Title of Invention

QUINOLINE AND QUINOXALINE COMPOUNDS OF FORMULA I AND A STENT DEVICE CONTAINING THE SAME

Abstract

This invention is directed to quinoline/quinoxaline compounds of formula (I), which inhibit platelet-derived growth factor or p56?lck¿ tyrosine kinase activity, to pharmaceutical compositions comprising theses compounds, and to the use of these compounds for treating a patient suffering from or subject to disorders/conditions involving cellular differentiation, proliferation, extracellular matrix production or mediator release and/or T cell activation and proliferation.

Full Text

QUINOLINE AND QUINOXALINE COMPOUNDS AS PDGF-pECEPTOR AND/OR LCK TYROSINE KINASE INHIBITORS CROSS REFERENCE TO RELATED APPLICATIONS This is a continuation-in-part of U.S. Patent Application No. 09/198,718, filed November 24, 1998, which is, in turn, a continuation-in-part of International Patent Application No. PCT/US98/] 1036. filed May 28, 1998, which is, in turn, a continuation-in-part of U.S. Patent Application No. 08/972,614, filed November 18, 1997, which is, in turn, a continuation-in-part of U.S. Patent Application No. 08/864,455, filed May 18, 1997, now abandoned. BACKGROUND OF THE INVENTION 1. Field of the Invention This invention is directed to the inhibition of cell proliferation and/or cell matrix production and/or cell movement (chennotaxis) and/or T cell activation and proliferation using of quinoline/quinoxaline compounds which are useful protein tyrosine kinase inhibitors (TKJs). Cellular signaling is mediated through a system of interactions which include cell-cell contact or cell-matrix contact or extracellular receptor-substrate contact. The extracellular signal is often communicated to other parts of the cell via a tyrosine kinase mediated phosphorylation event which affects substrate proteins downstream of the cell Membrane bound signaling complex. A specific set of receptor-enzymes such as the insulin receptor, epidermal grouch factor receptor (EGF-R) or platelet-derived growth factor receptor (PDGF-R) are examples of tyrosine kinase enzymes which are involved in cellular signaling. Autophosphorylation of the enzyme is required for efficient enzyme-mediated phosphorylation of substrate proteins containing tyrosine residues. These substrates are known to be responsible for a variety of cellular events including cellular proliferation, cellular matrix production. cellular migration and apoptosis to name a few. It is understood that a large number of disease states are caused by either uncontrolled reproduction of cells or overproduction of matrix or poorly regulated programmed cell death (apoptosis). These disease states involve a variety of cell types and include disorders such as leukemia, cancer, glioblastoma, psoriasis, inflammatory diseases, bone diseases, fibrotic diseases, atherosclerosis and restenosis occurring subsequent to angioplasty of the coronary, femoral or kidney arteries or, fibroproliferative disease such as in arthritis, fibrosis of the lung, kidney and liver. In addition, deregulated cellular proliferative conditions follow from coronary bypass surgery. The inhibition of tyrosine kinase activit>' is believed to have utility in the control of uncontrolled reproduction of cells or overproduction of matrix or poorly regulated programmed cell deatli (apoptosis). It is also known that certain tyrosine kinase inhibitors can interact with more than one type of tyrosine kinase enzyme. Several tyrosine kinase enzymes are critical for the normal function of the body. For instance, it would be undesirable to inhibit insulin action in most normal circumstances. Therefore, compounds which inhibit PDGF-R tyrosine kinase activity at concentrations less than the concentrations effective in inhibiting the insulin receptor kinase could provide valuable agents for the selective treatment of diseases characterized by cell proliferation and/or cell matrix production and/or cell movement (chemotaxis) such as restenosis. This invention relates to the modulation and/or inhibition of cell signaling, cell proliferation, extracellular matrix production, chemotaxis, the control of abnormal cell growth and cell inflammalorv response. More specifically, this invention relates to the use of substituted quinoxaline compounds which exhibit selective inhibition of differentiation, proliferation or mediator release by effectively inhibiting platelet-derived growth factor-receptor (PDGF-R) tyrosine kinase activir>' and/or Lck tyrosine kinase activity. 2. Reported Developments A number of literature reports describe tyrosine kinase inhibitors which are selective for tyrosine kinase receptor enzymes such as EGF-R or PDGF-R or non-receptor cytosolic tyrosine kinase enzymes such as v-abi, p56lck or c-src. Recent reviews by Spada and Myers {Exp. Opin. Ther, Patents 1995. j(8). 805) and Bridges (E^xp. Opin, Thcr. Patents 1995, 5(12), 1245) summarize the literature for tNrosinc kinase inhibitors and EGF-R selective inhibitors respectively. Additionally Law and Lydon have summarized the anticancer potential of tyrosine kinase inhibitors (Emerging; Drugs: The Prospect For Improved Medicines 1996, 241 "260). Known inhibitors of PDGF-R tyrosine kinase activirv' includes quinoline-based inhibitors reported by Maguire et al. U Med Chem. 1994, i7, 2129). and by Dolle et al. (J, Med, Cheni. 1994, 37, 2627), A class of phenylamino-pyrimidine-based inhibitors was recently reported by Traxler el al. in EP 564409 and by Zimmennan, J.: and Traxler, P. et al. {Biorg, & Med. Chem, Lett. 1996. The correlation between the multifactorial disease of restenosis with PDGF and PDGF-R is well-documented throughout the scientific literature. However, recent developments into the imderstanding of fibrotic diseases of the lung (Antoniadcs, H. N.: et al../ Clin, Invest, 1990, 86. 1055), kidney and liver (Peterson, T. C. Hepatohg}\ 1993, 77, 486) have also implicated PDGF and PDGF-R as playing a role. For instance glomerulonephritis is a major cause of renal failure and PDGF has been identified to be a potent mitogen for mesangial cells in vitro as demonstrated by Shultz et al. (Am. J. Physiol. 1988. 255, F674) and by Floege, et al. (Clin, Exp. Immim, 199L 86, 334). It has been reported by Thomton, S. C: et al. (Clin. Exp, Imimin. 1991. 86, 79) that TNF-alpha and PDGF (obtained from human rheumatoid arthritis patients) are the major cylokines involved in proliferation of synovial cells. Furthermore, specific tumor cell types have been identified (see Silver, B. J., BioFactors, 1992, i, 217) such as glioblastoma and Kaposi's sarcoma which overexpress either the PDGF protein or receptor thus leading to the uncontrolled growth of cancer ceils via an autocrine or paracrine mechanism. Therefore, it is anticipated that a PDGF tyrosine kinase inhibitor would be useful in treating a variety of seemingly unrelated human disease conditions that can be characterized by the involvement of PDGF and or PDGF-R in their etiology. The role of various non-receptor tyrosine kinases such as p56'* (hereinafter 'Lck') in infiammalion-relatcd conditions involving T cell activation and proliferation has been reviewed by Hankc, et al {Inflamm. Res, 1995, -/-/. 357) and by Bolen and Brugge (Ann. Rev. Immwioi, 1997, 15. 371). These inflammatory conditions include allergy, autoimmune disease, rheumatoid arthritis and transplant rejection. Another recent review summarizes various classes of tyrosine kinase inhibitors including compounds having Lck inhibitory activity (Groundwater, et. al Progress in MeJichinl Chcmistrv. 1996, 33, 233). Inhibitors of Lck tyrosine kinase activity include several natural products which arc generally non-selective tyrosine kinase inhibitors such as staurosporine, genistein. certain flavones and erbstatin. Damnacanthol was recently reported to be a low nM inhibitor of Lck (Faltynek, et. al. Biochemistry. 1995, 34. 12404). Examples of synthetic Lck inhibitors include: a series ofdihydroxy-isoquinoline inhibitors reported as having low micromolar to submicromolar activity (Burke, et. al J. Med. Cheni. 1993. 36. 425); and a quinoline derivative found to be much less active having an Lck IC50 of 610 micromolar. Researchers have also disclosed a series of 4-subsiilulcd quinazolines thai inhibit Lck in the low micromolar to submicromolar range (Myers et al, W095/15758 and Myers, et. al Bioorg Med. Chem. Lett. 1997, 7, 417). Researchers at Pfizer (Hanke, et. al J. Biol. Chem. 1996. 27L 695) have disclosed two specific pyrazolopyrimidine inhibitors known as PIN and PP2 which have low nanomolar potency against Lck and Fyn. (another Src-faniilv kinase). No Lck inhibitory has been reported regarding quinoline or quinoxaline based compounds. Therefore, it is anticipated that a quinoline or quinoxaline based inhibitor of Lck tyrosine kinase activity could be useful in treating a variety of seemingly unrelated human disease conditions that can be characterized by the involvement of Lck tyrosine kinase signaling in their etiology. wherein X is L,H or L3Z2; L, is (CR.,R,,X or {C%,R,^Xr^AC%.^y^)^. L, is (CR,,R,,)p-Z4-(CR33R3b)q or ethenyl; Z, isCHorN; Z2 is optionally substituted cycloalkyi, optionally substituted cycloalkenyl, optionally substituted heterocyclyl or optionally substituted helerocyclenyl; Z, isO, NR„S, SOorSO^; Z4 is O, "NRa, S, SO. SO: or a bond; m is 0 or 1; n is 2 or 3. and n + m = 2 or 3; p and q are independently 0, 1, 2, 3 or 4, and p ^ q = 0, K 2, 3 or 4 when Z4 is a bond, and p -^ q = 0, 1, 2 or 3 when Zj is other than a bond: r is 2, 3 or 4; R,3 and R,b are independently optionally substituted alkyl, optionally substituted aryl, optionally substituted heleroaryl, hydroxy, acyloxy. optionally substituted alkoxy, optionally substituted cycloalkyloxy, optionally substituted heterocyclyloxy, optionally substituted heterocyclylcarbonyloxy, optionally substituted aryloxy, optionally substituted heteroaryloxy, cyano. RsI^N- or acylRsN-, or one of R,3 and R,b is hydrogen or halo and the other is optionally substituted alkyl, optionally substituted aryl, optionally substituted heteroaryl, hydroxy, acyloxy, optionally substituted alkoxy, optionally substituted cycloalkyloxy, optionally substituted heterocyclyloxy, optionally substituted heterocyclylcarbonyloxy, optionally substituted aryloxy, optionally substituted heteroaryloxy, cyano, R5R(^N- or acylR^N-: R„ is hydrogen, optionally substituted alkyl, optionally substituted ar> I. optionally substituted heieroai7l, hydroxy, acyloxy, optionally substituted alkoxy, optionally substituted cycloalkyloxy, optionally substituted heterocyclyloxy. optionally substituted aryloxy, optionally substituted hcicroar>'loxy, halo, cyano. R^R^^N- or acylR^N-; R,.v R^h- Rj ;i 3nd Rr,, are independently hydrogen or alkyi: Rj is hydrogen, alkyl or acyl; and R. and R an N-oxide thereof, hydrate thereof, solvate thereof, prodrug thereof, or a phamiaceulically acceptable salt thereof Another aspect of the invention is directed to a pharmaceutical composition comprising a pharmaceutically effective amount of a compound of formula I or a pharmaceutically acceptable salt thereof and a pharmaceutically acceptable carrier. The invention is also directed to intermediates useful in preparing compounds of formula I, methods for the preparation of the intermediates and compounds of formula 1, and the use of a compound of formula 1 for treating a patient suffering from or subject to disorders/conditions involving cellular differentiation, proliferation, extracellular matrix production or mediator release and/or T cell activation and proliferation. DETAILED DESCRIPTION OF THE INVENTION As used above, and throughout the description of the invention, the following terms, unless otherwise indicated, shall be understood to have the following meanings: Definitions "Patient'* includes both human and other mammals, '"Effective amount*' means an amount of compound of the present invention effective in inhibiting PDGF-R tyrosine kinase activity and or Lck tyrosine kinase activity-, and thus producing the desired therapeutic effect. "Alkyl" means aliphatic hydrocarbon group which may be branched-or straight-chained having about 1 to about 10 carbon atoms. Preferred alkyl is "lovveralkyl" having about 1 to about 6 carbon atoms; more preferred having about 1 to about 4 carbon atoms. Branched means that one or more lower alkyl groups such as methyl, ethyl or propyl are attached to a linear alkyl chain. The alkyl group is also optionally substituted by alkoxy, halo, carboxy, hydroxy or R^R^N-. Examples of alkyl include methyl, fluoromethyl. difluoromethyL trifluoromethyl, ethyl, n-propyK isopropyl, butyl, sec-butyL /-bur\ L amyl and hexyl. "Alkenyl" means an aliphatic hydrocarbon group containing a carbon-carbon double bond and which may he straight or branched having about 2 to about 10 carbon atoms in the chain. Preferred alkenyl groups have 2 to about 6 carbon atoms in the chain; and more preferably about 2 to about 4 carbon atoms in the chain. Branched means that one or more lower alkyl groups such as methvL ethyl or propyl are attached to a linear alkenyl chain. 'Lower alkenyl" means about 2 to about 4 carbon atoms in the chain which may be straight or branched. The alkenyl group may be substituted by carbalkaxy. Exemplary alkenyl groups include ethenyl. propenyl, //-butenyk /-butenyk 3-methylbut-2-enyk //-pentcnyK hcptcnyl, octenyl, cyclohexylbutenyl and decenyl. "ElhylenyT' means a -CH=CH- group, "Cycloalkyl" means a non-aromatic mono- or multicyclic ring system of about 3 to about 10 carbon atoms. The cycloalkyl group as a portion of variables R,.