylaminopyrimidin-6-yl-oxy)-aniline (Stage 89.1; 271 mg, 1.177 mmol) in THF (5 ml) under N2-atmosphere, fran$-2-phenyl-cyclopropyl-isocyanate (188 mg, 1.18 mmol; Aldrich) is added. Then the solution is stirred for 8 h, whereas a precipitate is formed. Filtration and washing with THF and ether yields the title compound: m.p.: 205-206 °C; 1H-NMR (DMSO-de): 8.50 (s, HN), 8.11 (s, 1H), 7.42 (d( 2H), 7.27 (m, 3H), 7.15 (m, 3H), 7.01 (d, 2H), 6.67 (s, HN), 5.67 (s, 1H), 3.25 (m, 2H), 2.74 (m, 1H), 1.98 (m, 1H), 1.17 (m, 2H), 1.09 (t,3H); Anal.: CHN. The starting materials are prepared as follows: Stace 89.1: 4-(4-Ethvlaminopyrimidin-6-vl-oxY)-aniline A suspension of 4-(6-chIoro-pyrimidin-4-yl-oxy)-aniline (Stage 21.1; 5.0 g, 22.6 mmol) in ethyiamine dissolved in ethanol (« 35 %; 5 ml) under N2-atmosphere is stirred for 16h at rt. Then the resulting brown solution is diluted with water and AcOEt, the aqueous layer separated off and extracted twice with AcOEt. The organic phases are washed with 3 portions of water and brine, dried (Na2S04) and concentrated. Re-crystallisation from boiling AcOEt gives the title compound: m.p.: 143-145 CC; 1H-NMR (CDCI3): 8.24 (s, 1H), 7.24 (s, HN), 6.91 (d, 2H), 6.69 (d, 2H), 5.63 (s, 1H), 4.97 (s, H2N), 3.25 (m, 2H), 1.25 (t, 3H). More product can be isolated from the filtrate of the re-crystallization by column chromatography (Si02; AcOEt->AcOEt/EtOH 19:1). Example 90: N-(4-(4-Ethvlaminopvrimidin-6-vl-oxvVphenvl)-N'f(R)-5-bromo-indan-2-vn-urea (method B) A solution of triphosgene (117 mg, 0.393 mmol) in CH2CI2 (12 ml) under N2-atmosphere is cooled by an ice bath. A solution of [(R)-5-bromo-indan-2-yl-amine (250 mg, 1.178 mmol; preparation see Adv. Synth. Catal. 2001, 343, 461) and NEt3 (164 yd] 1.177 mmol) in CH2CI2 (10 ml) is added dropwise, the dropping funnel rinsed with CH2CI2 (2 ml) and the resulting suspension stirred for 60 min at rt. Then a solution of 4-(4-ethylaminopyrimidin-6-yI-oxy)-aniline (258 mg, 1.12 mmol) and NEt3 (164 jal; 1.177 mmol) in CH2CI2 (10 ml) is added dropwise and the dropping funnel rinsed with CH2CI2 (2 ml). A brown solution is formed, which is stirred for 16 h at rt. Si02 is then added to the resulting mixture. After concentration in vacuo, the powder is put on top of a MPLC column (Si02). Eluation with Si02/AcOEt 4:1 -» AcOEt, partial concentration and filtration of the crystallized material yields the title compound: m.p.: 247 °C; 1H-NMR (DMSO-d6): 8.33 (s, 1H), 8.06 (s, 1H), 7.43 (s, 1H), 7.36 (d, 2H), 7.30 (m, 1H), 7.26 (t, 1H), 7.19 (d, 1H), 6.96 (d, 2H), 6.43 (d, 1H), 5.63 (s, 1H), 4.40 (m, 1H), 3.2 (m, 4H), 2.75 (ABxd, 2H), 1.07 (t, 3H); Anal.: CHNBr. Example 91: The following compounds can be prepared analogously to the described procedures (Table 8): Stage 92.1: 4-(4-Amino-phenoxvV2-methoxv-pyridine Hydrogenation of 2-methoxy-4-(4-nitro-phenoxy)-pyridine (Stage 92.2; 0.12 g, 0.5 mmol) in AcOEt (10 ml) in the presence of Raney Nickel (20 mg) affords after filtration and concentration of the filtrate the title compound: 1H-NMR (CDCI3): 7.97 (d, 1H), 6.86 (d, 2H), 6.67 (d, 2H), 6.48 (d, 1H), 6.13 (s, 1H), 3.89 (s, H3CO), 3.70 (s, H2N). Staoe 92.2: 2-Methoxv-4-(4-nitro-phenoxy)-pyridine (A) and 1-methyl-4-(4-nitro-phenoxy)-1H-pvridin-2-one(B) In a sealed tube under N2-atmosphere, 4-(4-nitro-phenoxy)-1H-pyridin-2-one (Stage 92.3; 800 mg, 3.45 mmol), Ag2C03 (552 mg, 2.0 mmol), methyl-jodide (474 yi\y 7.6 mmol) and acetonitrile (70 ml) are stirred for 16 h at 60 °C. The reaction mixture is filtered through Celite, the filtrate concentrated and chromatographed (Si02; AcOEt) yielding (A) followed by (B): 1H-NMR (DMSOd5) (A): 8.32 (d, 2H), 8.18 (d, 1H), 7.37 (d, 2H), 6.78 (d, 1H), 6.49 (s, 1H), 3.86 (s, H3CO); (B): 8.30 (d, 2H), 7.80 (d, 1H), 7.40 (d, 2H), 6.15 (d, 1H), 5.80 (s, 1H), 3.40 (s, H3CO). Stage 92.3: 4-(4-Nitro-phenoxy)-1H-pyridin-2-one A suspension of 2,4-dihydroxy-pyridine (2.33 g, 21 mmol), 4-fluoro-nitrobenzene (2.22 ml, 21 mmol) and Cs2C03 (10.2 g, 31.3 mmol) in N-methyl-pyrrolidine (30 ml) is stirred for 3 h at 100 °C under N2-atmosphere. The reaction mixture is poured into water and the precipitate filtered off and washed with water. The solid is dissolved in CH2CI2/MeOH. Then Si02 (~ 20 g) is added and the mixture is concentrated in vacuo. The resulting powder is put on top of a Si02-column and eluted with toiuene/AcOEt 3:1 -> AcOEt -> AcOEt/EtOH 9:1, yielding the title compound: m.p.: 227-228 °C; 1H-NMR (DMSO-d6): 11.60 (s, HN), 8.31 (d, 2H), 7.47 (d, 1H), 7.39 (d, 2H), 6.07 (dd, 1H), 5.67 (d, 1H). Example 93: N-(4-(1-H-6-oxo-1 The title compound is prepared from 3-(4-amino-phenoxy)-1H-pyridin-6-one (Stage 93.1; 1.00 mmol) and 4-ferf-butyl-phenyl-isocyanate (346 }il, 2.0 mmol) in THF (10 ml) analogously to Example 89: m.p.: 234 °C; Anal.: CHN. The starting materials are prepared as follows: Stace 93.1: 3-(4-amino-phenoxvV1H-pyridin-6-one Hydrogenation of 3-(4-nitro-phenoxy)-1H-pyridin-6-one (Stage 93.2; 464 mg, 2.0 mmol) in DMEU (10 ml) in the presence of Raney Nickel (100 mg) affords after filtration and concentration of the filtrate the title compound: 1H-NMR (DMSO-d5): 11.2 (s, HN), 7.25 (dd, 1H), 7.11 (d, 1H), 6.68 (d, 2H), 6.51 (d, 2H), 6.35 (d, 1H), 4.87 (s, H2N). Stage 93.2: 3-(4-Nitro-phenoxy)-1H-pyridin-6-one A suspension of 2,5-dihydroxy-pyridine (4.65 g, 41.9 mmol), 4-fIuoro-nitrobenzene (2.22 ml, 21 mmol) and Cs2C03 (13.7 g, 41.9 mmol) in N-methyl-pyrrolidine (60 ml) is stirred for 18 h at 90 °C under N2-atmosphere. The reaction mixture is diluted with water and AcOEt, the aqueous layer separated off and extracted twice with AcOEt. The organic phases are washed with a NaHC03 solution and brine, dried (Na2S04) and partially concentrated. Thereby the title compound crystallizes and can be filtered off and washed with AcOEt: m.p.: 214-217 °C; 'H-NMR (DMSO-d5): 11.6 (s, HN), 8.22 (d, 2H), 7.57 (d, 1H), 7.43 (dd, 1H), 6.14 (d,2H),6.46(d,1H). Example 94: The following compounds can be prepared analogously to the described procedures (Table 9): The title compound is prepared from 4-(6-methoxy-pyridin-3-yImethyl)-phenylamine (Stage 95.1; 300 mg, 1.40 mmol) and 4-methyl-phenyl-isocyanate (0.35 ml, 2.8 mmoi) in THF (11 ml) analogously to Example 89:1H-NMR (DMSO-d6): 8.68 (s, 2 HN), 8.02 (d, 1H), 7.49 (dd, 1H), 7.33 (d, 2H), 7.29 (d, 2H), 7.09 (d, 2H), 7.03 (d, 2H), 6.70 (d, 1H), 3.79 (2s, 5H), 2.21 (s, 3H). The starting materials are prepared as follows: Stage 95.1: 4-(6-methoxv-pvridin-3-vlmethvl)-phenylamine Rac-(6-methoxy-pyridin-3-yl)-(4-nitro-phenyl)-methanol (Stage 95.2; 5.4 g, 21 mmol) in methanol (0.3 L) is hydrogenated with Pd/C 10 % ("Engelhard 4505"; « 5 g) as catalyst for 3 days under 1 atmosphere H2-pressure. Then the catalyst is filtered off, the filtrate concentrated and chromatographed (Si02; hexane/AcOEt 3:2 -^ 1:1) yielding the title compound: 1H-NMR (CDCI3): 7.99 (d, 1H), 7.34 (dd, 1H), 6.95 (d, 2H), 6.65 (d, 1H), 6.62 (df 2H)f 3.93 (s, H3CO), 378 (sf 2H), 3.6 (sb, H2N). Stage 95.2: RaC'(6-methoxv-pyridin-3-vl)-f4'nitro-phenvlVmethanol A solution of n-butyl-Iithium (1.6 m in hexane; 28 ml, 44.8 mmol) in ether (40 ml) is cooled down to -50 DC in a dried vessel under an atmosphere of N2. Then a solution of 5-bromo-2-methoxy-pyridine (5.7 ml, 44 mmol) in ether (48 ml) is added dropwise, whereby a yellowish suspension is formed, and the reaction mixture stirred for 1 h at -50 °C. In a second vessel, 4-nitro-benzaldehyde (6.04 g, 40 mmol) in THF (60 ml) is prepared at -60 °C. Then the yellowish suspension of 5-ifthio-2-methoxy-pyridine is transferred via canula into the second vessel. After 30 min stirring at-40 °C, a mixture of water (20 ml) and saturated NH4CI-solution (10 ml) is added. The resulting mixture is poured into water and AcOEt, the aqueous layer separated off and extracted twice with AcOEt. The organic phases are washed with water and brine, dried (Na2S04) and concentrated. Column chromatography (Si02; The title compound is prepared in analogy to Example 97 and purified by flash chromatography (Si02, gradient hexanes/ethyl acetate 7:3 to 4:6) to yield a white powder: m.p. = 180 -183 °C; 1H-NMR (DMSO-d6): 9.15 (s, 1H, HIM), 8.90 (s, 1H, HN), 8.81 (s, 1H), 8.00 (s, 1H), 7.59-7.40 (m, 3H), 7.37-7.29 (m, 2H), 7.16 (d, 2H). Example 99: 1 -r4-(6-Ethvl-pyrimidin-4-vloxv)phenvl1-3-p-tolvl-urea 1-[4-(6-Chioro-pyrimidin-4-yloxy)-phenyl]-3-p-toiyl-urea (Example 97; 106 mg, 0.3 mmol) is dissolved in THF (10 mL) under an argon atmosphere and CuCN (215 mg, 2.4 mmol) is added. The mixture is then cooled to -78 °C and EtMgBr (1.8 ml of a 3 M solution in THF) is added via a canula. The reaction mixture is allowed to stir for 30 min at -78 °C and then warmed to rt resulting in a brown suspension. It is stirred for additional 30 min at rt and then the solvent is removed in vacuo. The residual crude product is re-dissloved in CH2CI2/MeOH 1:1 and purified by flash chromatography (Si02, gradient hexanes/ethyl acetate 1:1 to 3:7) to give the title compound which is further purified by preparative TLC (Si02, hexanes /AcOEt 3:7): m.p. = 160-162 °C; C20H20N4O2: M+= 349.1; 1H-NMR (DMSO-d6): 9.55 (s, 1H, HN), 9.45 (s, 1H, HN), 8.64 (s, 1H), 7.55 (d, 2H); 7.40 (d, 2H), 7.10-7.06 (m, 4H), 6.92 (s, 1H), 2.70 (q, 2H), 2.24 (s, 3H), 1.22 (t,3H). The following Examples 100 a) - g) of Table 10 are prepared in analogy to the procedure of Example 99: 4-ChIoro-pyridine-2-carboxylic acid methylester (200 mg, 1.17 mmol) and MgCI2 (555 mg, 0.58 mmol) are suspended in THF (5 mL) at rt. The mixture is stirred for 5 min and then pyrrolidine (193 ^L, 2.33 mmol) is added and the mixture stirred for an additional 15 min. It is worked up by addition of aqueous HCI solution (1M, 1.2 mL) and extraction with ethyl acetate. The combined organic extracts are washed with brine dried over MgS04. The volatiles are removed under reduced pressure to give the title compound as a yellow oil: Ci0H1tCIN2O: M*= 211.3; 1H-NMR (DMSO-d6): 8.55 (d, 1H), 7.82 (s, 1H), 7.59 (d, 1H), 3.62-3.42 (m, 4H), 1.93-1.75 (m, 4H). Stage 101.2: [4-(4-Amino-phenoxv)-pyridin-2-vnpvrrolidin-1-vl-methanone 4-Aminophenol (122 mg, 1.12 mmol) is dissolved in DMF (3 ml) and treated with potassium-tert-butylate (131 mg, 1.16 mmol) at rt. The reaction mixture is stirred for 2 h to give a brown suspension, (4-Chloro-pyridin-2-yl)-pyrrolidin-1-yI-methanone (Stage 101.1; 236 mg, 1.12 mmol) and K2C03 (82 mg, 0.59 mmol) are added. The reaction mixture is then stirred for 12 h at 80 °C. It is allowed to cool to rt again and the solvent is removed in vacuo. The residual brown oil is taken up in ethyl acetate and washed with brine. The organic layer is dried over MgS04> concentrated and the residual crude product is purified by flash chromatography (Si02; gradient CH2CI2/MeOH 99:1 to 92:8) to give the title compound as a slightly brown solid: Cl6H17N302:M+= 284.2. 