„ R,b or R,^ is optionallv substituted bv one or more, preferably one to three, more preferably one to two, of the following 'cvcloalkvl subsiituents'\ alkyk hydroxy, acyloxy. alkoxy. halo, R^R^N-, acylR^Nv carboxy or R^R^NCO-subsiitucnts. or a bivalent oxygen (-0-) on two adjacent carbon atoms to form an epoxide, more preferred substiiucnts are alkyl. hydroxy, acyloxy, alkoxy, bivalent oxygen and R^R^NCO-. The cycloalkyl group as a portion of variables Z, is optionally substituted by one or more, preferably one to three, more preferably one to two, of the following "cycloalkyl substituents'\ alkyl, alkoxy, halo, R^R^^N-, acylR.N-. carboxy or R-;R^,NCO- substituents, or a bivalent oxygen (-O-) on two adjacent carbon atoms to form an epoxide, more preferred substituents are alkyl, hydroxy, acyloxy, alkoxy, bivalent oxygen and R^R^.NCO-. Furthermore, when the cycloalkyl group is substituted with at least two hydroxy substituents, then at least nvo of the hydroxy substituents may be ketalated or acetalated with an aldehyde or ketone of one to six carbon atoms to form the corresponding ketal or acetal. Ketalization of ag(?;;;-diol results in formation of a spiro fused ring system. A preferred spiro cycloalkyl ring is I,4-dioxaspiro[4,5]dec-8-yl-Preferred unsubstituted or substituted monocyclic cycloalkyl rings include cyclopentyl, fluorocyclopentyl. cyclohexyl, and cycloheptyl; more preferred are cyclohexyl and cyclopentyl. Exemplary multicyclic cycloalkyl rings include I-decalin, adamant"(l- or 2-)yl, [2.2.I]bicycloheptanyl (norbornyl) and [2.2.2]bicyclooctanyl; more preferred are [2.2.1]bicycloheptanyl, and [2.2.2]bicyclooctanyl. "Cycloalkenyl" means a non-aromatic monocyclic or multicyclic ring system containing a carbon-carbon double bond and having about 3 to about 10 carbon atoms. The cycloalkenyl group as a portion of variables R|y, Ru, or R,,, is optionally substituted by one or more, preferably one to three, more preferably one to two cycloalkyl substituents as described above. The cycloalkenyl group as a portion of variables Z^ is optionally substituted by one or more, preferably one to three, more preferably one to two cycloalkyl substituents as described above. Preferred unsubstituted or substituted monocyclic cycloalkenyl rings include cyclopentenyl, cyclohexenyl and cycloheptenyl; more preferred is cyciopenlenyl and cyclohexenyl. Preferred multicyclic cycloalkenyl rings include [2.2.1]bicycloheptenyl (norbomenyl) and [2.2.2]bicyclooctenyL "Aol" means aromatic carbocyclic radical containing about 6 to about 10 carbon atoms. Exemplary arj'l include phenyl or naphthyl, or phenyl or naphthyi substituted with one or more aryl group substiiuents which may be the same or different, where "aryl group substituent" includes hydrogen, hydroxy, halo, alkyl, alkoxy, carboxy. aikoxycarbonyl or Y'Y-NCO-, wherein Y' and Y" are independently hydrogen or alkyl. Preferred aryl group substhuents include hydrogen, halo and alkoxy. "Heteroar>r* means about a 5- to about a 10- membered aromatic monocyclic or multicyclic hydrocarbon ring system in which one or more of the carbon atoms in the ring system is/are element(s) other than carbon, for example nitrogen, oxygen or sulfur. The designation of the aza, oxa or thia as a prefix before heteroary I define that at least a nitrogen, oxygen or sulfur atom is present respectively as a ring atom. The "heteroar\'l" may also be substituted by one or more of the above-mentioned "aryl group substituents'". Exemplary heteroaryl groups inchide substituted pyrazinyl, furanyL thienyl, pyridyk pyrimidinyl, isoxazolyl, isothiazolyl, oxazolyK thiazolyl, pyrazolyl, furazanyk pyrrolyK imidazo[2J-b]thiazolyl, benzofurazanvL indolyl, azaindolyl, benzimidazolyl, benzothienyk quinolinvl. imidazolyl and isoquinolinyl. "Heterocyclyl" means an about 4 to about 10 member monocyclic or multicyclic rinsi system wherein one or more of the atoms in the ring system is an element other than carbon chosen amongst nitrogen, oxygen or sulfur. The heterocyclyl group as a portion of variables Rj^, R^^ or R,^ is optionally substituted by one or more, preferably one to three, more preferably one to tvvo cycloalkyi substituents as described above. The heterocyclyl group as a portion of variables Z, is optionally substituted by one or more, preferably one to three, more preferably one to two cycloalkyi substituents as described above. The designation of the aza, oxa or thia as a prefix before heterocyclyl define that at least a nitrogen, oxygen or sulfur atom is present respectively as a ring atom. Exemplary monocyclic heterocyclyl groups include piperidyl, pyrrolidinyl, piperazinyl, morpholinyl, thiomorpholinyL thiazolidinyl, 1,3-dioxolanyl, 1,4-dioxanyl, tetrahydrofuranyk tetrahydrothiophenyl. tetrahydrothiopyranyl, and the like. Exemplary heterocyclyl moieties include quinuclidyl, pentamethylenesulfide, tetrahydropyranyl, tetrahydrothiophenyl, pyrrolidinyl, tetrahydrofuranyl, 7-oxabicyclo[2.2,l]heptany| or 4-piperidinopiperidine. "Heterocyclylcarbonyloxy" means a heterocyclyl-C(0)0- group wherein the heterocyclyl is as defined herein. An exemplary heterocyclylcarbonyloxy group is [l,4']-biperidinyl-r-carbonyloxy (4-piperidinopiperid-I-ylcarbonyioxy). "Heterocyclenyl" means an about 4 to about 10 member monocyclic or multicyclic ring system which is partially unsaturated and wherein one or more of the atoms in the ring system is an element other than carbon chosen amongst nitrogen, oxygen or sulfur. The heterocyclenyl group as a portion of variables R,^, Rn, or Rj^ is optionally substituted by one or more, preferably one to three, more preferably one to two cycloalkyi substituents as described above. The heterocyclenyl group as a portion of variables Z: is optionally substituted by one or more, preferably one to three, more preferably one to two cycloalkyi substituents as described above. The designation of the aza, oxa or thia as a prefix before heterocyclenyl define that at least a nitrogen, oxygen or sulfur atom is present respectively as a ring atom. E.xemplary monocyclic azaheterocyclenyl groups include 1,2,3.4- tetrahydrohydropyridyl, 1,2-dihydropyridyl, 1.4-dihydropyridyK 1.2,3.6-tetrahydropyridyk K4,5,6-tetrahydropyrimidyL 2-pyrrolinyl, 3-pyrrolin\L 2-imidazolinyL 2-pyrazolinyL and the like. Exemplary oxaheterocyclenyl groups include 3,4-dihydro-2H-pyran, dihydrofuranvL and fliiorodihydrofuranyl. An exemplary muliicyclic oxaheterocyclenyl group is 7-oxabicyclo[2.2.i]heptenyI. Exemplary monocyclic ihiahcterocyclenyl groups include dihydrothiophenyl and dihydrothiopyranyl. "Acyl" means an H-CO- or alkyl-CO- group in which the alkyl group is as previously described. Preferred acyls contain a lower alkyi. Exemplary acyl groups include formyl, acetv!. propanoyl, 2-methylpropanoyl, butanoyi and caproyl. "Aroyl" means an aryl-CO- group in which the alkyl group is as previously described. Exemplary groups include benzoyl and I- and 2-naphthoyL "Alkoxv" means an alkyUO- group in which the alkyl group is as previously described. Preferred alkoxv is "lower alkoxy*' having about 1 to about 6 carbon atoms. The alkoxv may be optionally substituted by one or more amino, alkoxy, carboxy, alkoxycarbon> k carboxvaryl. carbamoyl or hetcrocycl) 1 groups. Exemplary alkoxy groups include methoxy, eihoxy, ^;-propox>, /-propoxy. n-butoxy. heptoxy. 2-(morpholin-4-yl)elhoxy. 2-(clhoxy)clhoxy. 2-(4-methylpiperazin-l-vl)ethoxy. carbamoyl. N-mcthyicarbamoyL N,N-dimcthylcarbamoyl- carboxymcthoxy and methoxycarbonylmcthoxy. "Cycloaikyloxy" means a cycloalkyl-O- group in which the cycloalk> 1 group is as previously described. Exemplar}- cycloalkyloxy groups include cyclopenlylpxy and cyclohcxyloxy. "Heterocyclyloxy" means a heterocyclyl-O group in which the heterocyclyl group is as previously described. Exemplary heterocyclyloxy groups include quinuclidyloxy. pentamethylencsulfideoxy, tetrahydropyranyloxy, tetrahydroihiophenyloxy, pyrrolidinylox>\ tetrahydrofuranyloxy and 7-oxabicyclo[2-2,1 Jheptanyloxy. "Ary loxy" means aryl-O- group in which the aryl group is as previously described. "Heteroaryloxy" means heteroaryl-O- group in which the heteroar>d group is as previously described. 'Acyloxy" means an acyl-O- group in which the acyl group is as previously described. "Carboxy' means a HO(0)C- (carboxylic acid) group. "RsRj.N-" means a substituted or unsubstituted amino group, wherein R5 and R^. are as previously described. Excmplai^ groups include amino (H2N-X methylamino. ethylmethykimino. dimethyiamino and dielhylamino. " RjR^jNCO-" means a substituted or unsubstituted carbamoyl group, wherein Rs and K^ are as previously described. Exemplary groups are carbamoyl (H2NCO-X N-methylcarbamoyI (MeNHCO-) and N.N-dimethylaminocarbamoyI (Me2NC0-). "AcylR^ N'" means an acylamino group wherein R, and acyl are as defined herein. "Halo" means fluoro, chloro, bromo, or iodo. Preferred are fluoro. chloro or bromo. and more prefen-ed are fluoro or chloro. "Prodrug" means a form of the compound of formula I suitable for administration to a patient without undue toxicity, irritation, allergic response, and the like, and effective for their intended use. including ketak ester and zwitterionic forms. A prodrug is transformed in vivo to yield the parent compound of the above formula, for example by hydrolysis in blood. A thorough discussion is provided in T. Higuchi and V. Stella, Pro-druiis as Novel Dclivcr\ Systems. Vol. N of tlie A. C. S. Symposium Series, and in Edward B. Roche, ed., Bioreversible Carriers in Drug Design, American Phamiaceutical Association and Pergamon Press, 1987. both of which are incorporated herein by reference. 'Solvate" means a physical association of a compound of this invention with one or more solvent molecules. This physical association involves varying degrees of ionic and covalent bonding, including hydrogen bonding. In certain instances the solvate will be capable of isolation, for example when one or more solvent molecules are incorporated in the crystal lattice of the cr>'stalline solid, 'Solvate" encompasses both solution-phase and isolable solvates. Exemplary solvates include ethanolates. methanolates. and the like. "Hydrate" is a solvate wherein the solvent molecule(s) is/are H,0. Prefened Embodiments A preferred compound aspect of the invention is a compound of formula I wherein L, is (CR33R3Jn,-Z3-(CR3 jR.vb),,^ L: is (CR,,R35)p-Z,-(CRv,RrhV Z-> is optionally substituted cycloalkyi, optionally substituted cycloalkenyl or optionally substituted heterocyclyl: Z4 is O and NR^; m is 0: n is 2 or 3; p + q = 0 or 1; Ria and R,b are independently optionally substituted alkyl, optionally substituted alkoxy. optionally substituted cycloalkyloxy, optionally substituted heterocyclyloxy or R^R^N-, or one of R, and R,H is hydrogen or halo and the other is optionally substituted alkyl, optionally substituted alkoxy, optionally substituted cycloalkyloxy, optionally substituted heterocyclyloxy or RjR^^N-; R,^. is hydrogen, optionally substituted alkyl or optionally substituted alkoxy: R:;,,, R^,H, R- a and Rvh are independently hydrogen or lower alkyl; R4 is hydrogen; and R5 and R^ taken together with the nitrogen atom to which R5 and R azaheterocyclyl, or an N'Oxide thereof, hydrate thereof, solvate thereof, prodrug thereof or pharniaceutically acceptable salt thereof Another preferred compound aspect of the invention is a compound of formula 1 wherein X is L.Z>; L> is (CR3,R3,VZ4-(CRv,Rru),; Zi is optionally substituted cycloalkyi or optionally substituted cycloalkenyl: Z, isOandNR^; p is 0: q is 0 or 1; R,n and R,h are independently optionally substituted alkyk optionally substituted alkoxy, optionally substituted cycloalkyloxy or optionally substituted heterocyclyloxy, or one of Riband R,b is hydrogen or halo: R,„ is hydrogen: R-, a and Rvb are independently hydrogen; and Rj is hydrogen, or an N-o\ide thereof, hydrate thereof, solvate thereof, prodrug thereof, or pharmaceutically acceptable salt thereof Another preferred compound aspect of the invention is a compound of formula I wherein L,H is lower alkyl Another preferred compound aspect of the invention is a compound of formula I wherein Z| is CH. Another preferred compound aspect of the invention is a compound of formula 1 wherein Z, is N. /Xnother preferred compound aspect of the invention is a compound of formula 1 wherein Z> is optionally substituted cycloalkyl. Another preferred compound aspect of the invention is a compound of formula 1 wherein Z. is alkyl substituted monocyclic cycloalkyl; more preferred methylcyclopentyl or methylc\clohe\\l. Another preferred compound aspect of the invention is a compound of formula I wherein Z> is multicyclic cycloalkyl; more preferred (2.2.1]bicycloheptanyl (norbornyl) and |2.2.2]bicyclooclanyl. Another preferred compound aspect of the invention is a compound of fomuila 1 wherein Z^ is optionally substituted cycloalkenyl: more preferred cyclopenlenyl and cyclohexenyl. Preferred multicyclic cycloalkenyl rings include |2.2.1]bicycloheptcnyl (norbornenyl) and (2.2.2]bicyclooctenyl. Another preferred compound aspect of the invention is a compound of formula I wherein Z^ is cyclopenlenyl or cyclohexenyl. Another preferred compound aspect of the invention is a compound of formula I wherein Z. is multicyclic cycloalkenyl; more preferred [2.2.1]bicycloheptenyl (norbornenyl) or [2.2.2]bicyclooctenyl. Another prefencd compound aspect of the invention is a compound of formula I wherein p and q are 0. Another preferred compound aspect of the invention is a compound of formula I wherein p + q = 1. Another preferred compound aspect of the invention is a compound of formula 1 wherein Z, is O. Another preferred compound aspect of the invention is a compound of fomuila 1 wherein Z^ is O, and p and q are 0. Another preferred compound aspect of the invention is a compound of formula 1 wherein Z4 is O. and p + q =^ 1. Another preferred compound aspect of the invention is a compound of formula I wherein Z^ is NR4. Another preferred compound aspect of the invention is a compound of formula I wherein Zj is NR,,, and p and q are 0. Another preferred compound aspect of the invention is a compound of formula I wherein Zj is NR4, and m -*- n =^ I. Another preferred compound aspect of the invention is a compound of formula I wherein Zj is S. Another prefen'ed compound aspect of the invention is a compound of formula I wherein Z4 is S. and p and q are 0. Another preferred compound aspect of the hiveniion is a compound of formula 1 wherein Z^ is S. and p + q = 1. Another preferred compound aspect of the invention is a compound of formula 1 wherein R,^ and R,^ are mdependently optionally hydroxy substituted lower alkyl, hydroxy, lower alko\y. cycloalkyloxy. helerocYclyloxy, or one of R,a and R,t, is hydrogen or halo. Another preferred compound aspect of the invention is a compound of formula 1 wherein R,3 and R,^ are mdependently heterocyclylcarbonyloxy or optionally substituted lower alkoxy: more preferably, the lower alkoxy is methoxy or ethoxy. Another preferred compound aspect of the invention is a compound of formula ! wherein R,^ and R,^ arc lower alkyl; more preferably the lower alkyl is methyl or ethyl. Another preferred compound aspect of the invention is a compound of formula 1 wherein one of R,, and R^, is lower alkoxy. and the other of R,;, and R^, is halo; more preferably the lower alkoxy is melhoxy or ethoxy, and the halo is chloro or bromo. Another preferred compound aspect of the invention is a compound of formula 1 wherein one of R,T and R|h is lower alkyk and the other of R,^ and R,|, is lower alkoxy; more preferably the lower alkoxy is methoxy or ethoxy, and the lower alkyl is methyl or ethyl. Another preferred compound aspect of the invention is a compound of formula I wherein one of R,3 and R„, Is lower alkoxy, and the other of Ri^ and R,b is cycloalkyloxy; more preferably the lower alkoxy is methoxy or ethoxy, and the cycloalkyloxy is cyclopentyloxy or cyclohexyloxy. Another preferred compound aspect of the invention is a compound of formula I wherein one of R,, and R,^ is hydrogen, and the other of R,« and R^, is lower alkoxy, cycloalkyloxy or helcrocyclyloxy: more preferably the lower alkoxy is methoxy or ethoxy, and the cycloalkyloxy is cyclopentyloxy or cyclohexyloxy, and the heterocyclyloxy is furanyloxy. Another preferred compound aspect of the invention is a compound of formula 1 wherein R,(. is hydrogen, lower alkyl or lower alkoxy: more preferably the lower alkoxy js methoxy or ethoxy. Another preferred compound aspect of the invention is a compound of formula 1 wherein Z; is (hydroxy or alkyl) substituted hydroxycycloalkyi, more preferred is (lower alkyl)hydroxycycloalkyl. Another preferred compound aspect of the invention is a compound of fonnula I wherein R,, and R,b are lower alkoxy wherein the lower alkoxy is optionally substituted with alkoxy, heterocyclyk carboxy, alkoxycarbonyl or carbamoyk Another preferred compound aspect of the invention is a compound of formula 1 wherein one of R,, and R,b is unsubstituted lower alkoxy and the other of R,3 and R^, is lower alkoxy substituted with alkoxy, heterocyclyl, carboxy, alkoxycarbonyl or carbamoyl. Another preferred compound aspect of the invention is a compound of formula 1 wherein one of R,3 and R^^ is methoxy and the other of R„ and R,b is [K4']-bipiperadin-r-ylcarbonyloxy. 