102.3: 1-f4-r2-Pvrrolidine"1-carbonvl)-pyridin-4-vloxv1-phenvlV3-p-tolvl-urea [4-(4-Amino-phenoxy)-pyridin-2-yI]pyrrolidin-1-yl-methanone (Stage 101.2; 118 mg, 0.42 mmol) is dissolved in DMF (3 mL) and cooled in an ice bath. Pyridine (37 yL, 0.46 mmol) and 3-(trifluoromethyl)phenyl-isocyanate (70 JIL, 0.50 mmol) are added and the reaction mixture allowed to reach rt. After 30 min it is worked up by removal of all volatiles under reduced pressure and purification of the residual crude product by flash chromatography (Si02; gradient CH2CI2/MeOH 99:1 to 95:5) to give the title compound as a slightly brown solid: C24H21F3N403: M+ = 471.5; 1H-NMR (DMSO-d6): 9.09 (s, 1H, HN), 8.92 (s, 1H, HN), 8.42 (d, 1H), 7.99 (s, 1H), 7.61-7.42 (m, 4H), 7.29 (d, 1H), 7.17 (d, 2H), 7.03 (d, 1H), 7.01 (dd, 1H), 3.62-3.58 (m, 2H), 3.49-3.39 (m, 2H), 1.87-1.72 (m, 4H). Stage 101.4: 144-(6-Acetvl-pvrimidin-4'Vloxy)-phenvn-3-(-trifluoromethvl-phenyl)-urea 1-{4-[2-Pyrrolidine-1-carbonyl)-pyridin-4-yloxy]-phenyI}-3-p-toIyl-urea (Stage 101.3; 23 mg, 0.05 mmo!) is dissolved in THF (200 nL) and cooled to -78 °C. Methyilithium (98 ^L, 0.10 mmol, of a 1.6 M solution in diethyl ether) is added dropwise. The reaction mixture is stirred for 30 min at -78 °C and then allowed to reach rt and stirred for additional 2 h. It is worked up by removal of all volatiles in vacuo, the residue is taken up in ethyl acetate and washed with brine and afterwards purified by preparative TLC (Si02, hexanes/ethyl acetate 7:3) to give the title compound as a white solid: m.p. = 149-151 °C; C21H16F3N3O3: M+= 416.1; 1H-NMR (DMSO-d6): 9.36 (s, 1H), 8.99 (s, 1H), 8.60 (d, 1H), 8.02 (s, 1H), 7.58 (d, 3H), 7.54-7,51 (m, 1H), 7.35-7.30 (m, 1H), 7.28-7.25 (m, 1H), 7.15 (d, 2H), 2.16 (s, 3H). Example 102: 1 -f4-(2-Cvano-pvridin-4-y[oxY)-phenvl1-3-p-tolyl-urea p-Tolylisocyanate (66.4 nL, 0.521 mmol, 1.1 equiv) is added to a solution of 4-(4-amino-phenoxy)-pyridine-2-carbonitriIe (100 mg, 0.473 mmol) in THF abs. (1.45 mL), under an argon atmosphere. The resulting mixture is stirred at rt for 2 h, diluted with 3 mL of a hexane/CH2CI2 (2/1) solution and filtered through a glass sintered funnel. The residue is washed with the above-mentioned solvents mixture and dried in vacuo to afford the title compound as a beige solid: ES-MS: 345.0 [M+H]+; single peak at tR= 9.04 min (System 2); Rf = 0.19 (CHzCb/EtzO, 90/10). 4-(4-Amino-phenoxy)-pyridine-2-carbonitrile: ^ -NH. 4-Amino-phenol (2.54 g, 22.8 mmol, 1.1 equiv) is added in one portion to a suspension of NaH (60% free-flowing powder moistened with oil, 1.25 g, 31.2 mmol, 1.5 equiv) in dioxane abs. (30 mL), under an argon atmosphere. When hydrogen evolution subsides, 4-nitro-pyridine N-oxide (3 g, 20.8 mmoi) is added in one portion. The resulting dark mixture is heated to 100 °C (oil bath temperature) for 22 h and then allowed to cool to rt. Me3SiCN (3.5 mL, 27.0 mmol, 1.3 equiv) is added. After 5 min, the reaction mixture is cooled with a 10 °C water bath and N,N-dimethyIcarbamoyl chloride (2.5 mL, 27.0 mmol, 1.3 equiv) is added dropwise. The reaction mixture is allowed to warm to rt. When the reaction becomes exothermic, the water bath (10 °C) is applied for a few minutes. The reaction mixture is allowed to warm to rt, stirred for 1 h, quenched by addition of MeOH (30 mL), and concentrated in vacuo. After addition of CH2CI2 to the residue, the resulting suspension is filtered through a glass sintered funnel (washing with copious amount of the same solvent). The filtrate is concentrated in vacuo and the residue is purified by silica gel (200 g) column chromatography (CH2Cl2/Et20, 90/10) to afford the title compound as a brownish solid: ES-MS: 211.9 [M+H]+; single peak at tR= 4.86 min (System 2); Rf = 0.44 (CH2CI2/Et20, 80/20). Example 103: 1 -['4-(2-Cvano-pvridin-4-vloxv)-phenvn-3-(4-ethvl-phenv)-urea The title compound is prepared as described in Example 102 but using 4-ethyl-phenyl-isocyanate. After a 2.5 h stirring, the reaction mixture is concentrated in vacuo and the residue is purified by silica gel (18 g) column chromatography (CH2Cl2/Et2Ol 90/10) to afford the title compound as a beige solid: ES-MS: 359.0 [M+H]*; single peak at tR= 9.41 min (System 2); Rf = 0.22 (CH2CI2/Et20. 90/10). Example 104:1 -f4-(2-Cvano-pyridin-4-yloxv)-phenvn-3-(3*trifluoromethvl-phenv)-urea The title compound is prepared as described in Example 102 but using a,a,ct-trifluoro-m-tolyl-isocyanate. After a 3 h stirring, the reaction mixture is concentrated in vacuo and the residue is purified by silica gel (18.5 g) column chromatography (CH2CI2, then CH2CI2/MeOH, 99/1) to afford the title compound as a light yellow solid: ES-MS: 398.9 [M+H]*; single peak at tR= 9.54 min (System 2); Rf = 0.067 (CH2CI2/MeOHt 99/1). Example 105: 1 -f4-(2-Chloro-pyridin-4-Yloxy)-phenvn-3-p-toly!-urea The title compound is prepared as described in Example 102 but using 4-(2-chloro-pyridin-4-yloxy)-phenylamine and stirring the reaction mixture for 3 h. The title compound is obtained as a white solid: ES-MS: 354.0 [M+Hf; single peak at tR= 9.53 min (System 2); R, = 0.19 (CH2CI2/Et20, 90/10). 4-(2-Chloro-pyridin-4-yIoxy)-phenyIamine: 4-Amino-phenol (1.05g, 9.40 mmol, 1.1 equiv) is added in one portion to a suspension of NaH (60% free-flowing powder moistened with oil, 0.513 g, 12.8 mmol, 1.5 equiv) in dioxane abs. (6.5 mL), under an argon atmosphere. When hydrogen evolution subsides, a solution of 2-chIoro-4-nitropyridine (1.35 g, 8.54 mmol) in dioxane (6 mL) is added. The resulting dark mixture is heated to 100 °C (oil bath temperature) for 70.5 h, allowed to cool to rt, quenched by addition of MeOH and partially concentrated in vacuo. The oily residue is dissolved in CH2Cl2/MeOH (80/20) and filtered through a glass sintered funnel containing silica gel (18 g), eluting with CH2CI2/MeOH (90/10). The filtrate is partially concentrated in vacuo, diluted with CH2CI2/MeOH (90/10) and purified by silica gel (70 g) column chromatography (CH2Ci2/Et20, 90/10, then 85/15). A second column chromatography purification affords the title compound as a yellow solid: ES-MS: 221.1 [M+H]+; single peak at tR= 6.56 min (System 2); R, = 0.27 (CH2CI2/Et20, 80/20). 2-Chloro-4-nitropyridine is prepared according to a literature procedure [M. A. Walters, J. J. Shay, Tetrahedron Letters, 36 (42), 7575-7578 (1995)] and used as a crude material. A suspension of 4-(4-nitro-phenoxy)-2-trifluoroniethyl-pyridine (1.16 g, 4.08 mmol) and Raney Nickel (0.4 g, in EtOH) in MeOH (70 mL) is stirred at rt and under a hydrogen atmosphere for 7 h. Additional Raney Nickel (tip of spatula) is then added and the reaction mixture is stirred for 17 h. The mixture is filtered through a pad of celite and the filter cake is washed with copious amount of MeOH. After removal of the solvents in vacuo, the residue is purified by silica gel (50 g) column chromatography (CH2Cl2/Et20, 95/5) to afford the title compound as a white solid: ES-MS: 255.0 [M+H]*; single peak at tR= 5.97 min (System 2); Rf = 0.40 (CH2CI2/Et20, 90/10). 4-(4-Nitro-phenoxy)-2-trifluoromethyl-pyridine: A mixture of 2-trifiuoromethyl-pyridin-4-ol (0.675 g, 4.14 mmol), 1-fIuoro-4-nitro-benzene (0.54 mL, 4.97 mmol, 1.2 equiv), and NaOH (0.203 g, 4.97 mmol, 1.2 equiv) in DMF abs. is heated to 100 °C (oil bath temperature) for 21.5 h, under an argon atmosphere. The reaction mixture is allowed to cool to rt, filtered through a glass sintered funnel and concentrated in vacuo. The residual yellow solid is purified by silica gel (100 g) column chromatography (CH2CI2/hexane, 70/30) to afford the title compound as a white solid: ES-MS: 285.0 [M+Hf; single peak at tR= 8.71 min (System 2); Rf = 0.25 (CH2CI2/hexane, 70/30). 2-TrifluoromethyI-pyridin-4-ol is prepared according to a reported three-step procedure [V. I. Tyvorskii, D. N. Bobrov; Chemistry of Heterocyclic Compounds, 33 (8), 995-996 (1997)]. Example 109: 1 -(4-Ethvl-phenvl)-3"f4-(2'trifluoromethvl-pyridin-4-vloxv)-phenvn-urea The title compound is prepared as described in Example 102 but using 4-(2-trifluoromethyi-pyridin-4-yloxy)-phenylamine (Example 108) and 4-ethyl-phenyl-isocyanate. The reaction vacuo to afford the title compound as a white solid: ES-MS: 389.0 [M+H]+; single peak at tR= 9.33 min (System 2). 4-(6-Trifluoromethyl-pyrimidin-4-yloxy)-phenylamine: 4-Amino-phenol (1.2 g, 10.9 mmol) is added in one portion to a suspension of NaH (60% free-flowing powder moistened with oil, 0.48 g, 12.0 mmol, 1.1 equiv) in dioxane abs. (18 mL). under an argon atmosphere. When hydrogen evolution subsides, a solution of 4-chloro-6-trifluoromethyl-pyrimidine (2.0 g, 10.9 mmol) in dioxane (2.0 mL) is added. The resulting dark mixture is heated to 60-65 °C (oil bath temperature) for 40 min, allowed to cool to rt, quenched by addition of MeOH and concentrated in vacuo. The residue is purified twice by silica gel (200 g) column chromatography (CH2Cl2/MeOH, 99/1, then 98/2) to afford the title compound as a white solid: ES-MS: 256.0 [M+H]+; single peak at tR= 6.35 min (System 2); Rf = 0.33 (CH2CI2/MeOH, 98/2). 4-Chloro-6-trifluoromethyl-pyrimidine is prepared according to a literature procedure (Kanne, David B.; Prisbylla, Michael P.: US Patent 5714438 A, 1998). Example 115: 1-(4-Ethvl-phenvl)-3-f4-(6-trifluoromethvl-pyrimidin-4-vloxv)-phenvn-urea The title compound is prepared as described in Example 102 but using 4-(6-trifluoromethyI-pyrimidin-4-yloxy)-phenyIamine (Example 114) and 4-ethyl-phenyl-isocyanate. The reaction mixture is stirred for 2.5 h. The title compound is obtained as a white solid: ES-MS: 403.0 [M+H]+; single peak at tR= 9.72 min (System 2). Example 116:1 -(3-Trifluoromethvl-phenvl)-3-f4-(6-trifluoromethyl-pvrimidin-4-vloxv)-phenvn-urea The title compound is prepared as described in Example 102 but using 4-(6-trifluoromethyl-pyrimidin-4-yloxy)-phenylamine (Example 114) and a,a,a-trifIuoro-m-tolyI-isocyanate. The reaction mixture is stirred for 2.5 h. The title compound is obtained as a white solid: ES-MS: 442.9 [M+H]+; single peak at tR= 9.83 min (System 2). Example 117: 1-f4-(6-Chloro-pyrimidin-4-vlmethyl)-phenvn-3-f4-ethyl-phenyl)-urea A 4 N solution of HCI in dioxane (1.2 mL, 4.96 mmol, 30 equiv) is added to a solution of [4-(6-chloro-pyrimidin-4-yimethyl)-phenyI]-carbamic acid tert-butyl ester (50 mg, 0.156 mmol) in CH2CI2 (0.67 mL), under an argon atmosphere. The resulting white suspension is stirred at rt for 4 h and concentrated in vacuo to afford 50.9 mg of crude 4-(6-chloro-pyrimidin-4-ylmethyl)-phenylamine as a white solid. DIEA (80 jiL, 0.454 mmol, 2 equiv) is added to a suspension of crude 4-(6-chloro-pyrimidin-4-ylmethyl)-phenylamine (50 mg, 0.227 mmol) in THF (0.4 mL), under an argon atmosphere. 4-Ethyl-phenyl-isocyanate (40 p.Lf 0.250 mmol, 1.1 equiv) is then added. The resulting yellow solution is stirred at rt for 2 h and concentrated in vacuo. The residue is purified by silica gel (20 g) column chromatography (CH2CI2/MeOH, 98/2). A second purification affords the title compound as a white solid: ES-MS: 367.0 [M+H]+; single peak at tR= 8.94 min (System 2); Rf = 0.32 (CH2CI2/MeOH, 95/5). [4-(6-ChIoro-pyrimidin-4-ylmethyl)-phenyl]-carbamic acid tert-butyl ester: Triethylamine hydrochloride (0.93 g 6.60 mmol), N.N-dimethylaniline (0.8 mL, 6.60 mmol), and POCI3 (3.7 mL, 39.6 mmol, 6 equiv) are added sequentially to a solution of [4-(6-hydroxy-pyrimidin-4-yImethyI)-phenyl]-carbamiC acid tert-butyl ester (2.0 g, 6.60 mmol) in CH3CN (16.5 mL), at rt and under an argon atmosphere. The resulting yellow solution is stirred at rt for 1 h and then added to a stirred mixture of H20/ice (1/1, v/v; 80 mL, total volume). The product is extracted in CH2CI2 (2 x 200 mL). The organic phase is washed with an aqueous saturated solution of Na2C03 (70 mL), dried (Na2S04), filtered and concentrated in vacuo. The residue is purified by silica gel (170 g) column chromatography (CH2CI2/Et20, 95/5, then 90/10) to afford the title compound: ES-MS: 320.1 [M+H]+; single peak at tR= 8.76 min (System 2); R, = 0.13 (CH2CI2/Et20, 95/5). 1.56 mmoi) in CH2CI2 (6.7 ml), under an argon atmosphere. The resulting white suspension is stirred at rt for 6.5 h. Additional 4 N HCI solution (1.1 mL, 4.6 mmol, 3.0 equiv) is added. The reaction mixture is allowed to stir for 0.5 h and concentrated in vacuo to afford 0.467 g of crude 4-(6-chloro-pyrimidin-4-ylmethyl)-phenylamine as a white solid. An 8 M solution of methylamine in EtOH (5.1 mL, 40.0 mmol, 30 equiv) is added to a solution of crude 4-(6-chloro-pyrimidin-4-ylmethyl)-phenylamine (0.300 g, 1.37 mmol) in EtOH (2.7 mL), under an argon atmosphere. The mixture is heated to 50 °C (oil bath temperature) for 5 h, allowed to cool to rt and concentrated in vacuo. The residue is purified by silica gel (48 g) column chromatography (CH2CI2/MeOH, 85/15) to afford the title compound as a light yellow oil: ES-MS: 215.0 [M+H]+; single peak at tR= 3.03 min (System 2); Rf = 0.49 (CHzCfe/MeOH, 85/15). Example 120: 1-(4-Ethvl-phenvl)-3-f4-(6-methvlamino-pyrimidin-4-vlmethvl)-phenyn-urea The title compound is prepared as described in Example 102 but using [6-(4-amino-benzyl)-pyrimidin-4-yl]-methyl-amine (Example 119) and 4-ethyl-phenyl-isocyanate. The reaction mixture is stirred for 6 h. The title compound is obtained as a white solid: ES-MS: 362.0 [M+H]+; single peak at tR= 7.14 min (System 2). Example 121:1 -f4-(6-methvlamino-pvrimidin-4-vlmethylVphenvlV3-(3-trifluoromethvl-phenyl)-urea The title compound is prepared as described in Example 102 but using [6-(4-amino-benzyl)-pyrimidin-4-yl]-methy!-amine (Example 119) and a.ct.a-trifluoro-m-tolyl-isocyanate. The reaction mixture is stirred for 3 h. The title compound is obtained as a white solid: ES-MS: 402.0 [M+H]+; single peak at tR= 7.34 min (System 2); Rf = 0.32 (CH2CI2/MeOH, 90/10). Example 122: 1 -{4-[2-(1 H-Tetrazol-5-yn-pyridin-4-vloxv1-phenyl}-3-(3-trifluoromethyl-phenylV urea The title compound is prepared as described in Example 102 but using 4-[2-(1H-tetrazoi-5-yl)-pyridin-4-yloxy]-phenylamine and a,a,a-trifluoro-m-tolyl-isocyanate. The reaction mixture is stirred for 4 h. The crude product is washed with a solution of CH2CI2/MeOH (95/5) and dried in vacuo to afford the title compound as a beige solid: ES-MS: 441.9 [M+H]+; single peak at tR= 7.93 min (System 2); Rf = 0.36 (CH2Ci2/MeOH, 80/20). 4-[2-(1H-tetrazol-5-yI)-pyridin-4-yloxy]-phenyIamine: A mixture of 4-(4-amino-phenoxy)-pyridine-2-carbonitrile (Example 102) (2.6 g, 12.3 mmol), sodium azide (6.6 g, 102 mmol, 8.3 equiv), and ammonium chloride in DMF abs. (180 mL) is heated to 70 °C for 7,5 h, under an argon atmosphere. The reaction mixture is allowed to cool to rt, filtered through a glass sintered funnel and concentrated in vacuo. The residue is purified by silica gel (390 g) column chromatography (CH2CI2/MeOH, 80/20) to afford the title compound as a beige solid: ES-MS: 255.0 [M+H]+; single peak at tR= 3.98 min (System 2); Rf = 0.20 (CH2CI2/MeOH, 75/25). Example 123: 1-(4-Ethyl-phenvl)-3-(4-r2-(1H-tetrazol-5-vl)-pvridin-4-vloxv1-Dhenvl}-urea The title compound is prepared as described in Example 102 but using 4-[2-(1H-tetrazol-5-yl)-pyridin-4-yloxy]-phenyIamine (Example 122) and 4-ethyl-phenyl-isocyanate. The reaction mixture is stirred for 4 h. The crude product is washed with a solution of CH2CI2/MeOH (95/5) and dried in vacuo to afford the title compound as a beige solid: ES-MS: 402.0 [M+H]+; single peak at tR= 7.73 min (System 2); Rf = 0.20 (CH2CI2/MeOH, 80/20). Example 124: 1-(4-f2-(1-Methvl-1H-tetrazol"5-vlVpvridin-4-vloxv1-phenvl>-3-(3-trifluoromethyl-phenvl)-urea lodomethane (0.21 mL, 3.40 mmol, 1.5 equiv) is added to a cold (0 °C) mixture of 1-{4-[2-(1H4etrazol-5-yl)-pyridin^-yloxy]-phenyl}-3-(3-triTIuoromethyl-phenyl)-urea (Example 122) (1.0 g, 2.27 mmol) and potassium carbonate (0.94 g, 6.80 mmol, 3.0 equiv) in DMF abs. (5.8 mL), under an argon atmosphere. The reaction mixture is stirred at 0 °C for 2 h, allowed to warm to rt and stirred for additional 20 h. The resulting brown suspension is filtered and concentrated in vacuo. MeOH (10 mL) and DMF (0.5 mL) are added to the residue and the resulting suspension is filtered. The white solid is washed with MeOH and dried in vacuo to afford the title compound as a white solid. The filtrate is concentrated in vacuo and the residue is purified by MPLC (CH3CN/H20/TFA) to afford additional title compound as a beige solid: ES-MS: 455.9 [M+H]+; single peak at tR= 9.15 min (System 2). Example 125: 1-(4-f2-(2-Methvl-2H-tetrazol-5-vn-pyridin-4-vloxv1-phenvl)-3-(3-trifluoromethvl-phenylVurea The MPLC purification of the residue obtained from the concentrated filtrate of Example 124 affords the title compound as a beige solid: ES-MS: 455.9 [M+H]+; single peak at tR= 8.24 min (System 2). Example 126: 1-(4-Ethvl-phenyl)-3^442-(1-methvl-1 H-tetrazol-5-ylVpvridin-4-vIoxvl-phenvl)-urea The title compound is prepared as described in Example 124 but using 1-(4-ethyl-phenyl)-3-{4-[2-(1H-tetrazol-5-yl)-pyridin-4-yloxy]-phenyl}-urea (Example 123). The crude product is purified by MPLC (CH3CN/H20yTFA) to afford the title compound as a white solid: ES-MS: 416.0 [M+H]+; single peak at tR= 8.97 min (System 2). Example 127: 1-f4-Ethvl-phenvlV3-f4-f2-f2-methvl-2H-tetrazol-5-vl)-pvridin-4*vloxv1-phenvlV urea The MPLC purification of the crude product of Example 126 affords the title compound as a white solid: ES-MS: 416.0 [M+H]*; single peak at tR= 8.06 min (System 2). Example 128: N-(4-(4-ChloroDyrimidin-6-vl-oxy)-phenvl)-N'-(3"trifluoromethvl-4-(piperidin-1-ylmethvD-phenvD-urea The title compound is prepared from 3-trifluormethyi-4-(piperidin-1-ylmethyl)-phenylamine (Stage 128.1) and 4-(6-chloro-pyrimidin-4-yl-oxy)-aniline (Stage 21.1) analogously to Example 85: MS: [M+1]+=505; 1H-NMR (DMSO-d6): 8.99 (s, 1H), 8.84 (s, 1H), 8.62 (s, 1H), 7.93 (s, 1H), 7.62 (d, 1H), 7.55 (m, 1H), 7.51 (d, 2H), 7.32 (s, 1H), 7.14 (d, 2H), 3.47 (s, 2H), 2.31 (sb, 4H), 1.49 (m, 4H), 1.39 (m, 2H). The starting materials are prepared as follows: Stage 128,1: 3-Trifluormethyi-4-fpiperidin-1'VlmethvlVphenylamine To a solution of 2l2t2-trifluorchN-(4-piperidin-1-yImethyi--3-trifluoromethyl-phenyi)-acetamide (Stage 128.2; 1.427 g, 4.03 mmol) in boiling methanol (42 ml), 20 ml of a 1 N solution of K2C03 in water are added dropwise. After 2 h stirring, the reaction mixture is cooled to rt, concentrated in vacuo and the residue re-dissolved in AcOEt and water. The aqueous layer is separated off and extracted twice with AcOEt. The organic phases are washed with water arid brine, dried (Na2S04) and concentrated to yield the title compound: MS: [M+1]+=259; 1H-NMR (DMSO-d6): 7.28 (d, 1H), 6.82 (d, 1H), 7.73 (dd, 1H), 5.40 (s, H2N), 3.32 (s, 2H), 2.27 (sb, 4H), 1.46 (m, 4H), 1.39 (m, 2H). Stage 128.2: 2,2,2-Trifluoro-N-(4-piperidin-1 -ylmethvl-3-trifluoromethvl-phenyl)-acetafnide To a solution of N-(4-bromomethyl-3-trifluoromethyl-phenyl)-2)2,2-trifluoro-acetamide (Stage 123.3; 1.465 g, 4.19 mmol) in acetonitril (35 ml) under ^-atmosphere, piperidine (1.25 ml, 12.7 mmol) is added. After 30 min at rt the reaction mixture is diluted with water and partially concentrated in vacuo. The aqueous residue is acidified to pH 5 by addition of 0.1 N HCI and extracted 3x with AcOEt. The organic layers are washed with water and brine, dried (Na2S04) and concentrated. Column chromatography (Si02; hexane/AcOEt 3:2) gives the title compound: MS: [M+1]+=355; 'H-NMR (DMSO-d6): 11.43 (s, HN), 8.02 (s, 1H), 7.91 (dd, 1H), 7.77 (d, 1H), 3.52 (s, 2H), 2.32 (sb, 4H), 1.50 (m, 4H), 1.40 (m, 2H). Stage 128.3: 2 N"(4-Bromomethvl-3>trifluoromethvl-phenyl)-2,2,2-trifluoro-acetamide Under N2-atmosphere, a suspension of N-(4-methyl-3-trifluoromethyl-phenyl)-2,2,2-trifluoro-acetamide (Stage 128.4; 5.21 g, 19.2 mmol), N-bromosuccinimide (15 g, 84 mmol) and azo-iso-butyronitrile (740 mg, 4.5 mmol) in 430 ml of CCI4 is heated to 85 °C for 15 h. The hot mixture is filtered, the solid washed with CCI4 and discarded. The filtrate is concentrated, the residue re-dissolved in CH2CI2 (0.7 L) and washed twice with 0.5 M solution of Na2S203 and brine. The inorganic phases are extracted with 2 portions of CH2CI2, the organic phases dried (Na2S04) and concentrated. Column chromatography (Si02; hexane/CH2CI21:1) yields the title compound: 1H-NMR (DMSO-d6): 11.59 (s, HN), 8.06 (d, 1H), 7.97 (dd, 1H), 7.76 (d, 1H), 4.77 (s, 2H). Stage 128.4: N-f4-Methvl-3-trifluoromethyl-phenvn-2 Example 129: N-(4-(4-Chloropyrimidin-6-vl-oxv)-phenv0-N,-(3-methoxv-4-(4-methvl- piperazin-1-ylmethyl)-phenvlVurea A solution of triphosgene (580 mg, 1.96 mmol) in CH2C(2 (60 ml) under N2-atmosphere is cooled by an ice bath. 4-(6-Chloro-pyrimidin-4-yl-oxy)-aniIine (Stage 21.1; 1.30 g, 5.86 mmol) and NEt3 (0.82 ml, 5.86 mmol) in CH2Ci2 (30 ml) is added dropwise and the suspension stirred for 15 min. Then a solution of 3-methoxy-4-(4-methyi-piperazin-1-ylmethyl)-phenylamine (Stage 129.1; 1.15 g, 4.89 mmol) and NEt3 (0.68 ml, 4.89 mmol) in CH2CI2 (30 ml) is added dropwise and the mixture stirred for 30 min in the ice bath, whereby a solution is formed. After stirring for 4.5 h at rt, the reaction mixture is added to a saturated NaHC03 solution and extracted 3x with CH2CI2. The organic phases are washed with water and brine, dried (Na2S04) and concentrated. Medium pressure reverse phase liquid chromatography (Nucleosil C18; water-acetonitrile gradient + TFA) yields after neutralization the title compound: MS: [M+1]+ = 483; 1H-NMR (DMSO-d6): 8.74 & 8.69 (2s, 2HN), 8.63 (s, 1H), 7.50 (d, 2H), 7.31 (s, 1H), 7.24 (s, 1H), 7.13 (m, 3H), 6.88 (d, 1H), 3.75 (s, H3C). 3.37 (s, 2H), 2.5-2.2 (m, 8H), 2.15 (s, H3C). The starting materials are prepared as described in Example 87: Stage 129.1: 3-Methoxv-4-(4-methvl-piperazin-1-vlmethvl)-phenylamine Hydrogenation of 3-methoxy-4-(4-methyl-piperazin-1-ylmethyl)-nitrobenzene (Raney Nickel, THF) yields the title compound: MS: [M+1]+= 236; 1H-NMR (DMSO-d6): 6.80 (d, 1H), 6.15 (s, 1H), 6.06 (d, 1H), 4.95 (s, 2H), 3.63 (s, H3C), 3.22 (s, 2H), 2.27 (sb, 8H), 2.10 (s, H3C). Stage 129,2: 3-Methoxv-4-(4-methvl-piperazin-1-vlmethvl)-nitrobenzene Reduction of (4-methy!