2-(cthoxy)ethoxy, 2-(4-niorpholinyl)eihoxy, 2-{4-methylpiperazin-1 -yl)ethoxy, carboxymcthoxy, methoxycarbonylmethoxy, aminocarbonylmethoxy, N-methylaminocarbonylmethoxy or N.N-dimethylaminocarbonylmethoxy. Preferred compounds according to the invention are selected from the follow ing species: 3-Cvclohexvloxv-6,7-dimethoxvuuinoline; 2-cyclohexylamino-6,7-dimethoxyquinoxaline; exo'bicycio [2.2.1]hept-2-yl' (6-chloro-7*methoxyquinoxalin-2-yl)amine: exo-bicyc(o [2.2. l]hept-2-yl- (7-ch)oro-6-melhoxyquinoxalin-2'yl)amine: BicycIo[2.2. i ]iiept-2-yl-(6,7-dimelhy l-quinoxalin-2-yl>amine: 2-cycloheptylamino-6.7-dijnethoxyquino.xaline: 2-cycl(>pentylamino-6,7-dimethoxyqiiinoxaline: 2-cyc!ohexylamino-6-methoxyquinoxaline; 3-Ani(nocyclohexyI-6,7-dimethoxy-quinoline; (6-7-dimethox>-quinoIino-yl)-cis-(3-{R)-methyl-cyclohexyI)amine; 2-Cyclohexylainino-6-methoxy-7-bromo-quinoxaline hydrochloride: (6,7-Dimethoxyquinolin-3-ylVcis//ran5-(3-{R)-methyl-cyclohexylVamiyie (6,7-Dimethoxyquinolin-3-yl)-/mw-(3-(R)-meihyt-cyc!ohexyl)'amine (6,7-Dimetho\yqi!inolin-3-yl)-c7.v-(3-(R)-methyl-cyclohexyi)-amine: (6.7-dimcthoxy-quinolin-3-yI)- (3-methyl-cyclopentyl) amine: Cyclohex-3-enyl-(6.7-diTnethoxyquinoxalin-2-yl)-amine; 2,7-Bjs-cyc!ohexyloxy-6-niethoxy-quinoxaline: Cyclohexyl-(6,7-dimethoxyquinoxalin'2'ylmethyl)-nmine; (6.7-Dimelhoxyquinolin-'3-yl)-isobur\l amine; Cyclohexyl-(6-methoxy'7-morpholin'4-yl-quinoxalin-2-yl)-amine; (H;;)-Bicyclo[2.2.1]hept-2-yl-(6,7-dimethoxyquinoxalin-2-ylVaminc; ^.Yo-bicyclo[2.2.1]hept-5-en-2-yl-(6.7-dimelhoxyqujnoxalin-2-yl)-amine; Cyclohexyl'(6,8-dimethyl~quinoxalin-2-yl)-amine; Endo-bicyclo[2.2.I)hept-2-yN(6,7-dimethoxyquinoxah'n-2-yI)-amine; (6,7-Dimethoxyquinoxalin-2-yl)-(4-methoxy-cyclohexyI)-amine;; Exo-bicyclo{2.2,!]hepl-2"yl-(6-methoxyquino\alin-2-yl)-amine; t^w-2-(Bicyclo[2-2.1]hept-2-yloxy)-6,7'dimeihoxyquinoxaline; 2-(Bicyclo[2.2.2]ocl-2-yloxy)-6,7-dimethoxy-quinoxaline; Endo-2-(bicyclo[2.2.1]hepl-2-yloxy)-6,7-dimethoxy-quinoxaiine: fA7>2-(BicycIo[2.2.]]hept-5-en-2-yloxy)-6,7-dimethoxyquinoxaline; 2-(Bicyc!o[2.2.! ]hept-5-en-2-yloxy)-6,7-dimethoxyqujnoxaUne; 2'Cyclohexyloxy-6,7-dimethoxyqurnGxaline; 2-cyclopentyhhio-6J-dimethoxy-quinoxaline; 6,7-dimethoxy-2-cyclopentyloxy-quinoxaline; 2-cyelopentyhiiethyloxy-6,7-dimethoxy-quinoxaline; 6,7-dimcthoxy-2-telrahydropyran-4-oxy-quinoxaline; exo,exo-6,7-dimethoxy-2-{5,6-epoxy-bicycIo[2.2.1]heptan-2'yloxy)-qinnoxah'nc; i:7.'i//ra77.v-4-(6,7-Dimethoxyquinoxalin-2-yloxy)-cyclohexanecarboxylic acid: 6.7-Dimethoxy-2-(4-methoxy-cyclohexyloxy)-quinoxaline: 3-Cyclohexy!oxy-6,7-dimethoxyquinoxaline 1 -oxide: (lR.2R.4S)-("i-)-Bicyclo[2.2.1]hept-2-yl-(6,7-dimethoxyquinoxaIin-2-yl)-amine: (IS.2S.4R)-(-)-Bicycio[2.2J]hept-2-yl-(6.7-dimeihoxyqiiinoxalin'2-yl)-amine: 2-(6,7-Dimethoxy-quinoxalin*2-yl)-2-a2a-bicyclo[2.2.2]oclan-3-one; Cis/trans-4-(6,7-Dimelhoxy-quinoxalin-2-ylamino)-cyclohexanecarboxylic acid methyl ester; Cis/trans-4-(6,7'dimethoxy-qi)inoxaiin-2-ylamino)-cyclohexanecarboxylic acid; Cis-4-(6,7-dimetlioxy-quinoxalin-2-ylamino)-cyclohexanecarboxyIic acid methyl ester; Trans-4-(6.7-dimethoxy'quinoxalin-2-yIamino)-cyclohexanecarboxylic acid methyl ester; (6,7-dimethoxy-quinoxaline-2-yl)-cis//r(^/;7.V'(3-(R)-methylcyclohexyi) amine; (6,7-dimethoxy-qiiinoxaline-2-yI) -/ra;75-(3-(R)-methylcyclohexyl) amine; (6.7-dimeihoxy-quinoxaline-2-yl)-c7"s-(3"{R)-methylcyclohexyl) amine: and methyl L/i7/ra775-4-{6,7-Dimethoxyquinoxalin'2-yloxy)-cyclohexanecarboxylate. or an N-oxide thereof, hydrate thereof, solvate thereof, prodrug thereof, or pharmaceiiticnily acceptable salt thereof.. More preferred compounds are the following: 2-cycloiiexylamino-6,7-dimetho\yquinoxaline; exo-bicycio [2.2.!]hept-2-yl- (6-chloro-7-methoxyquinoxalin-2-yl)aminc; exo-bicyclo [2.2.1]hept-2-yl- (7-chloro-6-methoxyquinoxalin-2-yl)amine; Bicyclo{2.2.1 ]hept-2-yl-(6,7-dimethyl-quinoxalin-2-yl)'amine; . 2-cycloheptylamino-6,7-dimelhoxyquinoxaline; 2-cyclopentylamino-6,7-dimethoxyquinoxaline; 3-Aminocyclohexyl-6.7-dimeihoxy-quinoline; (6.7-dimethoxy-quinolin-3-yl)-cis-(3-(R)-methyl-cyclohexyl) amine: (6,7-Dimethoxyquinolin-3-yl)-cis//r£/m-(3-(R)-methyl-cyclohexyl)-amine (6,7-Dimethoxyquinolin-3-yl)-//'am'-(3-{R)-methyl-cyclohexylVamine (6,7-Dimethoxyquinolin"3-yl)-<:.7a->amine; Cyclohex-3-enyl-(6,7-dimethoxyquinoxalin-2-yl)'amine: 2,7-'Bis-cyclohexyloxy-6-methoxy-quinoxaline; (6,7-Dimethoxyquinolin-3-yl)-isobutyI amine; (j:)-Bicyclo[2.2.1]hept-2-yl-(6,7-dimethoxyquino\alin-2-yl)"amine; t^.V(?-bicyclo[2.2.1]heplo-en-2-yl-(6,7-dimethoxyquinoxalin-2-yl)-amine; Endo-bicyclo[2.2J]hept-2-yl-(6,7-dimethoxyquinoxalin-2-yI)-amine; Exo-bicyclo[2.2.1]hept-'2-yl-(6-methoxyquinoxalin-2-yl)-amine; e\o-2-(Bicyclo[2.2J]hept-2-yloxy)-6,7-dimethoxyquinoxaline: 2-(Bicyclo[2.2.2]oct-2-yloxy)-6.7-dimethoxy-quinoxaline; Endo-2-(bicyclo[2.2.1]hept-2-yloxy)-6.7'dimethoxy-quinoxaline; L'.vo-2-(Bicyclo[2.2.1]hepl-5-en-2-yloxy)-6,7-dimethoxyquinoxaline: 2~{Bicyclot2.2.1]hept-5-en-2-yloxy)-6,7-dimethoxyquinoxaline; 2-Cyciohexyloxy-6.7-dimethoxyquinoxaline; 2-cyclopentylthio-6J-dimethoxy-quinoxaline; 6.7-dimethoxy-2-cyclopentyloxy-quinoxaline: 2-cyclopentylmethyloxy-6,7-dimethoxy-quinoxaline: 6.7-dimeihoxy-2-tetrahydropyran-4-oxy-quinoxaline; cxo,exo-6J-dimethoxy-2-(5,6-epoxy-bicycio[2,2.1]heptan-2-yloxy)-quinoxaline; 6,7-Dimeihoxy-2-(4-inethoxy-cyclohexyloxy)-quinoxaline; (IR,2R,4S>(+)-Bicyc]o[2.2.1]hept-2-yl-(6,7-dimethoxyquinoxalin-2-yl)-amine; (I S,2S.4 R)'(')-Bicyclo[2.2.1 ]hept-2-yl-(6,7-dimethoxyquinoxalin-2-yl)-amine: Cis/tran>-4-(6,7-Dimethoxy-quinoxalin-2-ylamino)-cycIohexanecarboxylic acid methyl ester; CiS"4-{6,7-dimeihoxy-quinoxalin-2-ylamino)-cyclohexanecarboxylic acid methyl ester; Trans-4-(6,7'dimethoxy-quinoxalin-2-ylaminoVcyclohexanecarboxyIic acid methyl ester; (6.7-dimelhoxy-quinoxaline-2-yl)-cis//nm5-(3-(R)'mcthy!cyclohexyl) amine: (6,7'dimcihoxy-quinoxaline-2-yl) -/ra77.v-(3-(R>methylcyclohexyl) amine; c (6,7-dimcthoxy-quinoxalinc-2-yl)-c/5-(3-(R)-methylcyclohexyl) amine; and methyl c7,v///Y//?A-4-(6.7-Dimethoxyquinoxalin-2-yloxy)-cyclohexanecarboxylate. or an N'Oxide thereof, hydrate thereof, solvate thereof, prodrug thereof, or pharmaccutically acceptable sail thereof.. It is to be understood that this invention covers all appropriate combinations of the particular and preferred groupings referred to herein. The compounds of this invention may be prepared by employing procedures known in the literature starting from known compounds or readily prepared intermediates. Exemplary general procedures follow. In addition, compounds of formula 1 arc prepared according to the following Schemes l-VIfK wherein the variables are as described above, excepting those variables which one skilled in the art would appreciate would be incongruent with the method described. 3. Reductive amination reaction with amino-quinolines and aldehydes or ketones. An appropriately substituted 3-amino quinoline (1 eq.) is stin-ed with I eq. of the appropriate aldehyde or ketone in methanol (or another suitable solvent mixture) until TLC indicates imine formation is complete. Excess NaCNBHj or NaBHj, or another suitable reducing agent is added and the mixture is stirred until TLC shows consumption of the intermediate imine. The mixture is concentrated and the residue is chromatographed on silica gel with hexane/ethyl acetate (0-100 %) or chlorofonn/methanol (0-20%) to give the desired product. 4. coupling reaction of 3-amino substituted quinolines and bromopheny! compounds. An appropriatf^ly substituted 3-amino quinoline (1 eq.) is stirred with -1.4 eq. of a strong base such as sodium /-butoxide, 1 eq. of the appropriate bromophenyl compound, and catalytic amounts of 2.2"-bis(diphcnylphosphino)-l-l '-binaphthyl (S-BINAP) and bis{dibenzylideneacetone)-Palladium (Pd(dba).) are mixed in an inert organic solvent such as toluene under an inert atmosphere such as argon and heated to about 80°C overnight. The mixture is cooled, diluted with a solvent such as ether, fdtered. concentrated and chromatographed with 50% EtOAc/hexane to give the desired product. 5. Ether formation from 3-hydroxy substituted quinolines via Mitsunobu conditions. A THF solution of an appropriately substituted hydroxyquinoxaline (at about 0 to about 25 °C) is treated with I eq. each of the desired alcohol, triphenylphosphlne and llnally diethylazodicarboxylate (DEAD) or a suitable equivalent. The reaction progress is monitored via TLC and upon completion of the reaction (about I to about 24 hours) the mixture is concentrated and the residue is chromatographed on silica gel to yield the desired product. 6. Dealkylation of a lower alkoxy substituted quinoline or quinoxaline, and subsequent alkylalion. An appropriate lower alkoxy substituted quinoline or quinoxaline (I eq.) in DMF is treated with excess sodium ethanihiolate (usually about 2 or more eq.) and the reaction mixture is stirred with heating from about I to about 24 hours. The mixture is partitioned between water and ethyl acetate. Extractive workup followed by chromatography, if necessary, provides the corresponding desired hydroxy substituted quinoline or quinoxaline product. The hydroxy substituted quinoline or quinoxaline product can be alkylated using the conditions for the Mitsunobu reaction as detailed above. Alternatively, simple alkylation using methods well-known in the art with a reactive alkyl- or benzyl- halide using NaH or another appropriate base in a suitable solvent provides the desired alkylated product. 7. Oxidation of a nitrogen in a quinoline or quinoxaline to the corresponding N-oxide. An imine (=N-) moiety in a quinoline or quinoxaline compound of formula (I), may be converted to the corresponding compound wherein the imine moiet\' is oxidized to an N-oxide, preferably by reacting with a pcracid, for example peracetic acid in acetic acid or m-chloroperoxybenzoic acid in an inert solvent such as dichioromethane, at a temperature from about room temperature to reflux, preferably at elevated temperature. The compounds of the present invention arc useful in the form of the free base or acid or in the form ot a pharmaceulically acceptable salt thereof. All forms are within the scope of the invention. Where the compound of the present invention is substituted with a basic moiet>\ acid,addition salts are formed and are simply a more convenient form for use; and in practice, use of the salt form inherently amounts to use of the free base form. The acids which can be used to prepare the acid addition salts include preferably those which produce, when combined with the free base, pharmaceutically acceptable salts, thai is, salts whose anions are non-toxic to the patient in pharmaceutical doses of the salts, so that the beneficial inhibitory effects on PDGF inherent in the free base are not vitiated by side effects ascribable to the anions. Although pharmaceutically acceptable salts of said basic compounds are preferred, all acid addition salts are useful as sources of the free base form even if the particular salt, per se, is desired only as an intermediate product as. for example, when the salt is formed only for purposes of purification, and identification, or when it is used as intermediate in preparing a pharmaceutically acceptable salt by ion exchange procedures. Pharmaceutically acceptable salts within the scope of the invention are those derived from the following acids: mineral adds such as hydrochloric acid, sulfuric acid, phosphoric acid and sulfamic acid; and organic acids such as acetic acid, citric acid, lactic acid, tartaric acid, malonic acid, methanesufonic acid, eihanesulfonic acid, benzenesulfonic acid, p-toluenesulfonic acid, cyclohexylsulfamic acid, quinic acid, and the like. The corresponding acid addition salts comprise the following: hydrohalides. e.g. hydrochloride and hydrobroniide. sulfate, phosphate, nitrate, sulfamate, acetate, citrate, lactate, tartarate, malonate, oxalate, salicylate, propionate, succinate, fumarate, maleate, methylene-bis-p-hydroxynaphthoates, gentisates, mesylates, isethionates and di-p-loluoyltartratesmethanesulfonate, elhanesulfonate, benzenesulfonate, p-toluenesulfonate, cyclohexylsulfamate and quinate, respectively. According to a further feature of the invention, acid addition salts of the compounds of this invention are prepared by reaction of the free base with the appropriate acid, by the application or adaptation of known methods. For example, the acid addition salts of the compounds of this invention are prepared either by dissolving the free base in aqueous or aqueous-alcohol solution or other suitable solvents containing the appropriate acid and isolating the sah by evaporating the solution, or by reacting the free base and acid in an organic solvent, in which case the salt separates directly or can be obtained by concentration of the solution. The compounds of this invention can be regenerated from the acid addition salts by the application or adaptation of known methods. For example, parent compounds of the invention can be regenerated from their acid addition salts by treatment with an alkali, e.g. aqueous sodium bicarbonate solution or aqueous ammonia solution. Where the compound of the invention is substituted with an acidic moiety, base addition salts may be formed and are simply a more convenient form for use; and in practice, use of the salt form inherently amounts to use of the free acid fonn. The bases which can be used to prepare the base addition salts include preferably those which produce, when combined with the free acid, pharmaccutically acceptable salts, that is, salts whose cations are non-toxic to the animal organism in pharmaceutical doses of the salts, so that the beneficial inhibitory effects on PDGF inherent in the free acid are not vitiated by side effects ascribable to the cations. Pharmaccutically acceptable salts, including for example alkali and alkaline earth metal salts, within the scope of the invention are those derived trom the following bases: sodium hydride, sodium hydroxide, potassium hydroxide, calcium hydroxide, aluminum hydroxide, lithium hydroxide, magnesium hydroxide, zinc hydroxide, ammonia, trimcthvlammonia. Iriethylammonia, ethylenediamine, ?7-methyI-glucamine, lysine, arginine, ornithine, choline. N.N'-dibenzylethylenediamine, chloroprocaine, diethanolamine, procaine, //-benzylphcnethylamine. diethylamine. piperazine, tris(hydroxymelhylVaminomethane, teiramcihylammonium hydroxide, and the like. Metal salts of compounds of the present invention may be obtained by contacting a