-piperazin-1-yl)-(4-nitro-2-methoxy-phenyl)-methanone (DIBAH, THF, .75 °c -» -40 °C) yields the title compound: MS: [M+lf = 266; Anal.: CHN. Stage 129.3: (4-Methyl-piperazin-1 -ylH4-nitro-2-methoxy-phenYl)-methanone Prepared from 2-methoxy-4-nitrobenzoic acid and 1-methyl-piperazine (TPTU, CH2CI2/CH3CN, Et3N): MS: [M+1]+= 280; Anal.: CHN. Hydrolysis of 2I2l24rifluoro-N-[4-(4-ethylpip^ acetamide gives the title compound: MS: [M+1]+= 288; 1H-NMR (DMSO-d5): 7.22 (d, 1H), 6.79 (d, 1H), 7.69 (dd, 1H), 5.38 (s, H2N), 3.32 (s, 2H), 2.29 (sb, 8H), 2.25 (q, 2H), 0.92 (t, H3C). Stage 133.2: 2.2.2-Trifluoro-N-(4-(4-ethylpiperazin-1-vlmethvlV3-trifluoromethvl-phenylV acetamide Reaction of N-(4-bromomethyl-3-trifluoromethyl-phenyl)-2,2,2-trifluoro-acetamide (Stage 128.3) with N-ethyipiperazine gives the title compound: MS: [M+1]* = 384; 1H-NMR (CDCI3): 8.0 (sb, HN), 7.8 (m, 3H), 3.63 (s, 2H), 2.51 (sb, 8H), 2.43 (q, 2H), 1.09 (t, H3C). Example 134: N-(4-(6-Chloroovrimidin-4-vl"OXv)-phenvl)-N'-(5-trifluoromethyl-3-f(4-ethylpiperazin-1-vlmethvl)1-phenyl)-urea To an ice-cold solution of 4-(6-chloro-pyrimidin-4-yl-oxy)-aniIine (Stage 21.1; 0.926 g, 4.18 mmol) and NEt3 (0.64 ml, 4.6 mmol) in CH2CI2 (30 ml) under N2-atmosphere, phosgene (2.32 mi of a 20 % solution in toluene, 4.39 mmol) in CH2CI2 (10 ml) is added dropwise. The resulting suspension is stirred for 1 h, then filtered under exclusion of moisture and the filtrate concentrated in vacuo. THF (20 ml) and NEt3 (0.64 ml, 4.6 mmol) is then added to the residue. After cooling in an ice bath, 3-(4-ethyl-piperazin-1-yImethyl)-5-trifluoromethyl-phenylamine (1.00 g, 3.48 mmol) dissolved in THF (20 ml) is added dropwise and the reaction mixture stirred for 30 min at 0 °C and 2 h at rt. Then it is diluted with water and AcOEt, the aqueous layer separated off and extracted twice with AcOEt. The organic phases are washed with water and brine, dried (Na2S04) and concentrated. Column chromatography (Si02; AcOEt/EtOH/Et3N 90:10:2 -> 80:20:2) and crystallization from ether affords the title compound: m.p.: 168-169 °C; MS: [M+1]+= 535; 1H-NMR (CD3OD): 8.54 (s, 1H), 7.82 (s, 1H), 7.60 (s, 1H), 7.54 (d, 2H), 7.30 (s, 1H), 7.14 (d, 2H), 7.09 (s, 1H), 3.60 (s, 2H), 2.57 (m, 8H), 2.47 (q,2H), 1.12 (t, 3H). The starting materials are prepared as follows: Stage 134.1: 3-(4-Ethyl-piperazin-1 -vlmethyl)-5-trifluoromethvl-phenvlamine To a solution of (3-amino-5-trifluoromethyl-phenyl)-(4-ethyl-piperazin-1-yl)-methanone (14.6 g, 48.5 mmoi) in THF (120 ml) under (^-atmosphere, a 1 M solution of BH3-THF (145.5 ml) is added dropwise (exothermic). The mixture is stirred for 14 h at rt and then 5 h at 65 °C. After cooling to rt, HCI conc./H20 1:1 (250 ml) is added and the mixture stirred for 15 h. The suspension is filtered, the filtrate extracted 3 times with AcOEt. The organic phases are washed twice with 1 N HCI and then discarded. The combined acidic phases are made basic by addition of saturated Na2C03 solution and extracted 3 times with AcOEt. The organic layers are washed twice with water and brine, dried (Na2S04) and concentrated. Column chromatography (Si02; AcOEt/EtOH/NH3 95:5:1 -> 90:10:1) followed by extraction between 3 portions of AcOEt, 3 portions of water and finally brine, drying (Na2S04) and concentration yields the title compound as an oil: MS: [M+1]* = 288; 1H-NMR (CDCI3): 6.94 (s, 1H), 6.82 (s, 1H), 6.78 (s, 1H),3.82(sb, H2N), 3.46 (s, 2H), 2.51 (m, 8H), 2.44 (q, 2H), 1.10 (t,3H). Stage 134.2: (3-Amino-5-trifluoromethvl-phenvl)-(4-ethyl-piperazin-1 -vQ-methanone Hydrogenation of (3-nitro-5-trifluoromethyl-phenyl)-(4-ethyl-piperazin-1-yl)-methanone (16.5 g, 50 mmol) in ethanol (300 ml) in the presence of Raney-Nickel (3 g), filtration through celite, concentration of the filtrate and crystallization from hexane gives the title compound: m.p.: 104 °C; MS: [M+1]+= 302; 1H-NMR (CDCI3): 6.96 (s, 1H), 6.91 (s, 1H), 6.83 (s, 1H), 3.99 (sb, H2N), 3.80 (m, 2H), 3.44 (m, 2H), 2.53 (m, 2H), 2.46 (q, 2H), 2.40 (m, 2H), 1.12 (t, 3H). Stage 134.3: (3-Nitro-5-trifluoromethvl-phenvlV(4-ethvl-piperazin-1 -vD-methanone In an ice bath under N2-atmosphere, 3-nitro~5-trifluoromethy!-benzoic acid (Lancaster; 11.8 g, 50 mmol), CH2CI2 (150 ml), a few drops of DMF and oxalylchloride (7.0 ml, 81 mmol) are mixed and then stirred for 3 h at rt. The resulting solution is concentrated in vacuo. The residue is dissolved in CH2CI2 (170 ml) and added dropwise to an ice cooled solution of N-ethyl-piperazine (12.7 ml, 0.10 mol) in CH2CI2 (100 ml). After stirring for 1 h at rt, the mixture is washed with a diluted solution of Na2C03, 2 portions of water and finally brine. The aqueous layers are re-extracted twice with AcOEt, the combined organic phases dried (Na2S04) and concentrated giving the title compound as an oil: MS: [M+1]+= 332; 1H-NMR (CDCI3): 8.53 (s, 1H), 8.44 (s, 1H), 8.00 (s, 1H), 3.84 (m, 2H), 3.43 (m, 2H), 2.57 (m, 2H), 2.48 (q, 2H), 2.44 (m, 2H), 1.12 (t, 3H). Example 135: N-(4-(6-Chloropvrirnidin-4-vl-oxv)-phenvl)-N,-f5-trifluororriethyl-3-(dimethvlamino-methvl)'Phenvll-urea A solution of 4-chloro-6-(4-isocyanato-phenoxy)-pyrimidine (Stage 135.1; 594 mg; 2.40 mmol) in THF (2 ml) is mixed under a N2-atmosphere with a solution of 3-dimethyIaminomethyl-5-trifluoromethyl-phenylamine (Stage 135.2; 524 mg; 2.40 mmol) in ether (10 ml). Stirring at rt affords the title compound: MS: [M+1]+=466. The starting materials are prepared as follows: Stage 135.1: 4-Chloro-6-(4-isocyanato-phenoxv)-pyrimidine Apparatus: 2 litre 3-neck-roundbottle flask, dropping funnel, short Vigreux column and condenser. A phosgene solution (20 % in toluene, 118 ml; 223 mmol) diluted with toluene (800 ml) under N2-atmosphere is cooled to approximately -20 °C. Then a solution of 4-(6-chloro-pyhmidin-4-yl-oxy)-aniIine (Stage 21.1; 18.52 g, 83.6 mmol) in CH2CI2 (400 ml) is added dropwise. The resulting suspension is heated to distil off approximately 400 ml of solvent. Distillation is continued (boiling point: 110 °C), while a mixture of phosgene solution (20 % in toluene, 59 ml) and toluene (500 ml) is added dropwise, followed by toluene (250 ml). The resulting clear solution (« 250 ml) in the reaction vessel is cooled to rt, filtered and the filtrate concentrated in vacuo. Distillation of the resulting waxy crude product on the Kugelrohr apparatus (0.2 mbar, 200 °C) gives the title compound as a solid: m.p.: 103 °C; MS: [M+1]+ = 302; 1H-NMR (CDCI3): 8.57 (s, 1H), 7.17 (d, 2H), 7.10 (d, 2H), 6.95 (s, 1H). Stage 135.2: 3-Dimethvlaminomethvl^5-trifluoromethvl-phenvlamine 3-Amino-N,N-dimethyl-5-trifluoromethyl-benzamide (2.0 g; 8.6 mmol) dissolved in THF (20 ml) is reduced with a 1 M solution of BH3-THF (26 ml) as described in Stage 134.1, yielding the title compound: MS: [M+1]+= 219, Stage 135.3: 3-Amino-N,N-dimethyl-5-trifluoromethvl-benzamide Hydrogenation of (3-nitro-N(N-dimethyi-5-trifluoromethyl-ben2amide (12.6 g, 48 mmol) in THF (250 mi) in the presence of Raney-Nickel (3 g), filtration through celite, concentration of the filtrate and crystallization from hexane gives the title compound: m.p.: 154 °C; MS: [M+1]*= 233; 1H-NMR (CD3OD): 6.97 (s, 1H)( 6.84 (s, 2H), 3.09 (s, 3H), 2.99 (s, 3H). Stage 135.4: (3-Nitro-N.N-dimethvl-5-trif]uoromethyl-benzamide In an ice bath under N2-atmosphere, 3-nitro-5-trifluoromethyl-benzoic acid (Lancaster; 11.8 g, 50 mmol), CH2CI2 (150 ml), 3 drops of DMF and oxalylchioride ( 7.0 ml, 81 mmol) are mixed and then stirred for 2.5 h at rt. The resulting solution is concentrated in vacuo. The residue is dissolved in CH2CI2 (170 ml) and added dropwise to an ice cooled solution of dimethylamine hydrochloride (4.5 g, 55 mmol) and NEt3 (21 ml; 0.15 mol) in CH2CI2 (100 ml). After stirring for 15 h at rt, the mixture is worked up as described in Stage 134.3, giving the title compound as an oil: MS: [M+1]+= 263; 1H-NMR (CDCI3): 8.53 (s, 1H),8.47(s, 1H), 8.03 (s, 1H), 3.18 (s, 3H), 3.04 (s, 3H). Example 136: The following compounds of Table 11 can be prepared analogously to the described procedures: 6-(4-Amino-phenoxv)-pvrimidin-4-ylamine (compound of Stage 144.1): Compound of Stage 56.1 (2.0 g, 9.725 mmol) dissolved in acqueous NH3(25 %, 80 mL) and EtOH (60 mL) is stirred in a sealed tube at 80 °C for 23 h. After evaporating the solvent under reduced pressure on a water bath at 40 °C, the residue is flash chromatographed (silica gel, 5.5 x 65 cm; CH2CI2/MeOH = 9:1) to give compound of Stage 144.1 as a white solid: M+H = 203.0; 1H-NMR (400 MHz, DMSO-d6): 8.01 (s, 1H, pyrimidinyi), 6.74 (d, 9 Hz, 2H, phenyl), 6.70 (s( 2H, NH2), 6.57 (d, 9Hz, 2H, phenyl), 5.51 (s, 1H, pyrimidinyi), 5.03 (s, 2H, NH2); Rf (CH2CI2/MeOH = 9:1): 0.37; HPLC: 3.75 min (System 1). 3-Pyridin-2-vl-5-trifluoromethyl-phenylamine (Compound of Stage 146.1V. The title compound is synthesized via Stille coupling analogously to the procedure of Zhang et al., Synthetic Commun. 31 (8), 1129-1139 (2001) 3-amino-5-bromo-benzotrifluoride (600 mg, 2.44mmol), 2-tributylstannyl-pyridine (1.0 g, 2.69 mmol), and tetrakistriphenylphosphin palladium (282 mg, 0.245 mmol) dissolved in THF (10 mL) is stirred under Ar at 90 °C for 7 d. After concentrating under reduced pressure, the reaction mixture is flash chromatographed (silica gel, 2.6 x 46 cm, AcOEt/hexane: 1:2 -> 2:3) to give compound of Stage 146.1 as a yellow oil: M+H = 239.1; 1H-NMR (400 MHz, DMSO-d6): 8.64 (d, 5.0 Hz, 1H), 7.82 (m, 2H), 7.54/7.45 (s/s, 1H/1H), 7.36 (m, 1H9, 6.90 (s, 1H), 5.73 (s/broad, 2H); HPLC: 3.49 min (System 1); R,(hexane/AcOEt = 2:1): 1.5. f6-f4-Amino-phenoxvVpyrimidin-4-vlVmethvl-amine (compound of Stage 148.1): Compound of Stage 148.2 (1.28 g, 5.2 mmol) dissolved in MeOH/THF (45 mL/15 mL) is hydrogenated (1 atm) in the presence of Raney-Ni during 8 h. After evaporating the solvent under reduced pressure, the residue is flash chromatographed (silica gel, 5.5 x 60 cm; AcOEt/hexane =1:1) to give compound of Stage 148.1 as a beige solid: M+H = 217.0; 1H-NMR (400 MHz, DMSO-d6): 8.04 (s, 1H, NH), 6.93 (s/broad, 1H, pyriminidyl), 6.75 (d, 9.0 Hz, 2H, phenyl), 6.53 (d, 9.0 Hz, 2H, phenyl), 5.85 (m/broad, 1H, pyrimidinyl), 5.03 (s, 2H, NH2), 2.66 (s/broad, 3H, Me); Rf (AcOEt/hexane =1:1): 0.12; HPLC: 3.60 min (System 1). Methyl-[4-(4-nitro-phenoxvVpvrimidin-2-vi1-amine (compound of Stage 148.2): Compound of Stage 148.3 (2 g, 7.95 mmol) is stirred in MeNH2 (30 % in EtOH, 40 mL) at rt for 50 min. After evaporating the solvent under reduced pressure, the residue is flash chromatographed (silica gel, 5.5 x 60 cm; AcOEt/hexane =1:1) to give compound of Stage 148.2 as a white solid: M+H = 247.1; Rf (AcOEt/hexane =1:1): 0.23; HPLC: 3.60 min (System 1). 2-Chloro-4-(4-nitro-phenoxy)-pyrimidine (compound of Stace 148.3): The title compound is synthesized analogously to the preparation compound of Stage 22.5: M+H = 252.0/253.8; HPLC: 5.97 min (System 1); 1H-NMR (400 MHz, DMSO-d6): 8.67 (d, 5.5 Hz, 1H, pyriminidyl), 8.35 (d, 9.0 Hz, 2H. phenyl), 7.55 (d, 9.0 Hz, 2H, phenyl), 76.32 d, 5.5 Hz, 1H, pyrimidinyl). 4-Methoxv-3-trifluoromethvl-phenylamine (compound of Stage 149.1): The title compound is prepared from 1-methoxy-4-nitro-2-trifluoromethyl-benzene (1 g, 4.43 mmoi) by hydrogenation (5 -> 1.4 bar) in the presence of Raney-Ni (0.3 g) in MeOH (20 mL) during 15 h. The product is isolated by filtration of the reaction suspension over Hyflo and evaporation of the solvent under reduced pressure to give compound of Stage 149.1 as a beige solid: M+H = 191.9; Rf (AcOEt/hexane = 1:1): 0.33. Example 152: 1 -(4-f6-(4-Methoxy-phenylamino)-pvrimidin-4-vloxvl-phenvlV344-(2-methvI' imidazol-1-ylV3-trifluoromethvl-phenvn-urea The title compound is synthesized analogously to the preparation of compound of Example 47 by urea formation with [6-(4-amino-phenoxy)-pyrimidin-4-yl]-(4-methoxy-phenyl)-amine (Stage 47.1) and 4-(2-methyl-imidazol-1-yl)-3-trifluoromethyl-phenylamine (Stage 152.1): M+H = 575.8; HPLC: 4.73 min (System 1); Rf (AcOEt/hexane =1:1): 0.33; 1H-NMR (400 MHz, DMSO-d5): 9.33 (s, 1H), 9.29 (s, 1H), 8.94 (s, 1H), 8.24 (s, 1H), 8.14 (s, 1H), 7.71 (d, 9.0 Hz, 1H, phenyl-CF3), 7.52 (d, 8.5 Hz, 2H), 7.44 (d, 9.0 Hz, 1H, phenyl-CF3), 7.39 (d, 8.5 Hz, 2H), 7.13 (s, 1H), 7.11 (d, 8.5 Hz, 2H), 6.S6 (d, 8.5 Hz. 2H), 5.94 (s, 1H, pyrimidinyl), 3.71 (s, 3H, CH3-0), 2.04 (s, 3H, CH3-imidazolyl). 