hydride, hydroxide, carbonate or similar reactive compound of the chosen metal in an aqueous or organic solvent with the free acid form of the compound. The aqueous solvent employed may be water or it may be a mixture of water with an organic solvent, preferably an alcohol such as methanol or ethanoL a ketone such as acetone, an aliphatic ether such as tetrahydrofuran. or an ester such as ethyl acetate. Such reactions are normally conducted at ambient temperature but they may. if desired, be conducted with heating. Amine salts of compounds of the present invention may be obtained by contacting an amine in an aqueous or organic solvent with the free acid form of the compound. Suitable aqueous solvents include water and mixtures of water with alcohols such as methanol or ethanol, ethers such as tetrahydrofuran. nitriles such as acetonitrile, or ketones such as acetone. Amino acid salts may be similarly prepared. The compounds of this invention can be regenerated from the base addition salts by the application or adaptation of known methods. For example, parent compounds of the invention can be regenerated from their base addition salts by treatment with an acid, e.g., hydrochloric acid. As well as being useful in themselves as active compounds, salts of compounds of the invention arc useful for the purposes of purification of the compounds, for example by exploitation of the solubility differences between the sails and the parent compounds, side products and/or starting materials by techniques well known to those skilled in the art-Compounds of the present invention may contain asymmetric centers. These asymmetric centers may independently be in either the R or S configuration. It will also be apparent to those skilled in the art thai certain compounds of formula I may exhibit geometrical isomerism. Geometrical isomers include the cis and frans forms of compounds of the invention, i.e., compounds having alkenyl moieties or substituents on the ring systems. In addition, bicyclo ring systems include encio and e.xo isomers. The present invention comprises the individual geometrical isomers, stereoisomers, enantiomers and mixtures thereof Such isomers can be separated from their mixtures^ by the application or adaptation of known methods, for example chromatographic techniques and recrysiallization techniques, or they are separately prepared from the appropriate isomers of their intermediates, for example by the application or adaptation of methods described herein. The starting materials and intermediates are prepared by the application or adaptation of known methods, for example methods as described in the Reference Examples or their obvious chemical equivalents, or by methods described according to the invention herein. The present invention is further exemplified but not limited by the following illustrative examples which describe the preparation of the compounds according to the invention-Further, the following examples are representative of the processes used to synthesize the compounds of this invention. EXAMPLE I 3-Cyclohexyloxy-6,7-dimetho\yquinoline To a TlIF solution (30 mL) at 0°C is added 3-hydroxy-6,7-dimethoxyquinoline (0.237 g, 1.15 nimoh, cyclohexanol (0.347 g, 3.46 mmol), Ph^^P (0.908 g, 3.46 mmol), Diethylazodicarboxylate is added portionwise until the solution retained a deep red color (0.663 g, 3.81 mmol). After 4 hours the solution is concentrated and the residue chromatographed (50% EtOAc in hexanes). The product is rccrystallized from isopropanol/hexanes as the HCl salt as a white solid (m.p, 229-232*^0, dec). EXAMPLE 2 2-Anilino-6-isopropoxy-quinoxaline hydrochloride To NaH (0.033 g. 0.84 mmol) under argon is added I mL DMF. 2-Anilino-6-quinoxa]inol (0.1 g. 0,42 mmol) in 1.5 mL DMF is added portionwise. After 30 minutes, 2-bromopropane is added dropwise and the solution is heated to 50°C for 1.5 hours. The cooled reaction mixture is quenched with water and partitioned between EtOAc and H^O, washed with H^O (3X), brine, dried (MgSOj), and concentrated. The resulting residue is chromatographed (30% EtOAc/hexanes) to provide 0,05 g dialkylated product and 0.1 g of the title compound. An analytical sample of the HCl salt is obtained by addition of IPA (isopropanol)/HCl to an Et>0/1PA solution of the free base to provide HCl salt (m.p. 205-210^Cdec.). Anal. Calcd. for CrH.^N^O •HCl: C, 64.65; H, 5.74: N, 13.31: Found: C, 64.51; R 5.90: N, 13.09. EXAMPLE 3 2-cyclohexylamino-6,7-dimethoxyquinoxaIine To 0.3 g (1.34 mmol) of 2-chloro-6,7-dimethoxyquinoxaline is added approx. 1 mL of cyclohexylamine. The mixture is heated overnight at 105 X and a further 10 hours at 135 °C. The mix is partitioned between CH^CI: and saturated NaHCO;,. The organic layer is dried (MgSO.,) and concentrated. The resulting syrup is chromatographed (1:1 EtOAc : CH^CL) to provide 0.265 g of the product as a It. brown solid in 69% yield (m.p. 188-189.5). Anal, calcd for C,^H:,N30.: C. 66.88: FL 7.37; N, 14.62- Found: C. 66.82; H. 7.28: N. 14,45. Using ihc standard coupling protocol above using the appropriate starling materials the following are prepared: exo-bicyclo [2.2.1 ]hept-2-yl- (6-chloro-7-melhoxyquinoxalin-2-Yl)amine (m.p. 17M73X). Anal, calcd for C^.H.sN.OCl'.C, 63,26; H. 5-97: N, 13.83. Found: C. 63.37; M, 5.91: N, 13.83. exo-bicyclo [2.2.1 ]hept-2-yl- {7-chloro-6-methoxyquinoxalin"2-yl)amine (m.p. 146-147.5^0. Anal, calcd for C„H,HN,OCI: C, 63.26; H, 5.97: N, 13.83. Found: C, 63.34: H, 5.93: N. 13.77. Bicyclo[2.2.1 jhcpt-2-yl-(6.7-dimethyl-quinoxalin-2-y))-amine (m.p. 155-57 °C). Anal, calcd for CpH^N,: C 76.37; H. 7.92: N, 15.72. Found: C 75.58: H, 7.55: N. 15.38. 2-cyclohept>'ianuno-6.7"dimethoxyquinoxaline (m.p. 134-I36°C). Anal. Calcd for CpH,,NA: C. 67.75: H. 7.69; N, J3.94. Found: C, 67.80; H, 7.61: NJ3.77. 2-cyclopentylamino-6,7-dimcthoxyquinoxaline (m.p. I49-15IX). Anal. Calcd for C„H,9N-A-C, 65.91; H, 7.01; N, 15.37. Found: C. 66.04; H, 6.96; N, 15.47. 2-cyclohexylamino-6-melhoxyquinoxaline (m.p. 242-248%'). EXAMPLE 4 3-Aminocyciohexyl-6J-dimethoxy-quinoline To a MeOH (3 mL) solution of 4A powdered molecular sieves (0.11 g) under argon is added 3-amino-6,7-dimethoxy-quinoline hydrochloride (0.17 g. 0.68 mmol) andNaOMe (0.039 g, 0.71 mmol). The reaction mixture is stirred at room temperature for 30 min., and cyclohexanone (0.074 mL, 0.71 mmol), then pyridine^borane (0.072 niL, 0.071 mmol) are added portionwise. The mixture is stirred for 4-5 h. then 5N HCl (1.4 mL, 6.8 mmol) is added poiiionwise. The reaction mixture is stirred 45 min., then made strongly basic with 5N NaOH. The mix is partitioned between EtOAC and H^O. and the aqueous layer is washed with EtOAc (2X). The combined organic layers are washed with brine. (IX), dried (MgSO^), chromatographed (50% EtOAc/he.xanes), and recrystallized from EtOAc/hexanes to obtain 0.112 g light-yellow solid in 57% yield (m.p. 164^165). Anal, calcd for Cpll,:NA: C 71.30; II 7.74;N,9.78. Found: C. 71.45:1 L 7.49; N, 9.80. EXAMPLE 5 2-Cyclohexylamino-6-niethoxy-7-bromo-quinoxaIine hydrochloride To 0,75 g (2,7 mmol) 7:1 7-bronio-6-methoxy-quinoxaliiv2-ol: 6-bronio-7'methoxy-quinoxahn-2-ol in a sealed tube is added 5 mL cyclohexyiamine. The reaction mixture is heated to 120° C for 2 h. Cyclohexyiamine is removed under reduced pressure, and the residue is partitioned between EtOAc/H.O. The organic layer is washed with H.O (2X). brine (IX), and dried (MgSOa). The resulting material is chromatographed (20% then 30% EtOAc/hexanes) to provide 0.81 g major product in 88% yield. An analytical sample is obtained by converting approximately 0.13 g of the free base into its hydrochloride salt (m.p. 280 dec.)- Anal, calcd for Cj^HjuN^OBr • HCI: C, 48.34: H. 5.14; R 11.27. Found; C. 48.51; H. 4.98; N, 11.09. EXAMPLE 6 (6,7-dimethoxy-quinolin-3-yl)'ci.s-(3-(R)-methyl-cyclohexyl)amine dihydrochloridcand(6,7-dimethoxy-quinolin-3-yl)'irans-{3-(R)-methyl-cyclohexyi) amine dihydrochloride A cis/trans mixture of (6,7-Dimctho\v-quinolin-3-yl)- (3"(R)-mclhyl-cyclohe\v|)^amine prepared by reductive amination of 3-amino-6.7,-dimethoxyquinoline and 3-(R)'methyl cyclohexanone is separated by RP-HPLC, Both samples are rc-chromatographed (70% EtOAc/hexanes) to obtain pure free base. An analytical sample of each isomer is obtained by converting separately the free bases into the amorphous and somewhat hygroscopic dihydrochloride salts. 500 MHz 'H NMR is consistent for the product and LC/MS and FAB confirmed M+H = 301 for each isomer. EXAMPLE 7 Cyclohex-3-enyI-(6,7'dimethoxyquinoxalin-2-yl)-amine To a solution of trans-4-(6J-dimethoxy-quinoxalin*2-ylamino)-cyclohexanol (303 mg, 1 mmoH in 10 niL of THF at -78" C are added triphenylphosphine (524 mg, 2 mmol) and diethyl azodicarbo.x) late (1 mL). The mixture is stirred at -78' C for one hour before addition of 4-nitrobenzoic acid (334 mg, 2 mmol). After being stirred at -78' C for one hour, the mixture is continued to stir at ROOM TEMPERATURE for additional hour and then concentrated. The residue is chromatographed on silica gel (ether) to give 250 mg (87.7%) of cyclohex-3-enyi-(6,7-dimcthoxyquinoxalin-2-yl)'amine. EXAMPLE 8 2-Anilino-6-quinoxalinol By the method of Feutrill, G, L: Mirrington, R. N. Te/, Lett. 1970, 1327: the aryl methyl ether is converted to the phenol derivative. To 2-anilino-6'methoxy-quinoxaline (0.27 g, 1,07 mmol) under argon in DMF is added the sodium salt of ethanethiol (0.19 g, 2 mmol). The reaction mixture is heated to I lO'^C overnight. The mixture is concentrated and partitioned between EtOAcand H:0/5% tartaric acid such that the pH of the aqueous layer is approximately 4. The organic layer is washed with FLO (4X), then with 2.5% NaOH (4X). The basic layers combined, washed with EtOAc (2X), re-acidified with 5% tartaric acid, and washed with multiple portions of EtOAc. The organic layers are combined, washed with brine, dried (Na^SO^), and concentrated. The resulting solid is chromatographed (50% EtOAc/ hexanes). An analytical sample is obtained by triturating the product with Et.O to provide a yellow powder (m.p. 211-213'C). Anal. Calcd. for CuH,,N,0: C, 70.88; H, 4,67; N, 17.71: Found: C. 70.64; H, 4.85: N, 17.58. EXAMPLE 9 Phenyl-[6-(tetraliydrofuran-3-(R)-yl-oxy)quinoxatin-2-yl]amine To a THF solution at 0°C under argon is added 2-aniIino-6-quinoxalinoI (0.23 g, 0.97 mmol), (S)-(+)-3-hydroxytetrahydrofuran (0.086 mL, 1.3 mmol), and triphenylphosphine (0.31 g, 1.2 mmol). DEAD (0.18 mL, 1.2 mmol) is added poitionvvise. The reaction is allowed to warm to room temperature and stirred for 1.5 hours. The mixture is concentrated and partitioned between ElOAc and H.O. The organic layer is washed with H.O, brine, dried (MgS04), and concentrated. The resulting yellow oil is chromaiographed (50% EtOAc/hexanes) and taken up in Et^O/IPA. HCI/ Et,0 solution is added dropwise and the resulting red-orange powder is dried in vacuo. The powder is free-based by stirring in McOH with washed (3X H.O, 5X MeOH) basic ion exchange resin. The mixture is stirred 30 minutes, filtered, concentrated, and recr>'stallized from EtOAc/hexanes to provide, in nvo crops, the product (m.p. 173-175X). Anal.Calcd. forC.gHnNA: C, 70.35: H. 5.57: N, 13.67; Found: C 70.19: H. 5.60; N, 13.66. EXAMPLE 10 2.7-Bis-cyclohexyloxy-6-melho\y-quinoxaline To a DMF solution (5 mL) of Nal I (0.32 g, 8 mmol) under argon, cyclohexanol (0.7 mU 6.7 mmol) is added dropwise. The mixture is stiircd at room temperature for 25 minutes, then 2-chloro-6,7-dimethoxyquinoxaiine is added portionwise. The reaction is stirred for 15 minutes at room temperature, at 90X for 2 hours, and at 110°C for 1 hour. The mixture is cooled, quenched with H,0, and partitioned between EtOAc/ H^O. The organic layer is washed with lUO and brine, dried (MgS04). and chromatographcd (10% EtOAc/hexanes) to provide a waxy while solid (m.p. 75-78°C). Anal. Calcd. for C2,H,,N:Ov C, 70.76; H, 7,92; N, 7.86: Found: C, 70.81; H, 7.79: N, 7.70. EXAMPLE 1 I Cyclohexyl-(6,7-dimethoxyquinoxalin-2-ylmethy|)-amine To a 0.067 M solution of 6,7-dimelhoxy-2-quinoxaline carboxaldehyde in 2:1 MeOH/1,2-dichloroethane (7.5 mL, 0.5 mmol) is added cyclohexylamine (0.11 mL, 0.9 mmol). The reaction is allowed to stir at room temperature overnight, then NaBFlj (0.038 g, I mmol) is added and the reaction mixture is stirred overnight. The mixture is then concentrated and chromatographcd (50% EtOAc/hexanes-approximately 5% MeOH in 50% EtOAc/hexanes). The oil is dissolved in EtOAc/ hexanes and treated with HCI in EtOH. The resulting solution is concentrated and the solids are triturated with isopropanol to provide a white solid after dr\'ing in vacuo at 60 X (m.p. 185-190*^0, dec). Anal. Calcd. for C„H,.,NA •HCI: C, 60.44; H, 7.16; N, 12,44; Found: C. 60.48; H, 6.88; N, 12.07. EXAMPLE 12 (6,7-Dimethoxyquinoiin-3-yl)-/ram-(3-(R)-methyl-cyclohexyl)-amine and (6.7- Dimethoxyquinolin-3-yl)-m-(3-(R)-metliyl-cyclohexyl)-amine The reaction is performed similarly to the above preparation using the free base of 3-amino-6,7-dimethoxyquinoline (0.32 g, 1.6 mmol) and (R)-(+)-3-methylcyclohexanone (0.23 mL. 1.9 mmol). The product mixture obtained is chromatographcd (70% EtOAc/hexanes). and recrystailized from EtOAc/hexanes to obtain a white solid (1:1 mixture of cw and nans isomers) (m.p. 153-160*^0. Anal. Calcd. for C,8ll:4NA; C, 71.97: H. 8.05; N, 9.33: Found: C. 72.12: H. 7.85; N, 9.29, Using the standard coupling protocol above using the appropriate starting material the following is prepared: (6,7-dimethoxy-quinoIin-3-yl)- (3-methyl-cyclopent>'l) amine (m.p. I06-109°C). Anal. Calcd for C,7H.,NA:C, 71.30; H. 7.74; N, 9.78. Found: C 71.24: R 7.56; N. 9.61. EXAMPLE 13 3-(6J-Dimethoxyquinolin-3-yl-amino)'2,2-dimethyl-propan-l-ol The reaction is run similar to the preparation in Example II. To a MeOH solution of 4A powdered molecular sieves (0.35 g) under argon is added 3-amino-6,7-dimethoxyquinoline (0.32 g, K6 mmol) and 2,2-dimethyl'3-hydroxypropionaldehyde (0.19 g, 1.9 mmol). The product mixture is chromalogrnphed (3% MeOH/CHCIa) to afford 0.10 g of material which is partitioned between CHXK/10% NaOH. The organic layer is washed with 10%NaOH, H.O, and brine, then dried (MgSO^), and recr>'stallizcd from EtOAc/hexanes to provide a light-orange solid (m.p. 170-173.5°C). Anal. Calcd. for C„IUN:0-,: C, 66.18: H, 7.64; N, 9.65; Foimd: C, 66.11; H, 7.49; N, 9.33. Using the standard coupling protocol above using the appropriate starting material the following is prepared: (6,7-Dimethoxyquinolin-3-yl)-isobutyl amine (m.p. 158-I62^C). Anal. Calcd for C.^H^nNA: C. 69.20; H, 7.74; N, 10J6. Found: C, 69.06; H, 7.82: N, 11.01. EXAMPLE 14 Cyclohexyl-(6-methoxy-7-morpholin-4-yl-quinoxalin-2-yl)-amine This preparation is based on an adaptation of the method described by Buchwald, et al J". Am. Chem, Soc, 1996, 775, 7215. To a toluene solution of 2-cyclohexylamino-6-methoxy-7-bromo-quinoxaline (0,1 g. 0.3 mmol) under argon is added morpholine (0.1 g, 0.3 mmol). sodium /er^butoxide (0.04 g. 0.42 mmol), S-(-)-BINAP (cat., 0.001 g), and bis(dibenzylideneacetone)-paIladium (cat.. 0.001 g). The reaction mixture is heated to 80°C overnight. The mixture is cooled, diluted with Et,0, filtered, concentrated, and chromatographed (50% EtOAc/hexanes). The product is recrystallized from HlOAc/hexanes to provide, in two crops, to provide a yellow solid (m.p. 194-196X). Anal. Calcd, for C„H,,NA: C, 66.64: H, 7.65; R 16.36; Found: C, 66.60: H, 7.60; N, 16.51. EXAMPLE 15 trans -4-(7-Chloro-6-melhoxy-quinoxalin-2-amino)-cycIohexanol and trans -4- (6-Chloro-7-methoxy-quino\alin-2-yl-amino)-cyclohexanol To a reaction flask under argon fitted with a Dean-Stark trap and a condenser is added 6:1 2,7-dichloro-6-methoxy-quinoxaline : 2,6-dichloro-7-methoxy-quinoxaline (0.30 g, 1.3 mmol) and trans-4-amino-cyclohexanol (0.35 g, 3 mmol). The reaction mixture is heated to 170X for approximately 10 hours, then concentrated and chromatographed twice. (7% MeOH/CHCh, then 5% MeOH/CHCl3). The product is recrystallized from ElOAc/hexanes lo provide a light-yellow solid (m.p. 144-147'C). Anal. Calcd. for C,.H:,N40: ^0.4 H.O: C, 57.20: H, 6.02; N. 13.34; Found: C, 57.21; H, 5.97; N, 13.08.1H NMR analysis revealed that the product is a 2:1 mixture of tram -4 -(7-chloro-6-metho\y-quinoxalin-2-amino)-cyclohexanol : irans -4 -(6-chloro-7-methoxy-quinoxalin-2-yl-amino)-cycIohexanol. EXAMPLE 16 //•a/75-4-(6,7-Dimethoxyquinoxalin-2-ylamino)-cycIohexanol trans- 4-aminocycIohexanol (0.11 g, 2 eq.) and 2-chloro-6.7-dimethoxyquinoxaIine (O.I g, I eq.) are combined and heated to 160-!80°C for a period of 4-8 hours. The dark-brown suspension is fihered and concentrated. The residue is purified on a flash column eluted with 3% methanol/methylene chloride to provide the product as a yellow powder with m.p. of I !9-123°C. Anal. Calcd. forC|Jl.iN30v C, 62 J3; W. 7.05; N, 13.63; Found: C, 62.35; H, 7.09: N. 13.18. The compound could be recrystallized by the following method. Stalling with 0.2 g of-yellow powder in a mixture of 2.5 mL of water and 1.25 mL of methanol a clear orange-colored sohition is obtained upon reflux. The hot solution is left standing and cooled gradually. Orange-colored needle4ike crystals are collected by filtration and dried under high vacuum to give a yellow solid (m.p. 119-I20°C). Alternatively, the HC! salt of the title compound is prepared as follows: To a solution ofiram-4-(6,7-dimethoxyquinoxalin-2-ylamino)-cyclohexanol in isopropanol is added a solution of HCI at 0°C. The mixture is stirred for 15 minutes before filtration. The solid collected is dried under a high vacuum lo provide the /r(v//.v-4-(6,7-dimethoxyquinoxalin-2-ylamino)-cyclohexanol hydrochloric acid salt. Anal. Calcd. for C,(iK,CIN,03 ♦1.2 H.O: C, 53.19; VI 6.80: N. 11.63; CI, 9.81; Found: C, 53.14; H, 6.85; N, 11.24; CI, 10.28. Alternatively, the sulfate salt of the title compound is prepared as follows: In a typical procedure, /r^;;.?-4-(6J-dimetho.xyquinoxalin-2-ylamino)-cycIohcxanol is dissolved in acetone or another suitable organic solvent with warming up to 45 °C as necessary. To the resultant solution is carefully added aqueous H^SO^ (1 equiv,, I M solution) with rapid stirring. The salt thus formed is collected and dried to provide the sulfate in >80% yield. EXAMPLE 17 (+)-Bicyclo[2.2T]hepi-2-yl-(6,7-dimethoxyquinoxalin-2-yl)-amJne Procedure A: A mixture of 2-chloro-6,7-dimethoxyquinoxaline (5 g, 22.3 mmol) and {±)'exo-norbornyl-2-amine (10 g. 90 mmol) is heated at 160-180°C overnight. The dark-brown residue is dissolved in 200 mL of methylene chloride and washed with IN NaOH (50 mL). The organic layer is dried over magnesium sulfate and then filtered. The residue after concentration is chromatographed on silica gel eluted with hexane/ethyl acetate (80%) to provide the desired product as a yellow solid which can be recrystallized in methanol. Procedure B: A mixture of 2-chloro-6J-dimethoxyquino.\aline (9 g, 40.1 mmol) and (±yexo-norbomyl-2-amine (5.77 g, 52 mmol). Sodium t-butoxide (4.22 g, 44 mmol), 2,2'-bis(diphenylphosphino)-l-r-binaphthyl (BINAP, 120 mg)and bis(dibenzylideneacelone)-palladium Pd(dba)., 40 mg in 80 mL of toluene is heated at 80°C for eight hours. Another portion of BINAP (60 mg) and Pd(dba)2(20 mg) is added and the mixture is heated at 100°C overnight. After being diluted with 200 niL of methylene chloride, the reaction mixture is washed with IN NaOH (100 mL). The organic layer is dried over magnesium sulfate and filtered. The residue after concentration is chromatographed on silica gel eluted with hcxane/ethyl acetate (80%) to provide the desired product as a light-yellow solid (m.p. 188-189°C). Anal. Calcd, for CpH.jNA: C, 68.20; H, 7.07: N. 14.04: Found: C. 68,18: H, 7.03; N, 14.03. The following compounds are prepared similarly beginning with the appropriate starting material (procedure A). f.To-bicyclo[2.2.1]hept-5-en'2-yl-{6,7-dimethoxyquinoxalin-2-yl)-amine (m.p. 175-]77^C). Anal. Calcd. for C,-11,,,N,0: 'O-^ H,0: C, 60.94; H, 6.56; N. 13.78; Found: C, 66.98; H. 6.62: N, 12.73. Cyclohe\yl-(6,8-dimelhyl-quinoxalin-2-yl)-amine [MS m/z: 255 (M+)]. Anal. Calcd. for Ci^HjiN,: C, 75.26; H. 8.29: N. 16.46: Found: C, 75.08; R 8.28: N, 15.86. Endo-bicyclo[2.2.]]hept-2-yl-(6,7-dimethoxyquinoxaiin-2-yl)-amine (m.p. 79-82" C). (6-7-Dimethoxyquinoxalin-2-yI)-(4-mcthoxy-cyclohexylVaminc (m.p. 58-68'^CV Anal. Calcd. for CpHr,N,0, •OS H.O: C, 62.56: H, 7.41; N J 2.87; Found: C, 62.53: H, 7.22; N, 12.22. Exo-bicyclo[2.2.1 ]hept-2-yl-(6-methoxyquinoxalin-2-yI)-amine (m.p. 98-100" C). Anal. Calcd forCH.oN^O: C, 71.35; H, 7.11:R 15.60. Found: C, 70.38: H. 7.03; N. 15.05. EXAMPLE 18 ejro-2"(Bicyclo[2.2.1 ]hept-2-yloxy)-6,7-dimethoxyquinoxaline A mixture of ^A7>-2-norborneol (223 mg, 2 mmol) and NaH (60%, 100 mg, 2.5 mmol) in 10 mL of anhydrous THE is refluxed for 0.5 hour before addition of 2-chloro-6.7-dimethoxyquinoxaIine (336 mg, 1.5 mmol). The resulting mixture is continued to refluxed for two hours. The residue after filtration and concentration is chromalographcd on silica gel (50% ether/hexane) to provide the desired product as a white solid (m.p. 135-137 X). Anal. Calcd. for CpH^oNA: C, 67.98; H, 6.71; N, 9.33; Found: C, 67.96; R 6.762: N, 9.19. Using the standard coupling protocol above using the appropriate starting materials the following are prepared: 2'(Bicyclo[2.2-2]oct-2-yloxy)-6,7-dimelhoxy-quinoxaline (m.p. 147-148'* C). Endo-2-(bicyclo[2.2.1]hept-2-yloxy)-6J-dimelhoxy-quinoxaline (m.p. 110-11 TC). £?-Yo-2-(Bicyclo[22.1]hept-5-en-2-yloxy)-6.7-dimethoxyquinoxaline (m.p. 108-110°C)- Anal. Calcd. for C,7H,KN A: C. 68.44; H, 6.08: N. 9.39; Found: C, 68.54; H, 6.23; N, 9.27. 2-(Bicyclo[2.2.1]hept-5-en-2-yIoxy)-6,7-dimethoxyquinoxaline (m.p. 93-95°C). Anal. Calcd. for CnHjgN.Ov C, 68.44; H, 6.08; N. 939: Found: C, 68.32; H. 5.98; N, 9.25. 2-Cyclohexyloxy-6,7-'dimethoxyquinoxaline (m.p. 104-106*" C). 2-cyclopentylthio-6,7-dimetho.\y-qiiinoxaline (m.p. 123-124* C). Anal. Caicd for C.^H.sN.O^S: C, 62.04; H, 6.25; N. 9.65, Found: C 61.90; hi 6.02; N, 9.48, 6,7-dimeilioxy-2-cyclopentyloxy-quinoxaline (m,p. 87-89" C), Anal. Calcd for Ci.H.sNA: C, 65.68; H. 6.61; R 10.21. Found: C 65.63; H, 6.52; N, 10.13. 2-cyclopcntyImethyloxy'6,7-dimelhoxy-quinoxaline (m.p. 99'102*'C). Anal. Calcd for CH^^NA- C, 66.65; H, 6.99; N, 9.72. Found: C 66.66; H, 7.03; N, 9.70. 6,7-dimethoxy-2-tetrahydropyran-4'Oxy-quinoxaline (m.p. 155-158*" C). Anal. Calcd for C^H.^NA: C. 62,06: H. 6.25; N, 9.65. Found: C. 62.26; H, 6.27: N, 9.67. exo.exo-6.7-dimethoxy-2~(5.6-cpoxy-bicyclo[2.2.1 ]heptan-2-yloxy)-quinoxaline (m.p. 173-175*" C). EXAMPLE 19 c7.v//yY//7.v-4-(6.7-Dimethoxyquinoxalin-2-yloxy)-cycIohexanecarboxylic acid. A mixture of c7'A//ra/M'4-hydroxy'Cyclohexanecarboxyiic acid (144 mg, 1 mmol) and Nail (60%, 160 mg. 4 mmol) in anhydrous THF/DMF(I0 mL/2 mL) is refluxcd for one hour before addition of 2-chloro-6,7-dimethoxyquinoxaline (225 mg. 1 mmol). The resulting mixture is continued to refluxed for four hours. The reaction mixture is neutralized to pH 5 and extracted with ethyl acetate (2x50 mL). The combined organic solutions are dried over magnesium sulfate and filtered. The residue after concentration is chromatographed on silica gel (ethyl acetate, followed by methanol) to provide the desired product as a white solid (m.p. 90-93 ""C). Anal. Calcd. for CnH^oN.Os ^O.S H.O: C, 59.89; H, 6.19; N, 8.22; Found: C, 59.91: H, 6.62; N, 7.90. EXAMPLE 20 6,7'Dimethoxy-2-(4-methoxy-cyclohexyloxy)-quinoxaline A mixture of cis/trans-4-(6J'dimethoxy-quinoxalin-2-yloxy)-cyclohexanol (170 mg. 0.56 mmole) and NaH (60%, 22.4 mg, 0.56 mmole) in anhydrous THF/DMF (10 mL/2 mL) is stirred at 0^ C for 10 min. before addition of methyl iodide (50 |iL, 0.56 mmole). After being stirred at ROOM TEMPERATURE for four hours, the reaction is quenched with water (0.5 mL) and concentrated. The aqueous layer is extracted with methylene chloride (2x20 mL) and the combined organic solutions are washed with brine (5 mL). The residue after concentration is chromatographed on silica gel (30% ethyl acetate/hexane) to give 80 mg (45%) of the desired product (m.p. 85-90° C). EXAMPLE 21 3-Cyclohexyloxy"6,7-dimelhoxyquinoxaIine 1-oxide. A mixture of 2-cyclohexyIoxy-6J-dimethoxyquinoxaline (110 mg, 0.38 mmol) and meta-chlorobenzoic peracid (70%* 113 mg, 0.46 mmol) in 10 mL of methylene chloride is stirred at room temperature for one day. The solution after filtration is concentrated and the residue is chromatographed on silica gel (20% ethyl acetate/hexane) to provide the desired product (m.p. 167-169X). /ra/75-4-(6,7-Dimethoxy-4-oxy-quinoxalin-2-yiamino)-cycIohexanol (m.p. 220-222^0 is prepared similarly, Anal. Calcd. for CH^jN-A •0.2 H.O: C. 59.42; H, 6.69; N, 12.99; Found: C, 59.43: H, 6.64; N, 12.95. EXAMPLE 22 (IR.2R,4SH+VBicyclo[2,2.1]hept-2-yN(6,7-dimethoxyquinoxalin'2-yl)-amine The (j:)-bicyclo(2.2.1]hept-2-yl-(6,7-dimethoxyquinoxalin-2-yl)-amine of Example 17 is resolved on a chiral HPLC column (Chiralpac AD, 25x2 cm. 60% hepiane/40% ethanol with 10 mM (lS)-(+)-camphorsulfonic acid. 12 mL/minute) and the above tilled product is obtained as the first eluent. The fractions collected arc combined and washed with 50 mL of 1 N NaOI 1 before drying (MnSOj). The solution after filtration is concentrated on a rotovap and then dried under a high vacuum. A yellow solid is obtained- [a]/*" + 19.5° (c=0.20, CH.CL) m.p. 184-186 °C. AnaK calcd for CnH^.N A >^ 0.3 H,0: C. 66.90; Yl 7.15; N. 13.77. Found: C, 66.86; H. 7.01: N, 13.86. EXAMPLE 23 (IS.2S.4R)-(-)-Bicyclo[2-2.1]hept-2-yl-(6.7^dimethoxyquinoxalin-2-yl)-amine (i) The (j:)-bicyclo[2.2.1]hept-2-yl-(6,7-dimethoxyquinoxalin-2-yl)-amine of Example 17 is resolved on a chiral HPLC (Chiralpac AD, 25x2 cm. 60% heptane/40% ethanol with 10 mM (LV)-(+)-camphorsulfonic acid. 12 ml/min) as the second elute. The fractions collected are combined and washed with 50 mL of IN NaOH before dried over magnesium sulfate. The solution after filtration is concentrated on a rotovap and then dried under a high vacuum. A yellow solid is obtained. (a]j"^ -19.5" (c=0.22.CH,CL) m.p. 185-187° C (ii) A mixture of 2-chloro-6,7-dimethoxyquinoxaline (462 mg, 2.06 mmole) and (15, 25, 47?)-norbomyl-2-amine (300 mg, 2.7 mmole). Sodium t-butoxide (220 mg, 2.3 mmole), BINAP (9 mg) and Pd(dba)2(3 mg) in 10 mL of toluene is heated at 80" -100" C overnight. The suspension is chromatographed on silica gel eluted with hexane/ethyl acetate (60%) to give 370 mg (60%) of the desired product as a yellow solid which had the same retention time as the first elute under the above chiral HPLC condition, [a]/" ^ 19° (c=0.19, CH.CU) EXAMPLE 24 2-(6.7-Dimethoxy-quinoxalin-2-yl)-2-aza-bicyclo[2.2.2]octan-3-one 2-Azabicyclo(2.2.2]octan-3-one (228 mg, 3.3 mmole) is dissolved in a mixture of THF/DMF (5 mL/3 mL) and treated with NaH (60%, 184 mg, 4.6 mmole). The resulting mixture is heated at 60° C for 0.5 hour before addition of 2-chloro-6,7-dimethoxyquinoxaline (344 mg, 1.5 mmole). After being heated at 80"" C overnight, the reaction mixture is concentrated . The residue is chromatographed on silica gel (50% ethyl acetate/hexane) to give 164 mg (23%) of a yellow solid (m.p. 158-I59*'C). V EXAMPLE 25 Cis/trans-4-(6J-Dimethoxy-quinoxalin-2-viamin6)-cyclohexanecarboxylic acid methyl ester To a solution of 2-(6,7-dJmethoxy-quinoxalin-2-yl)-2-aza-bicycIo[2,2.2Joctan-3-one (100 mg, 0.32 mmole) in 10 mL of methanol is added a freshly prepared NaOMe/methanol solution (54 mg. I mmolc) and the mixture is stirred at ROOM TEMPERATURE for 0.5 hour before concentrated. Methylene chloride is used to extract and then dried with magnesium sulfate. The residue after filtration and concentration is chromatographed on silica gel (40% ethyl acetate) to give 85 mg (77%) of cis/trans-4-(6.7-^dinietho.\y-quinoxalin-2'ylamino)-cyclohexanecarboxylic acid methyl ester as a light yellow solid (m.p. 68-80" C). I-'XAMPLE 26 Cis/trans-4-(6,7-dimethoxy-quinoxalin-2-ylamino)-cyclohexanecarboxyJic acid When NaOMe in above procedure is replaced with NaOll, 2-(6.7-dimethoxy-quinoxaiin'2-yl)-2-a/_a-bJcyclo[2.2.2]octan-3-one is converted into cis/trans-4-(6.7-dimethoxy-quinoxalin'2-yIamino)-cvclohcxnnecarboxylic acid. F.XAMPLE 27 Cis-4-(6.7-dimelhoxy-quinoxalin-2-ylamino)-cyclohcxanecarboxylic acid methyl ester and trans-4-(6,7-dimethoxy-qninoxalin-2-yIamino)-cyclohexanccarboxylic acid methyl ester-Cis-4-(6,7-dimethoxy-quinoxalin-2-ylamino)-cyc!ohe\anecarboxyIic acid methyl ester [MS mJz\ 345 (M')]and iranS'4-(6.7-dimethoxy-quinoxalin-2-ylamino)-cyclohexanecarboxylic acid methyl ester IMS m/z\ 345 (M)] are separated on preparative TLC from cis/trans-4-(6,7-dimethoxy-quinoxalin-2-ylamino)-cvclohexanecarboxylic acid ester with 65% ethyl acetatc/hexane as first and second elutes respectively. EXAMPLE 28 /'ram-4'[7-methoxy-6-(2-morphoIin-4-yl-ethoxy)-quinoxalin-2-yiamino]- cyclohexanol and /ra;75-4-[6-methoxy'7-(2-morpholin'4-yl-ethoxy)-quinoxalin-2-ylamino]-cyclohexanol The title compound is prepared by Mitsunobu coupling of 6-hydroxy-7-methoxy-2-chloroquinoxalinc; 7-(2-morpholin-4-ylethoxy)-6-methoxy'2-chioroquinoxaline and 2'(morphoIin-4-yOethanoI using the procedure of Example I and reaction of the resulting 6-(2-iiiorpholin-4-ylethoxy)-7-meihoxy-2-chloroquinoxaline: 7-(2-morpholin-4'ylethoxy)-6-methoxy-2-chloroquinoxaline and trans-4-amino-cyclohexanol using the procedure of Example 11. EXAMPLE 29 2-[2-(/ro/7A-4-Hydroxy-cyclohexylamino)-7-methoxy-quJnoxalin-6-yloxyl]-]- acetic acid and 2-[2-(/n7n.s-4-Hydroxy-cyclohexylamino)-6-methoxy-quinoxalin-7'yloxyI]-l-acetic acid Tlie title compound is prepared by dealkylation of 4'(6.7-dimethoxyquinoxaline-2-ylamino)cyclohexanol using the sodium salt of ethanethiol in DMF as described in Example 8. followed by alkylation with bromoacetic acid in the presence of base as described in general procedure 6. EXAMPLE 30 2-[2-(lrans-4-H>'droxy-cyclohexyIamino)-7-methoxy-quinoxalin-6-yloxyl]-N.N- dimethyl-acetamide and 2-[2-(trans-4-Hydroxy-cyclohexylamino)-6-methoxy-qinnoxalin-7-yloxyi]-N,N-dimethy|-acetamide The title compound is prepared by aminolysis of the compound of Example 29 using dimethylamine, EXAMPLE 31 (6,7-dimetboxy-quinoxaline-2-yl)-(3-(R)-methylcyclohexyl) amine and its cis and trans isomers The compounds are initially prepared as a mixture of cis and trans isomers. They are prepared from the cyclohexyl amine derived from reduction