4-(2-Methvl-ifnidazol-1-yl)-3-trifluoromethvl-phenylamine (compound of Stage 152.1): The title compound is generated from 2-methyl-1-(4-nitro-2-trifluoromethyl-phenyl)-1H-imidazole (Stage 152.2) by hydrogenation in the presence of Raney-Ni in MeOH during 14 h at rt: Rf (MeOH/CH2CI2 = 1:5): 0.42; M+H = 242.0; m.p. = 217-219 °C. 2-Methvl-1-(4-nitro-2-trifluoromethyl-phenyl)-1H-imidazole (compound of Stage 152.2): The title compound is prepared by heating 1-bromo-4-nitro-2-trifluoromethyl-benzene and 2-methyl-imidazole between 100 - 150 °C during 15 h: M+H = 272.0; Rf (MeOH/CH2CI2 = 1:5): 0.60. In accordance with the methods described hereinbefore, the following compounds [Examples 153a) - 153x)], with the substituents given in Table 15, are prepared: tris(dibenzylideneacetone)dipalladium (6 mg) dissolved in dioxane (3 mL) are stirred at 55 °C under Ar for 8 h. After evaporating the solvent under reduced pressure, the residue is partitioned between H20 (60 mL) and AcOEt (200 mL). The organic phase is separated, dried (MgS04) and concentrated under reduced pressure. The product is purified by preparative thin layer chromatography (four 20 x 20 cm silica gel plates, acetone/CH2CI2 = 3:7): M+H = 431.9; R, (acetone/CH2CI2 = 3:7): 0.29; 1H-NMR (400 MHz, DMSO-d5): 10.85 (s, 1H, pyrimidinyl), 9.03/8.84 (s/sf 1H/1H, urea). 8.45 (s, 1H, NH), 7.98 (s, 1H, pyrimidinyl), 7.56 (d, 8.5 Hz, 1H, phenyl-CF3), 7.50 (d/s, 9.0 Hz, 2H/1H, phenyl/phenyl-CF3), 7.49 (t, 1H, phenyi-CF3), 7.29 (d, 8.5 Hz, 1H, phenyi-CF3), 7.06 (d, 9.0 Hz, 2H, phenyl), 7.39 (d, 8.5 Hz, 2H), 7.13 (s, 1H), 7.11 (d, 8.5 Hz, 2H), 6.86 (d. 8.5 Hz, 2H), 5.94 (s, 1H, pyrimidinyl), 2.09 (s, 3H, CH3). Example 156: 1 -f3-Methvl-4-(6-methylamino-Dvrimidin-4-vloxy)-phenvlT3-(3-trifluoromethvl-phenylVurea [6-(4-Amino-2-methyl-phenoxy)-pyrimidin-4-yl]-methyl-amine (73 mg, 0.31 mmol), 3-trifluoromethyl-phenyl-isocyanate (118 mg, 0.63 mmol), NEt3 (63.5 mg, 0.63 mmol) dissolved in CH2CI2 (7 mL) are stirred at rt for 1.5 h. The precipitating product is filtered off and dried in vacuo: M+H = 431.9; R, (hexane/AcOEt = 1:1): 0.43; HPLC (System 1): 5.26 min; 1H-NMR (400 MHz, DMSO-d6): 10.85 (s, 1H, pyrimidinyl), 9.23/8.92 (s/s, 1H/1H, urea), 8.07 (s/broad, 1H, NH), 7.98 (s, 1H, pyrimidinyl), 7.56 (d, 8.5 Hz, 1H, phenyl-CF3), 7.50 (d, 9.0 Hz, 1H, phenyl-CF3), 7.49 (t, 9.0 Hz, 1H, phenyl-CF3), 7.39 (s, 1H), 7.36 (m, 3H), 6.95 (d, 9.0 Hz, 1H, phenyl-CF3), 7.13 (s, 1H>, 5.66 (s/broad, 1H, pyrimidinyl), 2.74 (s/broad, 3H, CHrNH), 2.04 (s, 3H, CH3). f6-r4-Amino-2-methvl-phenoxv)-pyrimidin-4-vn-methvl-amine (compound of Stage 156.1): The title compound is prepared from [3-methyl~4-(6-methylamino-pyrimidin-4-yloxy)-phenyl]-carbamic acid benzyl ester by hydrogenation in the presence of Pd/C in MeOH/THF: M+H = 230.9; Rf (acetone/CH2CI2 = 1:1): 0.20. [3-Methvl-4-(6-methvlamino-pvrimidin^-vloxv)-phenyl1-c3rfaarnic acid benzyl ester (compound of Stage 156.2): The title compound is prepared from [4-(6-chIoro-pyrimidin-4-yloxy)-3-methyl-phenyI]-carbamic acid benzyl ester by aminomethylation (30 % CH3NH2 in EtOH, 60 min, rt): M+H = 363.9; Rf (acetone/CH2CI2 = 3:7): 0.26. f4-(6-ChlorO'pyrimidin-4-yloxv)-3-methyl-phenyl1-carbamic acid benzyl ester (compound of Stage 156.3): (4-Hydroxy-3-methyl-phenyl)-carbamic acid benzyl ester (278 mg, 1.08 mmol) and NaH (29 mg, 1.2 mmol) dissolved in DMF (5 mL) are stirred at rt for 15 min. 4,6-Dichloro-pyrimidine (177 mg, 1.19 mmol) dissolved in DMF (5 mL) is added and the reaction solution is stirred for 1 h, concentrated under reduced pressure and flash chrornatographed (silica gel, 2.5 x 60 cm, AcOEt/hexane = 1:6): M+H = 370.8; Rf (AcOEt/hexane = 1:6): 0.31. (4-Hydroxy-3-methyl-phenyl)-carbamic acid benzyl ester (compound of Stage 156,4): 4-Amino-2-methyI-phenol (717 mg, 5.8 mmol) and benzyloxycarbony! chloride (1.09 g, 6.4 mmol) are stirred in a suspension of AcOEt/concentrated Na2C03 solution (50 mL/50 mL) for 7 h. The organic phase is concentrated under reduced pressure and flash chrornatographed (silica gel, 3.8 x 66 cm, AcOEt/hexane = 1:3): M+H = 257.9; HPLC (System 1): 5.43 min. Example 157: 1-f4-(6-Amino-pyrimidin-4-vlmethvlVphenyn-3-(4-ethvl-phenylVurea The title compound is prepared as described in Example 102 but using 6-(4-aminobenzy!)-pyrimidin-4-ylamine, 4-ethyi-phenyl-isocyanate, and DMF as the solvent. The reaction mixture is stirred for 2 h. The title compound is obtained as a white solid: ES-MS: 348.0 [M+H]+; single peak at tR= 6.94 min (System 2). 6-(4-Aminobenzyl)-pyrimidin-4-ylamine: A 4 N solution of HCI in dioxane (19.2 mL, 76.4 mmol, 30 equiv) is added to a solution of [4-(6-amino-pyrimidin-4-ylmethyl)-phenyl]-carbamic acid tert-butyl ester (770 mg, 2.56 mmol) in CH2C)2 (23 ml), under an argon atmosphere. The resulting white suspension is stirred at rt for 1.5 h and concentrated in vacuo. To the residue is added a 2 M methanolic solution of ammonia (3.8 mL, 7.68 mmol, 3 equiv) and the resulting yellow solution is concentrated in vacuo. The crude product is purified by silica gel (90 g) column chromatography CH2CI2/MeOH, 90/10, then 80/20). The title compound is obtained as a white solid: ES-MS: 201.0 [M+H]*; single peak at tR= 2.00 rr.in (System 2); Rf = 0.20 (CH2CI2/MeOH, 90/10). [4-(6-Amino-pyrimidin-4-ylmethy!)-pheny!]-carbamic acid tert-butyl ester: A suspension of [4-(6-azido-pyrimidin-4-ylmethyl)-phenyl]-carbamic acid tert-butyl ester (870 mg, 2.66 mmol) and 10% Pd/C (174 mg) in MeOH (35 mL) is stirred for 1.5 h at rt and a hydrogen atmosphere. The reaction mixture is filtered through a plug of celite (washing the filter cake with copious amounts of MeOH). The filtrate is concentrated in vacuo to afford the title compound as a beige solid: ES-MS: 301.1 [M+H]+; single peak at tR= 6.25 min (System 2). [4-(6-Azido~pyrimidin-4-ylmethyl)-phenyl]-carbamic acid tert-butyl ester: A suspension of [4-(6-chloro-pyrimidin-4-ylmethyl)-phenyl]-carbamic acid tert-butyl ester (see Example 117) (1.1 g, 3.44 mmol) and sodium azide (0.31 g, 4.81 mmol, 1.4 equiv) in DMF (13 mL) is heated to 80 °C for 2.5 h. The reaction mixture is allowed to cool to rt and concentrated in vacuo. The residue is diluted with EtOAc (25 mL) and H20 (66 mL). The layers are separated and the aqueous layer is extracted with EtOAc (2 x 40 mL and 2 x 50 mL). The organic phase is dried (Na2S04), filtered and concentrated. The residue is purified by silica gel (80 g) column chromatography CH2CI2/Et201 90/10). The title compound is obtained as a white solid: ES-MS: 327.0 [M+H]+; single peak at tR= 7.42 min (System 2); Rf = 0.26 (CH2CI2/Et20, 90/10). Example 158: 1"f4-(6-Amino-pyrimidin-4-ylmethyl)-phenvn-3-p-tolyl-urea solvent. The reaction mixture is stirred for 3 h. The title compound is obtained as a white solid: ES-MS: 348.0 [M+Hf; single peak at tR= 6.94 min (System 2). Example 162: 1-(4-(2-[2-(3-Dimethvlamino-propvl)-2H-tetrazol-5-vn-Pvridin-4-vloxy)-ohenvn-3-(3-trifluoromethyl-phenyl)-urea The title compound is prepared according to a procedure similar to that described in Example 125. Example 163: 5-(6-Chloro-pyrimidin-4-yloxy)-2,3-dihydro-indole-1-carboxylic acid (3-trifluoromethyl-phenyQ-amide To a solution of 5-(6-chloro-pyrimidin-4-yloxy)-1H-indole (Stage 163.1; 14.5 mmol) in acidic acid (80 ml), NaBH3CN (90 %; 5.06 g, 72.5 mmol) is added portionwise. After 45 min, ice (20 g) is added and the mixture partially concentrated on the rotation evaporator. Then a 1 N solution of NaOH is added to the residue (pH = 11), which then is diluted with water and AcOEt. The aqueous layer is separated off and extracted twice with AcOEt. The organic phases are washed with 2 portions of water and brine, dried (Na2S04) and concentrated to give crude 5-(6-chloro-pyrimidin-4-yIoxy)-2,3-dihydro-1H-indole: MS: [M+1]+ = 248. This crude 2,3-dihydro-1H-indole is then dissolved in THF (70 ml) and 3-trifluoromethyI-isocyanate (93 %; 3.0 g, 14.9 mmol) is added. After 16 h at rt, the mixture is diluted with AcOEt and washed twice with water. The aqueous layer is extracted twice with AcOEt, the organic phases washed with brine, dried (Na2S04) and concentrated. Column chromatography (Si02; hexane/AcOEt 3:1 ~»2:1 -> 1:1) gives the title compound: m.p.: 181 °C; MS:[M+1]+ = 435;1H-NMR(DMS0-d6):8.85(s, HN), 8.62 (s, 1H), 8.00 (s, 1H),7.88(d, 1H)/7.84 (d, 1H), 7.50 (t, 1H), 7.33 (d, 1H), 7.29 (s, 1H), 7.09 (s, 1H), 6.98 (d, 1H), 4.19 (t, 2H), 3.20 (t, 2H). j he starting materials are prepared as follows: Stage 163.1: 5-(6-Ch]oro-pyrimidin-4-v!oxv)-1H-indole To a mixture of NaOH (720 mg, 18 mmol) and acetone/water 1:1 (72 ml), 4,6-clchioropyrimidine (2.4 g, 18 mmol) and 5-hydroxy-indole (2.68 g, 18 mmol) are added. After stirring for 70 min at 65 °C, the brownish solution is cooled to rt and diluted with AcOEt and water. The aqueous layer is separated off and extracted twice with AcOEt. The organic layers are washed with water, saturated Na2C03 solution, water and brine, dried (Na2SO.t) and concentrated. The crude product can be used without further purification: m.p.: 137-138 CC; MS: [M+1]+^246. Examples 164a)-c): Starting from 5-(6-chioro-pyrimidin~4-yloxy)-2,3-dihydro-indole-1 -carboxylic acid (3-trifluoromethyl-phenyl)-amide (Example 163), the following derivatives are made analogously: - a): 5-(6-azido-pyrimidin-4-yioxy)-2,3-dihydro-indole-1 -carboxylic acid (3-trifluoromethyI-phenyl)-amide; - b): 5-(6-amino-pyrimidin-4-yloxy)-2,3-dihydro-indole-1-carboxylic acid (3-trifiuoromethyl-phenyl)-amide; and - c): 5-(6-methylamino-pyrimidin-4-yloxy)-2,3-dihydro-indole-1-carboxylic acid (3-trifluoromethyl-phenyl)-amide. Example 165: Pharmacokinetic data The compound of formula I or I* to be tested is formulated for administration to female MAG mice from BRL, Fuellinsdorf, Switzerland, by dissolving in DMSO/Tween 80 (90:10 v/v). The solution is diluted 1 :20 with distilled water and briefly sonicated to give a macroscopically homogenous suspension in 5 % v/v DMSO/0.5 % v/v Tween 80. Final concentrations of compound are 10, 3 and 1 mg/ml for dosed of 50 mg/kg, respectively. Each formulation is examined under a phase contrast microscope and particle form described and size are estimated. The formulated compound is administered by gavage to provide dosages of 50 mg/kg. At the alloted time points mice (4 at each time) are anesthesized with 3 % isoflurane in oxygen and heart blood is removed into heparinized tubes (ca. 30 lU/ml). The animals are subsequently killed without recovering from the anesthetic. Plasma is prepared from the blood by centrifu-gation (10,000 g, 5 min) and either analysed immediately