of the oxime of 3-(R)-methylcyclohexanone followed by coupling of the amine with 2-chloro-6J-dimethoxyquinoxaline using the standard conditions. An anaKlical sample of each isomer is obtained via preparative RP-HPLC. The 300 MHz 'H NMR and MS are consistent for both structures although the relative stereochemistry could not be assigned defmitively for the cyclohexyl -carbon bearinu the nitrogen. EXAMPLE 32 methyl c/A/rra/75-4-(6,7-Dimelhoxyquinoxalin-2-yioxy)-cyclohexanecarboxylate. The title compound is prepared by esterifying the product of Example 19 using standard techniques to afford the title compound. M,p. I30-132°C- AnaL Calcd for C,sH22N205: C, 62.42; H, 6.40; N, 8.09. Found: C 62,60; a 6.55: N, 7.89. INTERMEDIATE EXAMPLE 1 4-Bromo-5-methoxy-bcnzene-L2-diamine dihydrochloride To a solution of EtOAc (50 mL) and 5-bromo-4-methoxy-2-nitro-phenylamine (2,5 g. 10 mmol) under argon is added 5% Pd/C (0.5 g). The reaction mixture is hydrogenated at 50 psi for 1 hour. The mixture is filtered through Ceiite into a solution of HCl/lPA/EtOAc, and the pad is washed with additional EtOAc. The resulting precipitate is filtered off to provide white solid. INTERMEDIATE EXAMPLE 2 7-Bromo-6-methoxy-quinoxalin-2-oi and 6-Bromo-7'methoxy- quinoxalin-2-ol To a solution of MeOH (15 mL) under argon is added pulverized NaOH pellets (0.86 g, 21 mmol) and 4-bromo-5-methoxy"benzene-I,2-diamine dihydrochloride (2.7 g. 9.3 mmol). The mixture is stirred for 10 minutes, then a solution of 45% ethyl glyoxylate in toluene (2,7 g, 12 mmol) is added portionwise. The reaction mixture is refluxed for 1 hour, then cooled. Water is added, then the suspension is filtered. The resulting solid is washed successively with H.O. MeOH, IPA, and Et^O to provide a yellow powder. INTERMEDIATE EXAMPLE 3 7-Bromo-2-chloro-6-methoxy"quinoxaline and 6^Bromo-2' chloro-7-methoxy-quinoxaline To a mixture of 7-'bromo-6-methoxy-quinoxalin-2-ol and 6-bromo-7"methoxy-quinoxaIin-2-ol (I i^, 3.9 mmol is added POCl> (5 mL). The reaction mixture is refluxed 1 houn poured into ice water. filtered, then washed with water to provide a light-tan solid. Ratio of 7-bromo-2-chloro-6-methoxy-quinoxaline : 6-bromo-2-chIoro-7-methoxy"quinoxaline is approximately 7:1 by 'H NMR. INTERMEDIATE EXAMPLE 4 5-Chloro-4'nietho\y-2-nitroaniIine To a soUition of N-(5-chloro-4-methoxy-2'nitrophenyl)-acctamide (2 g, 8.2 mmol) in 5N HCI (20 mL) is added 1,4-dioxane (10 mL). and the mixture is stirred at 60°C for 1.5 hours. I he reaction mixture is concentrated and partitioned between EtOAc/2 N NaOH. The aqueous layers are washed with EtOAc (3XX brine, dried (MgSOj), adsorbed onto silica geL and chromatouraphed (70% EtOAc/hexanes) to provide an orange powder. INTERMEDIATE EXAMPLE 5 4-Chloro-5-methoxy-benzene-],2^diamine dihydrochloride To a solution of EtOAc (25 mL) and 5-chloro-4-mcthoxy-2-nitrO'phenylamine (1.6 g, 7.9 mmol) under argon is added 5% Pd/C (0.5 g). The reaction mixture is hydrogenated at 50 psi for 1 hour. The mixture is filtered under N^ through Celitc into a solution of I N HCI/ELO in EtOAc, and the pad is washed with additional EtOAc. The resulting precipitate is filtered off to provide a white solid. INTERMEDIATE EXAMPLE 6 7-Chloro-6-methoxy-qninoxalin-2'Ol and 6-Chloro-7-methoxy-quinoxalin-2-ol To a solution of 4-chloro-5-methoxy-benzene-K2-diamine dihydrochloride (1.8 g. 7.2 mmol) in Eton (] 5 mL) under argon is added TEA (2.5 mL. 1 8 mmol) at O'^C. The mixture is stirred for 20 minutes, then a solution of 45% ethyl glyoxylate in toluene (2.1 g, 9.3 mmol) is added portionwise. The reaction mixture is warmed to room temperature, refluxed for 1,5 hour then cooled, water is added, then the suspension is filtered and washed successively with H^O, IPA, and Et.O to provide a light-yellow powder. The product is azeotroped several times with toluene and dried in vacuo before use. INTERMEDIATE EXAMPLE 7 2J-Dichloro-6-methoxy-quinoxaline and 2,6- Dichloro-7-methoxy-quinoxaljne To a mixture of 7-chioro-6-methoxy-quinoxalin-2-ol and 6-chloro-7-melhoxy-quinoxalin-2-ol (I g. 4.7 mmol) under a CaCL drying tube is added POCI, (5 mL). The reaction mixture is refluxed 30 minutes, poured into cold saturated NaHCO^ solution, filtered, then washed with water to provide a solid. The ratio of 2J-dichloro-6-methoxy-quinoxaIine : 2,6-dichIoro-7-methoxy-quino\aline is approximately 6:1 by'H NMR. INTERMEDIATE EXAMPLE 8 (\S, IS, 4i?)-norbomyl-2-amine (3a): To a solution of R-(-H)-Endo-norborneol (2.24 g. 20 mmole) in 20 mL of THE at -78" C are added triphenylphosphine (6.55 g. 25 mmole). phthalimide (3.68 g, 25 mmole) and diethyl azodicarboxylale (4.4 mL. 28 mmole). The mixture is stirred at ROOM TEMPERATURE overnight and then concentrated- The residue is chromatographed on silica gel (20 % ethyl acciate/hexanc) to give 4.6 g (95%) of (U9. 2.^. 4/? )-2-bicyclo[2,2-l]hept'-2-yl isoindole-IJ-dione. (3b): A mixtureof (15, 2i'. 4^ )-2-bicyclo[2.2.11hept-2-yl isoindole-1.3-dione (1.2 g, 5 mmole) and monohydrated H.NNH. (300 mg, 6 mmole) in 10 mL of methanol is refluxed for tour hours before concentrated to dryness, methylene chloride (2x100 mL) is used lo extract and the soHd is removed by nitration. Evaporation of methylene chloride affords 300 mg (54%) of (I.S, 25", 47?)-norbomyi-2-amine. INTERMEDIATE EXAMPLE 9 £',xt)-Bicyclo[2.2. ] ]hept-5-en'2-amine L\rr>-bicyclo[2.2T]hept-5-en-2-amine is prepared with the same procedures as in INTERMEDIATE EXAMPLE 12 from 5-norbornen-2-ol via a versatile intermediate exo- 2-bicyclo(2.2. l]hept-5-en-2-yl isoindole-K3-dione INTERMEDIATE EXAMPLE 10 2-Methyl-6,7-dimethoxyquinoxaline The title compound is prepared using an adaptation of the published method of Tamao, et al. Tetrahedron, 1982, 38, 3347-3354. To a THF solution under argon is added 2-Chloro^6,7-dimethoxyquinoxaline (5 g, 26 mmol) and NiCl2(dppp) (0,14 g, 0.26 mmol). The reaction mixture is cooled lo 0*^C, and a 3 M solution of MeMgBr in Et^O (13 mL, 39 mmol) is added portionwise. The reaction mixture is allowed to warm to room temperature, stirred for 1 hour, then refluxed for 1.5 hours. The mixture is cooled, quenched with 10% HCL stirred 10 minutes, then made basic with 5% NaOH. CfLCU and 1 LO are added to the reaction, and the mixture stirred overnight. Additional CH^CI, FLO, and NaCI are then added and the mixture is filtered. The resulting solution is poured into a separator/ funnel, and the aqueous layers are washed 3X with CH2CI.. The organic layers are combined, washed with brine, dried (MgS04), concentrated onto silica gel, and chromatographed (50%-80% EtOAc/hexanes) to provide a orange solid (49% yield), fNTERMEDIATE EXAMPLE 11 6,7-Dimethoxy-2-quinoxaline carboxaldehyde To a reaction flask under argon is added 1,4-dioxane (20 mL), 2-methyl-6,7-dimethoxyquinoxaline(L09 g, 5.3 mmol) and Se02(L8 g, 16 mmol). The mixture is heated to I00°C for 2 hours 45 minutes, cooled, and filtered through Celite. The pad is washed with portions of EtOAc and CH^CU. The resulting solution is concentrated, taken up in MeOH/ CH2CI2, loaded onto a silica gel column, and chromatographed (30% EtOAc/CfLCL) to provide an off-white solid (73% yield). INTERMEDIATE EXAMPLE 12 {2exo, 5 evO'5-Acetoxybicyclo[2.2T]heptan-2-one and eTO'6-acetoxybicyclo[2.2.1] heptan-2-one are obtained from the bicyclo[2.2. l]hepta-2,5-diene according to the procedure of R. Gagnon {J. Chem. Soc, Perkin trans. K 1505 1995) with minor modification. To a solution of e%Y;-5-acetoxybicyclo[2.2.1]heptan-2-one (350 mg, 2.08 mmol) in 10 mL of THF at room temperature is added a IM borane/THF solution (1.2 mL, L2 mmol). The mixture is stirred for 0.5 hour before quenched at 0"C with methanol (3 mL) and IN HCl (1,5 mL). Ethyl acetate (3x 30 mL) is used to extract and dried over magnesium sulfate. The residue after filtration and concentration is chromatographed on silica gel to provide (2£?/;£/a5t'.xf?)-5-acetoxybicyclo [2.2J] heptan-2-0I. To a solution of (2^77^o,5e.Yo)-5-acetoxybicyclo [2.2.1] heptan-2-ol (350 mg, 2.06 mmol ) in THF (10 mL) is added phthalimide (454 mg, 3.09 mmol). triphenylphosphine (810 mg, 3.09 mmol )and diethyl azodicarboxylaie (0.49 niL, 3.09 mmol ) at 0X\ The reaction is left to stir overnight and then is condensed on the rotovap and the residue is purified by column chromatography (20% ethyl acetate/hcxane) to provide the desired product as a yellow solid. A mixture of the above solid (300 mg. I mmol ) and hydrazine (0.126 mU 2.2 mmol) in 5 niL of methanol is heated to reflux for six hours. Af»cr removal of methanol, dichloromethane (jx 30 niL) is used to extract the residue. Concentration of the .solvent affords (eA7;,cw)-5-aminobicyclo[2.2.1 jheptan-2^acetaie (127 mc, 75%) which is used in the coupling reaction without further purification. Similarly, (2ew^a5ew)-5-aminobicyc|{>(2.2.1 ]heptan-2-acetate, (2endo.6e.xo)-6-aminobicyclo[2.2.1 ]heptan-2-acetaie and (2c^x^;/>c^Yo)-6-aminobicyc!o[22J ]heptan-2-acetaie are prepared from proper starting material. INTERMEDIATE EXAMPLE 13 2-methoxy-4.5-diaminophenol dihydrochloride The title compound is prepared by hydr(»genation of 2-methoxy-4,5-dinitrophenol according to the procedure of Ehrlich et al.../ Or^.Chem., I'M?, 12. 522. INTERMEDIATE EXAMPLE 14 7-hydr(>xy-6-metho.xy-quinoxaline-2-ol and 6-hydroxy-7-methoxy'quinoxaline-2-ol. The title compounds are prepared Iron) 'l-mcthoxy-5-hydro\yhcnzene-1.2-diaminc dihydrochloride by reaction with NaOH and ethyl glyoxalate using the procedure of Intermediate Example 2. INTERMEDIATE EXAMPLE 15 7.hydr 6-hydroxy-7-methoxy-2-chloroquinoxaiine. The title compounds are prepared from 7-hydroxy-6-methoxy-quinoxaline-2-ol and 64iydroxy-7-methoxy-quinoxaline-2-ol by reacti The compounds of formula I as described herein inhibit inhibition of cell proliferation and/or cell matrix production and/or cell movement (chemotaxis) via inhibition of PDGF-R tyrosine kinase activity. A large number of disease states are caused by cither uncontrolled reproduction of cells or overproduction of matrix or poorly regulated prr^sirammed cell death (apoptosis). These disease states involve a variety of cell types and include disorders such as leukemia, cancer, glioblastoma, psoriasis, innammatory diseases, bone diseases, fibrotic diseases, atherosclerosis and occurring subsequent to angioplasty of the coronary, femoral or kidney arteries or, flbroproliferative disease such as in aHhritis, fibrosis of the lung, kidney and liver. In particular, PDGF and PDGF-R have been reported to be implicated in specific types of cancers and tumor% such as brain cancer, ovarian cancer, colon cancer, prostate cancer lung cancer, Kaposi's sarcoma and malignant melanoma. In addition, deregulated cellular proliferative conditions follow from c(^r'.nary bypass surgery. The inhibition of tyrosine kinase activity is believed to have utility in the control ^A uncontrolled reproduction of cells or overproduction of matrix or poorly regulated programmed cell 'i'^'i'h (apoptosis). This invention relates lo the modulation and/or inhibition of cell signaling, cell proliferation and/or cell matrix production and/or cell moveri^'-ni (chemotaxis). the control of abnormal cell growth and cell inflammatory response. More specifically, this invention reJates to the use of substituted quinoline and quinoxaline compounds which exhibit selective inhibition of differentiation, proliferation, matrix production, chemotaxis or mediator release by effectively inhibiting platelet-derived grovvth factor-receptor (PDGF-R) t\TOsine kinase activity. Initiation of auiophosphorylation, i.e., phosphorylation of the growth factor receptor itself, and of the phosphorylation of a host of intracellular substrates are some of the biochemical events which are involved m cell signaling, cell proliferation, matrix production, chemotaxis and mediator release. By effectively inhibiting Lck tyrosine kinase activity, the compounds of this invention are also useful in the treatment of resistance to transplantation and autoimmune diseases such as rheumatoid arthritis, multiple sclerosis and systemic lupus erythematosus, in transplant rejection, in graft vs. host disease, in hyperproliferative disorders such as tumors and psoriasis, and in diseases in which cells receive pro-inflammatory signals such as asthma, inflammatory bowel disease and pancreatitis. In the treaimcni of resistance to transplantation, a compound of this invention may be used either prophylaclically or in response to an adverse reaction by the human subject to a transplanted organ or tissue. When used prophylaclically. a compound of this invention is administered to the patient or to the tissue or organ to be transplanted in advance of the transplantation operation. Prophylactic treatment may also include administration of the medication after the transplantation operation but before any signs of adverse reaction to transplantation are observed. When administered in response to an adverse reaction, a compound of this invention is administered directly to the patient in order to treat resistance to transplantation after outward signs of the resistance have been manifested. According to a further feature of the invention there is provided a method of inhibiting PDGF tyrosine kinase activity comprising contacting a compound according to claim 1 with a composition containing a PDGF tyrosine kinase. According to a further feature of the invention there is provided method of inhibiting Lck tyrosine kinase activity comprising contacting a compound according to claim I with a composition containing a Lck tyrosine kinase. According to a further feature of the invention there is provided a method for the treatment of a patient suffering from, or subject to, conditions which may be ameliorated or prevented by the administration of an inhibitor of PDGF-R tyrosine kinase activity and/or Lck tyrosine kinase activity, for example conditions as hereinbefore described, which comprises the administration to the patient of an effective amount of compound of formula I or a composition containing a compound of formula K or a pharmaceulically acceptable salt thereof Reference herein to treatment should be understood to include prophylactic therapy as well as treatment of established conditions. The present invention also includes within its scope pharmaceutical compositions which comprise pharmaceutically acceptable amount of at least one of the compounds of fonnula I in association with a pharmaceutically acceptable carrier, for example, an adjuvant, diluent, coating and excipient. In practice compounds or compositions for treating according to the present invention may administered in any variety of suitable forms, for example, by inhalation, topically, parenterally, rectally or orallv: more preferably orally. More specific routes of administration include intravenous. intramuscular, subcutaneous, intraocular, intrasynovial, colonical, peritoneal, transepithelial including iransdermaL ophthalmic, sublingual, buccal, dermal, ocular, nasal inhalation via insufflation, and aerosol. The compounds of formula I may be presented in forms permitting administration by the most suitable route and the invention also relates to pharmaceutical compositions containing at least one compovmd according to the invention which are suitable for use as a medicament in a patient. These compositions may be prepared according to the customary methods, using one or more pharmaceutically acceptable adjuvants or excipients. The adjuvants comprise, inter alia, diluents, sterile aqueous media and the various non-toxic organic solvents. The compositions may be presented in the form of tablets, pills, granules, powders, aqueous solutions or suspensions, injectable solutions, elixirs or syrups, and may contain one or more agents chosen from the group comprising sweeteners such as sucrose, lactose, fructose, saccharin or Nutrasweet^ flavorings such as peppermint oil, oil of winiergrcen. or cherry or orange Havorings. colorings, or stabilizers such as methyl- or propyl-paraben in order to obtain pharmaceutically acceptable preparations. The choice of vehicle and the content of active substance in the vehicle are generally determined in accordance with the solubility and chemical properties of the product, the particular mode of administration and the provisions to be observed in pharmaceutical practice. For example, excipients such as lactose, sodium citrate, calcium carbonate, dicalcium phosphate and disintegrating agents such as starch, alginic acids and certain complex silica gels combined with lubricants such as magnesium stearate, sodium lauryl sulfate and talc may be used for preparing tablets, troches, pills, capsules and the like. To prepare a capsule, it is advantageous to use lactose and liquid carrier, such as high molecular weight polyethylene glycols. Various other materials may be present as coatings or to otherwise modify the physical form of the dosage unit. For instance, tablets, pills, or capsules may be coated with shellac, sugar or both. When aqueous suspensions are used they may contain emulsifying agents or agents which facilitate suspension. Diluents such as sucrose, ethanol, polyols such as polyethylene glycol, propylene glycol and glycerol, and chloroform or mixtures thereof may also be used. In addition, the active compound may be incorporated into sustained-release preparations and formulations. For oral administration, the active compound may be administered, for example, with an inert diluent or with an assimilable edible carrier, or it may be enclosed in hard or soft shell gelatin capsules, or it may be compressed into tablets, or it may be incorporated directly with the food of the diet, or may be incorporated with excipient and used in the form of ingestible tablets, buccal tablets, troches, capsules, elixirs, suspensions, syrups, wafers, and the like. For parenteral administration, emulsions, suspensions or solutions of the compounds according to the invention in vegetable oil, for example sesame oil, groundnut oil or olive oil, or aqueous-organic solutions such as water and propylene glycol, injectable organic esters such as ethyl oleate, as well as sterile aqueous solutions of the pharmaceutically acceptable salts, are used. The injectable forms must be fluid to the extent that it can be easily syringed, and proper fluidity can be maintained, for example, by the use of a coating such as lecithin, by the maintenance of the required particle size in the case of dispersion and by the use of surfactants. Prolonged absorption of the injectable compositions can be brought about by use of agents delaying absorption, for example, aluminum monostearate and gelatin. The solutions of the salts of the products according to the invention are especially useful for administration by intramuscular or subcutaneous injection. Solutions of the active compound as a free base or pharmacologically acceptable salt can be prepared in water suitably mixed with a surfactant such as hydroxypropyl-cellulose. Dispersion can also be prepared in glycerol, liquid polyethylene glycols, and mixtures thereof and in oils. The aqueous solutions, also comprising solutions of the salts in pure distilled water, may be used for intravenous administration with the proviso that their pH is suitably adjusted- that they are judiciously buffered and rendered isotonic with a sufficient quantity of glucose or sodium chloride and that they are sterilized by heating, irradiation, microfillration, and/or by various antibacterial and antifungal agents, for example, parabens. chlorobuianol, phenol, sorbic acid, thimerosal, and the like. Sterile injectable solutions are prepared by incorporating the active compound in the required amount in the appropriate solvent with various of the other ingredients enumerated above, as required, followed by filtered sterilization. Generally, dispersions are prepared by incorporating the various sterilized active ingredient into a sterile vehicle which contains the basic dispersion medium and the required other ingredients from those enumerated above. In the case of sterile powders for the preparation of sterile injectable solutions, the preferred methods of preparation are vacuum drying and the freeze drying technique which yield a powder of the active ingredient plus any additional desired ingredient from previously sterile-filtered solution thereof Topical administration, gels (water or alcohol based), creams or ointments containing compounds of the invention may be used. Compounds of the invention may be also incorporated in a gel or matrix base for application in a patch, which would allow a controlled release of compound through /ra/7jdermal barrier. For administration by inhalation, compounds of the invention may be dissolved or suspended in a suitable carrier for use in a nebulizer or a suspension or solution aerosol, or may be absorbed or adsorbed onto a suitable solid carrier for use in a dry powder inhaler-Solid compositions for rectal administration include suppositories formulated in accordance with known methods and containing at least one compound of formula I. Compositions according to the invention may also be formulated in a manner which resists rapid clearance from the vascular (arterial or venous) wall by convection and/or diffusion, thereby increasing the residence time of the viral particles at the desired site of action. A periadventitial depot comprising a compound according to the invention may be used for sustained release. One such useful depot for administering a compound according to the invention may be a copolymer matrix, such as ethylene-vinyl acetate, or a polyvinyl alcohol gel surrounded by a Silastic shell. Alternatively, a compound according to the invention may be delivered locally from a silicone polymer implanted in the adventitia. An alternative approach for minimizing washout of a compound according to the invention during percutaneous, transvascular delivery comprises the use of nondiffusible, drug-eluting microparticles. The microparticles may be comprised of a variety of synthetic polymers, such as polylactide for example, or natural substances, including proteins or polysaccharides. Such microparticles enable strategic manipulation of variables including total dose of drug and kinetics of its release. Microparticles can be injected efficiently into the arterial or venous wall through a porous balloon catheter or a balloon over stent, and are retained in Uie vascular wall and the periadventitial tissue for at least about two weeks. Formulations and methodologies for local, intravascular site-specific delivery of therapeutic agents are discussed in Reissen et al. (J. Am. Coli Cardioi. 1994; 23: 1234-1244), ilic entire contents of which are hereby incorporated by reference. A composition according to the invention may also comprise a hydrogel which is prepared from any biocompatible or non-c\lotoxic (homo or hetero) polymer, such as a bydrophilic polyacrylic acid polymer that can act as a drug absorbing sponge. Such polymers have been described, for example, in application WO93/08845, the entire contents of which are hereby incorporated by reference, Cenain of them, such as, in particular, those obtained from ethylene and/or propylene oxide are commercially .ivailable. In the use of compounds according to the invention for treating pathologies which are linked to Mypeiprolifcrative disorders, the compounds according to the invention can be administered in'different ways. For the treatment of restenosis, the compounds of the invention are administered directly to the \Aoo6 vessel wall by means of an angioplasty balloon which is coated with a hydrophilic film (for t \ample a hydrogel) which is saturated with the compoimd. or by means of any other catheter containing ;in infusion chanibcr for the compound, which can thus be applied in a precise manner to the site to be licated and allow the compound to be liberated locally and efficiently at the location of the cells to be luMied. This method of administration advantageously makes it possible for the compound to contact .|iiickly the cells in need of treatment. The treatment method of the invention preferably consists in introducing a compound according tu the invention at the site to be treated. For example, a hydrogel containing composition can be dtposited directly onto the surface of the tissue to be treated, for example during a surgical intervention. Nilvantageously. the hydrogel is introduced at the desired intravascular site by coating a catheter, for r.\a/iiple a balloon catheter, and delivery to the vascular wall, preferably at the time of angioplasty. In a p;iriicularly advantageous manner, the saturated hydrogel is introduced at the site to be treated by means ( t a balloon catheter. The balloon may be chaperoned by a protective sheath as the catheter is advanced (c>dstream. Another embodiment of the invention provides for a compound according to the invention to be uiministered by means of perfusion balloons. These perfusion balloons, which make it possible to maintain a blood flow and thus to decrease the risks of ischaemia of the myocardium, on inflation of the halioon. also enable the compound to be delivered locally at normal pressure for a relatively long time, \\\ The use of a perfusion balloon catheter is especially advantageous, as it Has the advantages of \n^\\\ keeping the balloon inflated for a longer period of time by retaining the properties of facilitated Jhiini: and of site-spccificily of the hydrogeL are gained simultaneously. Another aspect of the present invention relates to a pharmaceutical composition comprising a compound according to the invention and poloxamer, such as Poloxamer 407 is a non-toxic, biocompatible polyol, commercially available (BASF, Parsippany, NJ). A poloxamer impregnated with a compound according to the invention may be deposited directly on the surface of the tissue to be treated, for example during a surgical intervention. Poloxamer possesses essentially the same advantages as hydrogei while having a lower viscosity, I he use of a channel balloon catheter with a poloxamer impregnated with a compound according to the invention is especially advantageous. In this case, the advantages of both keeping the balloon inflated for a longer period of time, while retaining the properties of facilitated sliding, and of site-spccificity of the poloxamer, are gained simultaneously. The percentage of active ingredient in the compositions of the invention may be varied, it being necessary that it should constitute a proportion such that a suitable dosage shall be obtained. Obviouslv, several unit dosage forms may be administered at about the same time. A dose employed may be dctcmiined by a physician or qualified medical professional, and depends upon the desired therapeutic effect, the route of administration and the duration of the treatment, and the condition of the patient. In the adult, the doses are generally from about 0.001 to about 50, preferably about 0.001 to about 5, mg/kg body weight per day by inhalation, from about 0.01 to about 100, preferably 0.1 to 70, more especially 0.5 to 10. mg/kg body weight per day by oral administration, and from about 0.001 to about 10, preferably 0.01 to 10, mg/kg body weight per day by intravenous administration. In each particular case. the doses are detennined in accordance with the factors distinctive to the patient to be treated, such as age, weight, general state of health and other characteristics which can influence the efficacy of the compound according to the invention. The compounds/compositions according to the invention may be administered as frequently as necessary in order to obtain the desired therapeutic effect. Some patients may respond rapidly to a higher or lower dose and may find much weaker maintenance doses adequate. For other patients, it maybe necessary to have long-term treatments at the rate of 1 to 4 doses per day. in accordance with the physiological requirements of each particular patient. Generally, the active product may be administered orally 1 to 4 times per day. Of course, for other patients, it will be necessary to prescribe not more than one or two doses per day. The compounds of the present invention may also be formulated for use in conjunction with other therapeutic agents such as agents or in connection with the application of therapeutic techniques to address pharmacological conditions which may be ameliorated through the application of a compound of formula I, such as in the following: The compounds of the present invention may be used in the treatment of restenosis post angioplasty using any device such as balloon, ablation or laser techniques. The compounds of the present invention may be used in the treatment of restenosis following stent placement in the vasculature either as I) primary treatment for vascular blockage, or 2) in the instance where angioplasty using any device fails to give a patent artery. The compounds of the present invention may be used either orally, by parenteral administration or the compound could be applied topically through the intervention of a specific device or as a properly formulated coating on a stent device. In one aspect, the coating on a stent device is formed by applying polymeric material in which the compound of the invention is incorporated to at least one surface of the stent device. Polymeric materials suitable for incorporating the compound of the invention include polymers having relatively low processing temperatures such as polycaprolactonc, poly(ethyIene-co-vinyl acetate) or poly(vinyl acetate or silicone gum rubber and polymers having similar relatively low processing temperatures. Other suitable polymers include non-degradable polymers capable of carrying and delivering therapeutic drugs such as latexes, urethanes, polysiloxanes. styrene-ethylene/butylene-stN'rene block copolymers (SEES) and biodegradable, bioabsorbable polymers capable of carr>'ing and delivering therapeutic drugs, such as poly-DL-laciic acid (DL-PLA), and poly-L-lactic acid (L-PLA), polyonhoesters, polyiminocarbonates, aliphatic polycarbonates, and polyphosphazenes. A porosigen may also be incorporated in the drug loaded polymer by adding the porosigen to the polymer along with the therapeutic drug to form a porous, drug loaded polymeric