or stored frozen at - 70 °C. The plasma samples are mixed with an equal volume of acetonitrile and allowed to stand at rt for 20-30 min. The protein precipitate is removed by centrifucation (10,000 x g) and a sample of the supernatant is analysed by reversed-phase HPLC on Merck-Hitachi LaChrom® equipment. The sample (100 ul) is injected onto a Nucleosil® 100-5 C18 column (Macherey & Nagel, Dtiren, F.R.G.) (125 x 4 mm) with a guard column (8x4 mm) of the same material. The column is equilibrated e.g. with a 5 % v/v acetonitrile in water containing 0.05 % trifluo-roacetic acid (TFA). The sample is eluted e.g. with a gradient of 5 % v/v acetonitrile to 95 % v/v acetonitrile (in water with 0.05 % v/v TFA) over a period of 10 min. The column is then prepared for the next sample by holding the gradient at the final conditions for 5 min, then returning to the starting conditions and reequilibrating for 5 min. The compound is detected by absorbance, e.g. at 320 nm. The identity of the peak can be confirmed by retention time and UV absorption spectrum (diode array detector 205 - 400 nm) compared to controls. The amount of compound is quantified by the external standard method. A calibration curve is constructed with known amounts of compound in plasma which is processed as described above. Compounds of the formula I or I* according to the invention here show plasma concentrations in the area of e.g. 1 to 50 ^M. Example 166: In vitro inhibition data Enzymatic (c-Abl, KDR, Flt3) data are given on Table 17 (% inhibition at 10 nM). (Measurements are made as described above in the general description). Manufacture: The active ingredient is mixed with the carrier materials and compressed by means of a tabietting machine (Korsch EKO, Stempeidurchmesser 10 mm). Avicel is microcrystaliine cellulose (FMC, Philadelphia, USA). PVPPXL is polyvinylpolypyrrolidone, cross-linked (BASF, Germany). Aerosil is silcium dioxide (Degussa, Germany). Example 168: Capsules Capsules, comprising, as active ingredient, 100 mg of any one of the compounds of formula I or I* given in Examples 1 to 164c), of the following composition are prepared accoding to standard procedures: Manufacturing is done by mixing the components and filling them into hard gelatine capsules, size 1. What is claimed is: 1. Use of a diaryl urea derivative of She formula I wherein G is either not present, lower alkyiene or C3-C5cyc!oalkyiene and Z is a radical of the formula la or G is not present and Z is a radical of the formula lb A is CH, N or N-»0 and A1 is N or N~»0, with the proviso that not more than one of A and A can be N-»0; n is 1 or 2; m is 0, 1 or 2; p is 0, 2 or 3; r is 0 to 5; X is NR if p is 0, wherein R is hydrogen or an organic moiety, or if p is 2 or 3, X is nitrogen which together with (CH2)P and the bonds represented in dotted (interrupted) lines (including the atoms to which they are bound) forms a ring, or X is CHK wherein K is lower a!kyl or hydrogen and p is zero, with the proviso that the bonds represented in dotted line.?, if p is zero, are absent; YT is O, S or CH2; Y;isO, Sor NH; with the proviso that (Y1)ri-(Y2)-. dees not include O-O, S-S. NH-O, NH-S or S-0 groups; each of R,, R2) R3 and R5, independency of the others, is hydrogen or an inorganic 0^ organic moiety or any two of them together form a lower a'kylene-dioxy bridge bound via the oxygen atoms, and the remaining one of these moieties is hydrogen or an inorganic or organic moiety; and R4 (if present, that is, if r is not zero) is an inorganic or organic moiety; or a tautomer thereof; or a pharmaceutical^ acceptable salt thereof; for the manufacture of pharmaceutical compositions for use in the treatment of protein kinase dependent diseases. 2. The use according to claim 1 wherein the diaryl urea derivative is a compound of the formula I according to claim 1 wherein G is either not present, lower aikylene, especially methylene or ethylene, or C3- C5cycloalkylene, especially cyclopropylene, and Z is a radical of the formula la according to claim 1, or G is not present and Z is a radical of the formula lb according to claim 1; A is CH or N and A' is N or N->0; n is 1; misOoM; p is 0, 2 or 3; r is 0 or 1; X is NR if p is 0, wherein R is hydrogen or lower alkyl, or if p is 2 or 3, X is nitrogen which together with (CH2)? and the bonds represented in dotted (interrupted) lines (including the atoms to which they are bound) forms a ring, or X is CHK wherein K is hydrogen and p is zero, with the proviso that the bonds represented in dotted lines, if p is zero, are absent; Yi isO, SorCH2; Y: is O; with the proviso that (Y1)n-(Y2)n c!oes not include 0-0, or S--0 groups; each of R), R2 and R3, independently of the others, is hydrogen, lower alkyl, especially methyl, ethyl, n-propyl, isopropy! or tert-biit\!, lower alken;. -, especially iscpropenyl, hydroxy-lower alkyl, especially hydroxy-propyl, lower alkoxy, especially rnethoxy, halo, especially chioro or brorno, halo-lower alky!, especiaw' trifliioromethy. halo-lower alkoxy, especially wfkiorornethoxy or trifluoroethoxy, amino-iower alkyi, especially aniinomeihyl, amino-lower aY-'.oxy, especially arninoethoxy di-lower alkyl-amino, especially diethylamide, hydrcxydower a'kyl-amino, especially hydroxy-propylarnino, bis-(lower alkoxy-lower a'kylj-arnino, especially ti3-(2-mothoxy-ethyl)-aminoI di-iower alkyl-amino-Iower alkyl, especially ciimethylaminomethyl, phenyl, morpholinyl, especially morpholin-4-yl, piperidyl, especially piperidin-1-yI, piperidyl-lower alkyl, especially piperidin-1-y'methyl, lower alkyl-piperazinyl, especially 4-methyl-piperazin-1-yl or 4-ethyl-piperazin-1-yl, lower alkyl-piperazinyl-lower alkyl, especially 4-methyl-piperazin-1-y!methyl or 4-ethyl-piperazin-1-yImethyl, pyridyl, especially pyridin-2-yI, or lower alkyl-imidazolyl, especially 2- or 4-methyl-imidazol-1-yl; if r is 1, RA is lower alkyl, especially methyl, ethyl or ispropyl, hydroxy, aminocarbonvl, lower alkyl-carbonyl, especially methylcarbonyl, cyclohexyl, halo, especially chloro or fluoro, halo-lower alkyl, especially trifluoromethyl, lower alkoxy, especially rnethoxy, amino, lower alkyl-amino, especially methylamino, ethylamino, isopropylamino or tert-butylamino, di-lower alkyl-amino, especially dimethylamino, lower alkenyl-amino, especially prop-2-enylamino or but-3-enylamino, lower alkyl-carbonyl-amino, especially methylcarbonylamino, cyano, azido, hydroxy-phenyl-amino, especially 3- or 4-hydroxy-phenyl-amino, mono or tri-lower alkoxy-phenyl-amino, especially methoxy-phenyl-amino or trimethoxy-phenyl-amino, lower alkoxy-halo-phenyl-amino, especially methoxy-fluoro-phenyl-amino, phenyl-lower alkylamino, especially benzylamino, (mono or di-lower alkoxy)-phenyMower alkylamino, especially methoxy-benzylamino or dimethoxy-benzylamino, aminosulfonyl-phenyl-lower alkylamino, especially aminosulfonyl-benzylamino, amino-lower alkoxy-phenyl-amino, especially aminoethoxy-phenyl-amino, lower alkyl-amino-sulfonyl-lower alkyl-phenylamino, especially methylamino-sulfonylmethyl-phenylamino, lower alkyl-piperazinyl-lower alkylamino, especially 4-methylpiperazin-1-yl-propylamino, morpholinyl-Iower alkylamino, especially morphoIin-4-yl-propylamino, lower alkyl-piperidyl-amino, especially 1-methyI-piperidin-4-ylamino, tetrazolyl, especially 1H-tetrazoi-5-yl, lower alkyl-tetrazolyl, especially lower alkyl-tetrazoi-5-yl such as 1-methyl-1H-tetrazol-5-yl or 2-methyl-2H-tetrazol-5-yl, or (di-lov/er alkyI)-amino-Iower alkyl-tetrazolyl, especially (di-lower alkyl)-amino-lower alkyl-tetrazol-5-yl such as 2-(3-dimethylaminopropyl)-2H-tetrazol-5-yl; R5 is most preferably hydrogen, or lower aikyl, especially methyl, or halo, especially chloro; cf a tautomer thereof; cr a pharmaceutically acceptable salt thereof. 3. The use according to claim 1 wherein the diaryl urea derivative is a compound of the formula I according tcrclaim 1 wherein A and A' are both N, n is 1, m is 0, p is 0 or 2, r is 1, X is NH if p is 0, Of if p is 2, X is nitrogen which together with (CH2)2 and the bonds represented in dotted (interrupted) lines (including the atoms to which they are bound) forms a ring, Yj is O, G is not present, Z is a radical of the formula la according to claim 1, at least one of Ri, R2 and R3 is a basic organic moiety, R4 is amino or lower alkylamino and R5 is hydrogen. 4. The use according to claim 1 wherein the diaryl urea derivative is a compound of the formula I* wherein A, A', n, m, p, r, X, Ylf Y2 and RrR5 have the meanings as defined for a compound of formula I according to claim 1; or a tautomer thereof; or a pharmaceutically acceptable salt thereof. 5. The use according to claim 4 of a compound of the formula I* or a tautomer thereof, or a pharmaceutically acceptable salt thereof, where, in the compound of the formula I*, A is CH, N or N->0 and A' is N or N-»0, with the proviso that not more than one of A and A' can be N->0; n is 1; m is 0; p is 0, 2 or 3; r is 0, 1 or 2; X is NR if p is 0, wherein R is hydrogen or lower alkyl, or if p is 2 or 3, X is nitrogen which together with (CH2)? and the bonds represented in dotted '.interrupted) lines (including the atoms to which they are bound) forms a ring, or X is CH2 and p is zero, with the proviso that the bonds represented in dotted lines, if p is zero, are absent; Y- is O or CH2; each of R1( R2 and R3 independently of the others, is hydrogen, lower alkyl, halo, especially tromo or chloro, halo-lower alkyl, especially trifluoromethyl, lower alkoxy, especially methoxy, halo-lower alkoxy, especially 2,2,2-trifluoroethoxy, phenyl, piperidyl, especially piperidin-1-yl, piperazinyl, especially piperazin-1-yl, morpholinyl, especially morpholine, thiomorpho-linyl, especially thiomorpholino, or any two of them together form a lower alkylene-dioxy bridge bound via the oxygen atoms, and the remaining one of these moieties is hydrogen or one of the moieties mentioned; if r is not zero, R4 is lower alkyl, especially methyl or ethyl, lower alkoxy, especially methoxy, lower alkanoylamino, especially acetylamino, hydroxyphenylamino, especially p-hydroxyphenylamino, amino-lower alkyl-oxyphenyl-amino, especially 4-[(2-aminoethyl)-oxyphenylj-amino, sulfamoylphenylamino, especially 4-sulfamoylphenylamino, carbamo-yiphenylamino, especially 4-carbamoylphenylamino, [N-(hydroxy-lower alkyl)-carbamoyl]-phenylamino, especially [N-(2-hydroxyethyl)-carbamoyl]-phenylamino, halo, especially chloro, or hydroxy!; and R5 is hydrogen, lower alkyl or halo, especially hydrogen. 6. The use according to any one of claims 1 to 5 where the protein kinase dependent disease is a tyrosine protein kinase dependent disease, especially a proliferative disease depending on any one or more of of the following tyrosine protein kinases: ras, Abl, VEGF-receptor tyrosine kinase, Flt3, and/or Bcr-Abl activity. 7. A compound of the formula I according to claim 1 or a tautomer thereof, or a pharmaceutical^ acceptable salt thereof, where, in the compound of the formula I, A is CH, N or N->0 and A' is N or N->0, with the proviso that not more than one of A and A' can be N->0; n is 1 or 2; m is 0, 1 or 2; p is 0, 2 or 3; r is 1 to 5; X is NR if p is 0, wherein R is hydrogen or an organic moiety, or if p is 2 of 3, X is nitrogen which together with (CH2)P and the bc~ds represented in dotted (interrupted) lines (including the atoms to which they are bound) fcrms a ring, with the proviso that if X is NH, each of PM. independently of the others if r>1, is a moiety as defined in claim 1 but not bound to the rest of formula I via a -C(=0)-, -C(NR)- cr -S(02)- bridge, or X is CHK wherein K is lower alkyl or hydrogen and p is zero, with the proviso that the bonds represented in dotted lines, if p is zero, are absent; YT is O, S or CH2; Y2 is O, S or NH; with the proviso that (Y1)n-(Y2)m does not include O-O, S-S, NH-O, NH-S or S-0 groups; each of Rlt R2, R3 and R5( independently of the others, is hydrogen or an inorganic or organic moiety or any two of Ru R2 and R3 together form a lower alkylene-dioxy bridge bound via the oxygen atoms, and the remaining one of these moieties is hydrogen or an inorganic or organic moiety, with the proviso that if G is not present and Z is a radical of the formula la according to claim 1, Rlt R2 and R3 cannot all be hydrogen and with the further proviso that if one of Rlf R2 and R3 is halo or lower alkyl-sulfonyl, the other two cannot both be hydrogen; R4 is an inorganic or organic moiety, with the proviso that if n is 1, m is 0, p is 0, r is 1, X is NH, Y1 is O, G is not present and Z is a radical of the formula la according to claim 1, R4, together with the benzene ring containing A and A', does not form methylpyridinyl, 2- hydroxy-pyridin-4-yl or 1-H-2-oxo-1,2-dihydropyridin-4-yl; and G and Z have the meanings given under formula I in claim 1. 8. A compound of the formula I according to claim 7 wherein G is either not present, lower alkylene, especially methylene or ethylene, or C3- C5cycloalkylene) especially cyclopropylene, and Z is a radical of the formula la according to claim 1, or G is not present and Z is a radical of the formula lb according to claim 1; A is CH or N and A' is N or N->0; n is 1; m is 0 or 1; p is 0, 2 or 3; r is 1; X is NR if p is 0, wherein R is hydrogen or lower alkyl, or if p is 2 or 3, X is nitrogen, which together with (CH2)P and the bonds represented in dotted (interrupted) lines (including the atoms to which they are bound) forms a ring, or X is CHK wherein K is hydrogen and p is zero, with the proviso that the bonds represented in dotted lines, if p is zero, are absent; Y, is O, S or CH2; Y2 is O; with the proviso that (Y1)n-(Y2)m does not include O-O, or S-0 groups; each of R1( R2 and R3, independently of the others, is hydrogen, lower alkyl, especially methyl, ethyl, n-propyl, isopropyl or tert-butyl, lower alkenyl, especially isopropenyl, hydroxy- lower alkyl, especially hydroxy-propyl, lower alkoxy, especially methoxy, halo, especially chloro or bromo, halo-lower alkyl, especially trifluoromethyl, halo-lower alkoxy, especially trifluoromethoxy or trifluoroethoxy, amino-lower alkyl, especially aminomethyl, amino-lower alkoxy, especially aminoethoxy, di-lower alkyl-amino, especially diethylamino, hydroxy-lower alkyl-amino, especially hydroxy-propylamino, bis-(lower alkoxy-lower aikyl)-amino, especially bis-(2-methoxy-ethyl)-amino, di-lower alkyl-amino-lower aikyJ, especially dimethylaminomethyl, phenyl, morpholinyl, especially morpholin-4-yl, piperidyl, especially piperidin-1-yl, piperidyl-lower alkyl, especially piperidin-1-ylmethy!, lower alkyi-piperazinyl, especially 4-methyI-piperazin-t-yI or 4-ethyl-piperazin-1-yl, lower alkyl-piperazinyl-lower alkyl, especially 4-methyl-piperazin-1-ylmethyl or4-ethyl-piperazin-1-ylmethyI, pyridyl, especially pyridin-2-yl, or lower alkyl-imidazolyl, especially 2- or 4-methyl-imidazoi-1-yl, with the proviso that if G is not present and Z is a radical of the formula la according to claim 1, R1( R2 and R3 cannot all be hydrogen and with the further proviso that if one of R1( R2 and R3 is halo, the other two cannot both be hydrogen; R4 is lower alkyl, especially methyl, ethyl or ispropyl, hydroxy, aminocarbonyl, lower alkyl- carbonyl, especially methylcarbonyl, cyclohexyl, halo, especially chloro or fluoro, halo-lower alkyl, especially trifluoromethyl, lower alkoxy, especially methoxy, amino, lower alkyl-amino, especially methylamino, ethylamino, isopropylamino o( tert-butylamino, di-lower alkyl-amino, especially dimethylamino, lower alkenyl-amino, especially prop-2-enylamino or but-3- enylamino, lower alkyl-carbonyl-amino, especially methylcarbonylamino, cyano, azido, hydroxy-phenyl-amino, especially 3- or 4-hydroxy-phenyi-amino, mono or tri-lower alkoxy-phenyl-amino, especially methoxy-phenyl-amino or trimethoxy-phenyl-amino, lower alkoxy-halo-phenyl-amino, especially methoxy-fluoro-phenyl-amino, phenyl-Iower alkylamino, especially benzylamino, (mono or di-iov/er alkoxy)-phen\ '-lower alkylamino, especially methoxy-benzylamino or dimethoxy-ber.zylamino, aminosulfonyl-phenyl-Iower alkylamino, especially aminosulfonyl-benzylamino, amino-lower alkoxy-phenyl-aminc. especially aminoethoxy-phenyl-amino, lower alkyl-amino-sulfonyl-lower alkyl-phenylamino. especially methylamino-sulfonylmethyl-phenylamino, lower alkyl-piperazinyl-lower alkylamino, especially 4-methy!piperazin-1-yl-propy!amino, morpholinyl-lower alkylamino, especially morpholin-4-yl-propylamino, lower alkyl-piperidyl-amino, especially 1 -methyl-piperidin-4-ylamino, tetrazolyl, especially 1 H-tetrazol-5-yl, lower alkyl-tetrazolyl, especially lower alkyl-tetrazol-5-yl such as 1 -methyl-1 H-tetrazol-5-yl or 2-methyI-2H-tetrazol-5-yl, or (di-lower a!kyl)-amino-lower alkyl-tetrazolyl, especially (di-lower a!kyI)-amino-lower alkyl-tetrazol-5-yl such as 2-(3-dimethylaminopropyl)-2H-tetrazol-5-yl, with the proviso that if X is NH, R4 is not aminocarbonyl or lower alkyl-carbonyl and with the further proviso that if n is 1, m is 0, p is 0, r is 1, X is NH, Y, is 0, G is not present and Z is a radical of the formula la according to claim 1, R4, together with the benzene ring containing A and A', does not form methylpyridinyl, 2-hydroxy-pyridin-4-yl or 1-H-2-oxo-1,2-dihydropyridin-4-yl; R5 is most preferably hydrogen, or lower alkyl, especially methyl, or halo, especially chloro; or a tautomer thereof; or a pharmaceutical^ acceptable salt thereof. 9. A compound of the formula I according to claim 7 wherein A and A' are both N, n is 1, m is 0, p is 0 or 2, r is 1, X is NH if p is 0, or if p is 2, X is nitrogen which together with (CH2)2 and the bonds represented in dotted (interrupted) lines (including the atoms to which they are bound) forms a ring, Yj is 0, G is not present, Z is a radical of the formula la according to claim 1, at least one of R1( R2 and R3 is a basic organic moiety, R4 is amino or lower alkylamino and R5 is hydrogen, or a tautomer thereof, or a pharmaceutical^ acceptable salt thereof. 10. A compound of the formula I* according to claim 4 or a tautomer thereof, or a pharmaceutical^ acceptable salt thereof, where, in the compound of the formula I*, A is CH, N or N->0 and A' is N or N-»0, with the proviso that not more than one of A and A' can be N-»0; n is 1; m is 0; p is 0, 2 or 3; r is 1; X is NR if p is 0, wherein R is hydrogen or lower alkyi, or if p is 2 or 3, X is nitrogen which together with (CH2)P and the bonds represented in dotted (interrupted) lines (including the atoms to which they are bound) forms a ring, or X is CH2 and p is zero, with the proviso that the bonds represented in dotted lines, if p is zero, are absent; Y, is OorCH2; each of Ru R2 and R3 independently of the others, is hydrogen, lower alkyl, halo, especially bromo or chloro, halo-lower alkyl, especially trifluoromethyl, lower alkoxy, especially metho- xy, halo-lower alkoxy, especially 2,2,2-trifluoroethoxy, phenyl, piperidyl, especially piperidin- 1-yl, piperazinyl, especially piperazin-1-yl, morpholinyl, especially morpholine, thiomorpho- iinyl, especially thiomorphoiino, or any two of them together form a lower aikylene-dioxy bridge bound via the oxygen atoms, and the remaining one of these moieties is hydrogen or one of the moieties mentioned, with the proviso that R,, R2 and R3 cannot al) be hydrogen and with the further proviso that if one of R1( R2 and R3 is halo, the other two cannot both be hydrogen; R4 is lower alkoxy, especially methoxy, lower alkanoylamino, especially acetyfamino, hydroxyphenylamino, especially p-hydroxyphenylamino, amino-lower alkyl-oxyphenyl-amino, especially 4-[(2-aminoethyl)~oxyphenyl]-amino, sulfamoylphenylamino, especially 4- sulfamoylphenylamino, carbamoylphenylamino, especially 4-carbamoyIphenylamino, [N- (hydroxy-lower alkyO-carbamoylj-phenylamino, especially [N-(2-hydroxyethyl)-carbamoyl]- phenylamino, or halo, especially chloro; and R5 is hydrogen, lower alkyl or halo, especially hydrogen. 11. A compound of the formula I* according to claim 4 or a tautomer thereof, or a pharmaceutical^ acceptable salt thereof, where, in the compound of the formula I*, A, A', n, m, p, Y1, Y2, Ri, R2, R3 and R4 have the meanings given under formula I* in claim 4, and r is 1 to 5, X is NR if p is 0, wherein R is hydrogen or an organic moiety, or if p is 2 or 3, X is nitrogen which together with (CH2)P and the bonds represented in dotted (interrupted) lines (including the atoms to which they are bound) forms a ring, or X is CH2 and p is zero, and, if p is zero, the bonds represented in dotted lines are absent; with the proviso that if X is NH, each of R^, independently of the others, if present, is a moiety as defined in claim 4 but not bound to the rest of formula 1* via a -C(=0)-, -C(NR)- or -S(02)- bridge, and the substituents R-. R- and R3 are se'ected from the following moieties, ■/.-hereby positions (o = ortho, m = me:a. p = para) are indicated with regard to the position .vhere the ring is bound to the rest of -he molecule in formula I* (via the NH-C(=0)-X-moiety): : only Ri is other than hydrogen: RT = p-lower alkyl, especially p-methyl, p-ethyl, p-n-propyl; m-halo-lower alkyl, especially m-trifluoromethyi; or phenyl, p-piperidin-1-yl or p-piperazin-1-yl; if both Ri and R2 are other than hydrogen: Rt = m-halo-lower alkyl, especially m-trifluoromethyi, and R2 = p-halo, especially p- bromo; R, = m-halo-lower alkyl, especially m-trifluoromethyi, and R2 = p-halo-lower alkoxy, especially p-(2,2,2-trifluoroethoxy); R, = m-halo-lower alkyl, especially m-trifluoromethyl, and R2 = m-lower alkoxy, especially m-methoxy; RT = m-halo-lower alkyl, especially m-trifluoromethyl, and R2 = p-phenyl; Ri = m-halo-lower alkyl, especially m-trifluoromethyl, and R2 = p-piperidin-1-yl or p- piperazin-1-yl; Ri = m-halo-lower alkyl, especially m-trifluoromethyl, and R2 = p-N-morpholino or p-N- thiomorpholino; Ri = m-lower alkoxy, especially m-methoxy, and R2 = p-halo, especially p-bromo (less preferred); RT = m-lower alkoxy, especially m-methoxy, and R2 = p-halo-lower alkoxy, especially p-2,2,2-trifluoroethoxy; Ri = m-lower alkoxy, especially m-methoxy, and R2 = p-phenyl; or Ri = m-lower alkoxy, especially m-methoxy, and R2 = p-piperidin-1-yl or p-piperazin-1- yi; or, if Ri, R2 and R3are other than hydrogen: R, = m-lower alkoxy, especially m-methoxy; R2 = m-lower alkoxy, especially m-methoxy; and R3 = p-lower alkoxy, especially p-methoxy; or RT = lower aikoxy, especially methoxy, and R2 and R3 together form a lov/er-alkylene- dioxy, especially-0-CH2-CH2-O, bridge; and R5 is hydrogen, lower aikyi or ha'c. especialiy hydrogen; with the proviso that if n is 1, m is 0, p is 0, r is 1, X is NH and Y} is C. R4, together with the benzene ring containing A and A', does not form methylpyridinyl, 2-hydroxy-pyridin-4-yI or 1-H-2-oxo-1,2-dihydropyridin-4-yI. 12. A compound of the formula I* according to claim 4 or a tautomer thereof, cr a pharmaceutical^ acceptable salt thereof, where, in the compound of the formula I*, A is CH, N or N^O and A' is N or N--0, with the proviso that not more than one of A and A' can be N->0; n is 1; m is 0; p is 0, 2 or 3; r is 1 or 2; X is NR if p is 0, wherein R is hydrogen or lower aikyi, or if p is 2 or 3, X is nitrogen which together with (CH2)P and the bonds represented in dotted (interrupted) lines (including the atoms to which they are bound) forms a ring, or X is CH2 and p is zero, with the proviso that the bonds represented in dotted lines, if p is zero, are absent; YT is O or CH2; Ru R2 and R3 are selected from the following moieties, whereby positions (o = ortho, m = meta, p = para) are indicated with regard to the position where the ring is bound to the rest of the molecule in formula I* (via the NH-C(=0)-X-moiety): if only Ri is other than hydrogen: R, = p-lower aikyi, especially p-methyl, p-ethyl, p-n-propyl; m-halo-Iower alkyl, especially m-trifluoromethyl; or phenyl, p-piperidin-1-yl or p-piperazin-1-yl; if both Ri and R2 are other than hydrogen: R} = m-halo-lower alkyl, especially m-trifluoromethyl, and R2 = p-halo, especialiy p-bromo; Ri = m-halo-lower alkyl, especially m-trifluoromethyl, and R2 = p-halo-lower aikoxy, especially p-(2,2,2-trifluoroethoxy); R, = m-halo-lower alkyl, especially m-trifluoromethyl, and R2 = m-lower aikoxy, especially m-methoxy; Rt = m-halo-lower alkyl, especially m-trifluoromethyl, and R2 = p-phenyl; R, = m-halo-lower alkyl, especially m-trifluoromethyl, and R2 = p-piperidin-1-yl or p- piperazin-1-yl; R, = m-halo-lower alkyl. especially m-trifluoromethyl, and R2 = p-N-morpholino or p-N- thiomorpholino; PM = m-lov/er alkoxy, especially m-methoxy, and R: = p-halo, especially p-bromo (less preferred); R, = m-lower alkoxy, especially m-methoxy, and R: = p-ha!o-!ov/er alkoxy. especially p-2,2,2-trif)uoroethoxy; R, = m-lower alkoxy, especially m-methoxy, and R; = p-phenyl; or RT = m-lower alkoxy, especially m-methoxy, and R? = p-piperidin-1-yl or p-piperazin-1- yi; or, if Ru R2 and R3are other than hydrogen: Ri = m-lower alkoxy, especially m-methoxy; R2 = m-lower alkoxy, especially m-methoxy; and R3 = p-lower alkoxy, especially p-methoxy; oc RT = lower alkoxy, especially methoxy, and R2 and R3 together form a lower-alkylene-dioxy, especially -0-CH2-CH2-O, bridge; and, if r is not zero, R4 is lower alkoxy, especially methoxy, lower alkanoylamino, especially acetyiamino, hydroxyphenylamino, especially p-hydroxyphenylamino, amino-lower alkyl-oxyphenyl-amino, especially 4-[(2-aminoethyl)-oxyphenyl]-amino, sulfamoylphenylamino, especially 4-sulfamoylphenyiamino, carbamoylphenylamino, especially 4-carbamoylphenylamino, [N-(hydroxy-lower alkyl)-carbamoyi]-phenylamino, especially [N-(2-hydroxyethyO-carbamoylj-phenylamino, or halo, especially chloro; and R5 is halo, especially chloro, lower alkyl, especially methyl, or preferably hydrogen. 13. A compound of the formula I* selected from the group consisting of N-(4-pyridin-4-yl-oxy-phenyl)-N,-(4-ethyl-phenyl)-ureaJ N-(4-pyridin-4-yl-oxy-phenyI)-N'-(3-trifluoromethyl-phenyl)-urea, N-(4-pyridin-4-yl-oxy-phenyl)-N'-(4-(2,2,2-trifluoroethoxy)-3-trifIuoromethyl-phenyl)-urea; N-(4-(4-(4-hydroxyphenylamino)-pyrimidin-6-y!)-oxyphenyl)-N'-(3-trifluoromethyiphenyl)-urea; and N-(4-(2-methyl-pyridin-4-yl)-oxyphenyl)-N'-(3-trifluoromethyl-phenyl)-urea; or a pharmaceutical/ acceptable salt thereof. 14. A compound of the formula I* selected from the group consisting of N-(4-pyridin-4-yl-oxy-phenyl)-N'-(4-n-prop>l-phenyl)-urea, N-(4-pyridin-4-yi-oxy-phenyl)-N,-(4-methyl-phenyl)-urea, N-methyi-N-(4-pyridin-4-yl-oxy-phenyi)-N'-i4-ethyi-phenyl)-urea1 N-methyl-N-(4-pyridin-4-yl-oxy-phenyl)-N'-;3-trifiuoromethyl-phenyl)-urea, N-methyI-N-(4-pyridin-4-yl-oxy-phenyl)-N,-i4-n-propyl-phenyl)-urea, N-methyI-N-(4-pyridin-4-yl-oxy-phenyl)-N'^4-methyl-phenyi)-urea, N-(4-pyridin-4-yI-oxy-phenyl)-N,-(4-bromo-3-trif!uoromethy!-phenyI)-urea, N-(4-pyridin-4-yl-oxy-phenyl)-N'-(3-methox"/-54rifluoromethyl-phenyi)-urea1 N-(4-pyridin-4-ylmethyl-phenyI)-N,-(4-n-prcpyI-phenyl)-urea1 N-(4-pyridin-4-ylmethyI-phenyl)-N'-(4-ethy!-phenyI)-urea, N-(4-pyridin-4-ylmethyl-phenyi)-N,-(4-rnethyl-phenyI)-urea, N-(4-pyridin-4-ylmethyl-phenyl)-N,-(3-trifluoromethyl-phenyl)-urea, N-(4-pyridin-4-y!-oxy-phenyl)acetyl-(4-ethyl-phenyl)-amide, N-(4-pyridin-4-yl-oxy-phenyl)acetyl-(4-methyl-phenyl)-amide, N-(4-pyridin-4-yI-oxy-phenyi)acetyl-(4-n-propyl-phenyl)-amide, 5-(4-pyridyl-oxy)-N-(3-trifluoromethyl-phenyl)amino-carbonyl-2)3-dihydroindole, 5-(4-pyridyl-oxy)-N-(3-trifluoromethyl-phenyl)amino-carbonyl-1l2,3l4-tetrahydroquinolinel N-(4-(4-Chloropyrimidin-6-y!)-oxyphenyl)-N'-(3-trif!uoromethylphenyl)-urea, N-(4-pyridin-4-y!-oxyphenyl)-N,-(4-phenyl-3-trifluoromethyl-phenyl)-urea) N-(4-pyridin-4-yl-oxyphenyl)-N'-(4-(piperidin-1-yl)-3-trifluoromethyl-phenyI)-urea, N-(4-pyridin^-yl-oxyphenyl)-N'-(4-(morphoiino)-3-trifluoromethyi-phenyl)-urea, N-(4-pyridin-4-yl-oxyphenyl)-N'-(3,4t5-tnmethoxy-phenyl)-urea, N-(4-pyridin-4-yl-oxyphenyl)-N'-(3-methoxy-4-phenyl-phenyl)-urea, N-(4-pyridin-4-yI-oxyphenyl)-N'-(3-methoxy-4,5-(ethylen-1,2-dioxy)-phenyl)-urea, N-(4-pyridin-4-yl-oxyphenyl)-NX3-methoxy-4-(2,2,2-trifluoroethoxy)-phenyi^ N-(4-pyridin-4-yl-oxyphenyl)-N,-(3-methoxy-4-piperidin-1-yl-phenyl)-urea, N-(4-pyridin-4'yl-oxyphenyl)-N'-(4-piperidin-1-yl-phenyl)-urea, N-(4-[2-(44iydroxyphenyl)-amino-pyrimidi^ urea, N-(4-[4-(4-sulfamoylphenyl)-amino-pyrimidin-6-yl]-oxyphenyl-N,-(3-trifluoromethyl-phenyl)- urea, N-(4-[4-(4-carbamoylphenyl)-amino-pyrimidin-6-yl]-oxyphenyl-N'-(3-trifluoromethyl-phenyl)- urea, N-(4-[4^(4-(N-2-hydroxyethylcarbamoyl)-prenyl)-amino-pyrimidin-6-yl]-oxyphenyl-N'-(3- trifluoromethyl-phenyl)-urea, N-(4-[4-(4-hydroxyphenyl)-amino-pyrimidir-3-yl]-oxyphenyl-N'-(3-trifluoromethyI-4-(212,2- trifluoroethoxy)-phenyl)-urea, N-(4-(N-oxido-pyridin-4-yl)-oxyphenyl)-N,-(3-trifluoromthy!-phenyl)-ureaI N-(4-(2-methoxypyridin-5-yl)-ox7phenylrN,-(3-trifluorom9ihyl-phenyl)-urea. N-(4-(2-pyridon-5-yl)-oxyphenyl)-N'-(3-trif!,joromethyl-phenyl)-urea, N-[4-{(2-acetylamino)-pyridin-4-yl}-oxy]-phenyl-N'-(3-trifluoromethyl-phenyl)-urea) N-^-fpyridin^-yl-oxyJ^-chloro-phenylJ-N'-S-trifluoromethyl-phenylJ-urea, N-[4-(pyridin-4-yl-oxy)-2-meLhyl-phenylj-N'-i3-trifluorometnyl-phenyl)-urea, and N-(4-[4-(2-aminoethoxyphenyl)-amino-pyrimidin-6-yl]-oxyphenyl-N'-(3-trifluoromethyl-phenyl)- urea, or a pharmaceutically acceptable salt thereof. 15. A compound selected from the group consisting of the compounds of Examples 1 164c) as described in the description and pharmaceutically acceptable salts thereof. 16. A pharmaceutical preparation comprising a compound of the formula I or I* according to any one of claims 7 to 15, or a tautomer thereof, or a pharmaceutically acceptable salt thereof, and a pharmaceutically acceptable carrier material. 17. A compound of the formula I or I* according to any one of claims 7 to 15, or a tautomer thereof, or a pharmaceutically acceptable salt thereof, for use in the treatment of the animal or human body, especially in the treatment of. a tyrosine kinase dependent disease. 18. Use of a compound of the formula I or I* according to any one of claims 1 to 15 for use in the treatment of a tyrosine protein kinase dependent disease. 19. A method of treatment for a disease that responds to inhibition of an (especially tyrosine) protein kinase; which comprises administering a prophylactically or especially therapeutically effective amount of a compound of formula I or I* as shown in any one of claims 1 to 15 to a warm-blooded animal, for example a human, that, on account of one of the mentioned diseases, requires such treatment. 20. A process for the preparation of a compound of the forrrtula I according to claim 7, or a tautomer thereof, or a pharmaceuticaily acceptable salt thereof, characterized in that (a) for the synthesis of a compound of the formula I wherein X NR if p is 0, or if p is 2 or 3, X is nitrogen which together with (CH2)P and the bonds represented in dotted (interrupted) lines (including the atoms to which they are bound) forms a ring, and G, Z, A, A', Yi, Y2l R, Ru R2, R3, R4, R5, m, n, p and r have the meanings as defined for a compound of formula I according to claim 7, an amino compound of the formula II wherein X is as just defined and R4, R5, A, A\ Y^ Y2, rri, n, p, r and the bonds . represented in dotted (interrupted) lines have the meanings as defined for a compound of formula I according to claim 7, is reacted with an isocvanate of the formula III 0=C=N — G~Z (III) wherein G, Z, R1f R2 and R3 have the meanings as defilned for a compound of formula I according to claim 7, or (b) for the synthesis of a compound of the formula I wherein m is 0 (and thus Y2 is missing), n is 1, Yi is O and G, Z, X, R1f R2, R3, R4, R5, A, A', p and r have the meanings as defined for a compound of formula I according to claim 7, a hydroxy compound of the formula IV wherein R4, A, A', Yi, Y2, m, n, r and R5 have the meanings as defined for a compound of formula I according to claim 7, is reacted with an arino compound of the formula IX wherein G, Z, R1( R2 and R3 have the meanings as de'ined for a compound of formula I according to claim 7, and, if desired, after reaction (a), (b), (c) or (d) an obtainable compound of formula I is transformed into a different compound of formula I, a salt of 5n obtainable compound of formula I is transformed into the free compound or a differen ; salt, or an obtainable free compound of formula I is transformed into a salt; and/or an c otainable mixture of isomers of compounds of formula i is separated into the individual isom ;rs; where for all reactions mentioned functional groups in the stc rting materials that shall not take part in the reaction are, if required, present in protected Form by readily removable protecting groups, and any protecting groups are subsequently 1 amoved. 21. A use of a diary! urea derivative substantially as herein described and exemplified. 22. A method of treatment for a disease substantially as herein described and exemplified. Dated this 25 day of Ncu ember 2004

Documents:

2670-chenp-2004 abstract duplicate.pdf

2670-chenp-2004 claims duplicate.pdf

2670-chenp-2004 description (complete) duplicate 1.pdf

2670-chenp-2004 description (complete) duplicate.pdf

2670-chenp-2004-abstract.pdf

2670-chenp-2004-claims.pdf

2670-chenp-2004-correspondnece-others.pdf

2670-chenp-2004-correspondnece-po.pdf

2670-chenp-2004-description(complete).pdf

2670-chenp-2004-form 1.pdf

2670-chenp-2004-form 19.pdf

2670-chenp-2004-form 3.pdf

2670-chenp-2004-form 5.pdf

2670-chenp-2004-pct.pdf