membrane. "Porosigen'* means as any moiety, such as microgranules of sodium chloride, lactose, or sodium heparin, for example, which will dissolve or otherwise be degraded when immersed in body fluids to leave behind a porous network in the polymeric material. The pores left by such porosignes can typically be a large as 10 microns. The pores formed by porosignes such as polyethylene glycol (PEG), polyethylene oxide/polypropylene oxide (PEO/PPO) copolymers, for example, can also be smaller than one micron, although other similar materials which form phase separations from the continuous drug loaded polymeric matrix and can later be leached out by body fluids can also be suitable for forming pores smaller than one micron. The polymeric material can be applied to the stent while the therapeutic drug and porosigen material are contained within the polymeric material, to allow the porosigen to be dissolved or degraded by body fluids when the stent is placed in a blood vessel, or alternatively, the porosigen can be dissolved and removed from the polymeric material to form pores in the polymeric material prior to placement of the polymeric material combined with the stent within a blood vessel. If desired, a rate-controlling membrane can also be applied over the drug loaded polymer, to limit the release rate of the compound of the invention. The rate-controlling membrane can be added by applying a coating form a solution, or a lamination. The rate-controlling membrane applied over the polymeric material can be fomied to include a uniform dispersion of a porosigen in the rate-controlling membrane, and the porosigen in the rate-controlling membrane can be dissolved to leave pores in the rate-controlling membrane t>'pically as large as 10 microns, or as small as 1 micron, for example, although the pores can also be smaller than 1 micron. The porosigen in the rate-controlling membrane can be, for example sodium chloride, lactose, sodium heparin, polyethylene glycol polyethylene oxide/polypropylene oxide copolymers, and mixtures thereof. In another aspect, the coating on the stent device can be formed by applying the compound of the invention to at least one surface of the stent device to form a bioaclive layer and then applying one or more coats of porous polymeric material over the bioactive layer, such that the porous polymeric material has a thickness adequate to provide a controlled release of the compound. The porous polymeric material may be composed of a polyamide, parylene or a paiylene derivative applied by catalyst-free vapor desposition. "Parylene" refers to a polymer based on p-xylylene and made by vapor phase polymerization as described in U.S. Pat. No. 5,824.049, incorporated herein by reference. Alternatively, the porous polymeric material is applied by plasma deposition. Representative polymers suitable for plasm deposition include poly(etliylene oxide). poly(ethylene glycol), poly(propylene oxide), and polymers of methane, silicone, tetrafluoroelhylene tetramethyldisiloxane, and the like. Other suitable polymer systems include polymers derived from photopolymerizable monomers such as liquid monomers preferably having at least two cross linkable C-C (Carbon to Carbon) double bonds, and being a non-gaseous addition polymerizable ethylenically unsaturated compound, having a boiling point above 100 "^C, at atmospheric pressure, a molecular weight of about 100-1500 and being capable of forming high molecular weight addition polymers readily. More preferably, the monomer is preferably an addition photopolymerizable polyethylcnically unsaturated acrylic or methacrylic acid ester containing two or more acrylate or methacrylate groups per molecule or mixtures thereof. Representative examples of such multifuntional acrylates are ethylene glycol diacrylate. ethylene glycol dimethacrylate, trimethylopropane triacrylate, trimethylopropane trimelhacryiate, pentaerjlhritol Tetraacr\'late or pentaerythritol tetramethacrylatc, 1,6-hexanediol dimcthacr\'iate, and diethyleneglycol dimelhacrylate. Also useful in some special instances are monoacr>'lates such as n-buiyl-acrylate, n-butyl methacrylate, 2-ethylhexyl acrylate, lauryl-acrylate. and 2-hydro.\y-propyl acr>'late. Small quantities of amides of (meth)acrylic acid such as N-methylol melhacrylamide butyl ether are also suitable, N-vinyl compounds such as N-vinyl pyrrolidone, vinyl esters of aliphatic monocarboxylic acids such as vinyl oleate, vinyl ethers of diols such as butanediol-l.4-divinyl ether and allyl ether and allyl ester are also suitable. Also included are other monomers such as the reaction products of di- or polyepoxides such as butanediol-1. 4-diglycidyl ether or bisphenol A diglycidyl ether with {meth)acrylic acid. The characteristics of the photopolymerizable liquid dispersing medium can be modified for the specific purpose by a suitable selection of monomers or mixtures thereof. Other useful polymer systems include a polymer that is biocompatible and minimizes irritation to the vessel wall when the stent is implanted. The polymer may be either a biostable or a bioabsorbable polymer depending on the desired rate of release or the desired degree of polymer stability. Bioabsorbable polymers that could be used include poiy(L-lactic acid), polycaprolactone, poly(Iactide-co-glycolide), poly(hydroxybutyrate). poly (hydroxybutyrate-co-valerate), polydioxanone, polyorthoester, polyanhydride, poly(glycolic acid), poly(D, L-lactic acid), poly(glycolic acid-coirimethylene carbonate), polyphosphoester, polyphosphoester urethane, poly(amino acids), cyanoacrylates, poly(trimethylene carbonate), poly (iminocarbonate), copoly(ether-esters) (e.g., PEO/PLA), polyalkylene oxiales, polyphoosphazenes and biomolecules such as fibrin, fibrinogen, cellulose, starch, collagen and hyaluronic acid. Also, biostable polymers with a relatively low chronic tissue response such as poiyurethanes, silicones, and polyesters could be used and other polymers could also be used if they can be dissolved and cured or polymerized on the stent such as polyolefins, polyisobutylene and ethylene-alphaolefme copolymers; acrylic polymers and copolymers, vinyl halide polymers and copolymers, such as polyvinyl chloride; polyvinyl ethers, such as polyvinyl methyl ether; polyvinylidene halides, such as polyvinylidene fluoride and polyvinylidene chloride; polyacrylonitrile, poly\'invl ketones, polyvinyl aromatics. such as polystyrene, pol>Tinyl esters, such as polyvinyl acetate; copolymers of vinyl monomers with each other and olefms, such as ethylene-meihyl methacrylate copolymers, acrylonitril-styrene copolyers, ABS resins, and ethylene-vinyl acetate copolymers; polyamides, such as Nylone 66 and polycaprolaciam; alkyl reins, polycarbonates; polyoxymethylenes; polyimides, polyethers; epoxy reins, polyiirethanes; rayon; rayon-triacetate; cellulose, cellulose acetate, cellulose buiyraic; cellulose acetate buryrate; cellophane, cellulose nitrate; cellulose propionate; cellulose ethers; and carboxymethyl cellulose. In addition to plasma deposition and vapor phase deposition, other techniques for applying the various coalings on the stent surfaces may be employed. For example, a polymer solution may be applied to the stent and the solvent allowed to evaporate, thereby leaving on the stent surface a coating of the poi> nicr and the therapeutic substance. Typically, the solution can be applied to the stent by either spraying the solution onto the stent or immersing the stent in the solution. The compounds of the present invention may be used in the treatment of restenosis in combination with any anticoagulant, antiplatelet, antithrombotic or proHbrinolytic agent. Often patients are concurrently treated prior, during and after interventional procedures with agents of these classes cither in order to safely perform the interventional procedure or to prevent deleterious effects of thrombus fornuition. Some examples of classes of agents known to be anticoagulant, antiplatelet, antithrombotic or profibrinolytic agents include any formulation of heparin, low molecular weight heparins, pentasaccharides, fibrinogen receptor antagonists, thrombin inhibitors. Factor Xa inhibitors, or Factor Vila inhibitors. The compounds of the present invention may be used in combination with any antihypertensive agent or cholesterol or lipid regulating agent in the treatment of restenosis or atherosclerosis concurrently with the treatment of high blood pressure or atherosclerosis. Some examples of agents that are useful in the treatment of high blood pressure include compounds of the following classes; beta-blockers, ACE inhibitors, calcium channel antagonists and alpha-receptor antagonists. Some examples of agents that are useful in the treatment of elevated cholesterol levels or disregulated lipid levels include compounds known to be HMGCoA reductase inhibitors, compounds of the fibrate class. The compounds of the present invention may be used in the treatment of various forms of cancer either alone or in combination with compounds known to be useful in the treatment of cancer. It is understood that the present invention includes combinations of compounds of the present invention with one or more of the aforementioned therapeutic class agents Compounds within the scope of the present invention exhibit marked pharmacological activities according to tests described in the literature which tests results are believed to correlate to pharmacological activity in humans and other mammals. The following pharmacological in vitro and in vivo test results are typical for characterizing compounds of the present invention. Preparation of Pharmaceutical Compositions and Pharmacological Test Section Compounds within the scope of this invention exhibit significant activity as protein tyrosine kinase inhibitors and possess therapeutic value as cellular antiproliferative agents for the treatment of certain conditions including psoriasis, atherosclerosis and restenosis injuries. Compounds within the scope of the present invention exhibit the modulation and/or inhibition of cell signaling and/or cell proliferation and/or matrix production and/or chemoiaxis and/or cell inllammatory response, and can be used in preventing or delaying the occurrence or reoccurrence of such conditions or otherwise treating the condition. To determine the effectiveness of compounds of this invention, the pharmacological tests described below, which are accepted in the art and recognized to correlate with pharmacological activity in mammals, are utilized. Compounds within the scope of this invention have been subjected to these various tests, and the results obtained are believed to cojTelate to useful cellular differentiation mediator activiiN. The results of these tests are believed to provide sufficient information to persons skilled in the pharmacological and medicinal chemistry arts to determine the parameters for using the studied compounds in one or more of the therapies described herein. 1. PDGF-R Tyrosine Kinase Antophosphorylation ELISA assay The titled assay is perfonned as described by Dolle et al. (./ Med. Chem. 1994. 37. 2627). which is incorporated herein by reference, with the exception of using the cell lysates derived from Human aortic smooth muscle cells (HAMSC) as described below. 2. Mitouenesis Assay General Procedure a Cell Culture Human aortic smooth muscle cells (passage 4-9) are plated in 96 well plates in a growih supporting medium al 6000 cells/well and allowed to grow 2-3 days. At approximately 85% confluence, cells are growth arrested with serum free media (SFM). b. Mitogenesis Assay After 24 hour serum deprivation, medium is removed and replaced with test compound/vehicle in SFM (200 |il/well). Compounds are solubilized in cell culture DMSO al a concentration of ]0 mM and further dilutions are made in SFM. After 30 min preincubation with compound, cells are stimulated with PDGF at 10 ng/mL. Determinations are performed in duplicate with stimulated and unstimulated wxlis at each compound concentration. Four hours later, 1 fiCi "'H thymidine/well is added. Cultures are terminated 24 hours after addition of growth factor. Cells are lifted with trypsin and harvested onto a filter mat using an automated cell harvester (WaJIac MachII96). The filter mat is counted in a scintillation counter (Wallac Betaplate) to determine DNA-incorporated label. 3. Chemotaxis Assay Human aortic smooth muscle cells (HASMC) at earlier passages are obtained from ATCC. Cells are grown in Clonetics SmGM 2 SingleQuots (media and cells at passages 4-10 are used. When cells are 80% confluent, a fluorescent probe, calcein AM (5 mM, Molecular Probe), is added to the media and cells are incubated for 30 minutes. After washing with HEPES buffered saline, cells are lifted with trypsin and neutralized with MCDB 131 buffer (Gibco) with 0.1% BSA, 10 mM glutamine and 10% fetal bovine serum. After centrifugation, cells are washed one more time and resuspended in the same buffer without fetal bovine serum at 30000 cells/50 mL. Cells are incubated with different concentrations of a compound of formula 1 (final DMSO concentration - I %) for 30 min at 37^C. For chemotaxis studies, 96 well modified Boyden chambers (Neuroprobe, Jnc.) and a polycarbonate membrane with 8 mm pore size (Porelics, CA) are used. The membrane is coated with collagen (Sigma C3657, 0.1 mg/mL). PDGF-Pp (3 ng/mL) in buffer with and without a compound of formula I are placed in the lower chamber. Ceils (30,000), with and without inhibitor, are placed in the upper chamber. Cells are incubated for 4 hours. The filter membrane is removed and cells on the upper membrane side are removed. After drying, fluoresce on the membrane is detciTnined using C>lofiuor II (Millipore) at excitation/emission wavelengths of 485/530 nm. In each experiment, an average cell migration is obtained from six replicates. Percent inhibition is determined from DMSO treated control values. From five points concentration-dependent inhibitions, IC^o value is calculated. Results are presented as a mean±S[:M from five such experiments, 4. BGF-Rcceptor Purification EGF-receplor purification is based on the procedure of Yarden and Schlessinger. A431 cells are grown in 80 cm^ bottles to confiuency (2 x 10' cells per bottle). The cells are washed twice with PBS and har\'esled with PBS containing 11.0 mmol EDTA (1 hour at 37'C, and ccntrifuged at 600g for 10 minutes. The cells are solubilizcd in I mLper2x 10'cells of cold solubilization buffer (50 mmol Hepes buffer, p\\ 7.6, 1% Triton X-100, 150 mmol NaCL 5 mmol EGTA, I mmol PMSF. 50 mg/mL aprotinin, 25 mmol benzamidine, 5 mg/mL leupeptic. and 10 mg/mL soybean trypsin inhibitor) for 20 minutes at 4°C. After centrifugation at lOO.OOOg for 30 minutes, the supernatant is loaded onto a WGA- agarose column (100 mL of packed resin per 2 x 10^ cells) and shaken for 2 hours at 4"C. The unabsorbed material is removed and the resin washed twice with HTN buffer (50 mmol Hepes, pH 7.6, 0.1% Triton X-100, 150 mmol NaCI), twice with HTN buffer containing I M NaCl, and twice with HTNG buffer (50 mmol Hepes, pH 7,6, 0.1% Triton X-100, 150 mmol NaCI, and 10% glycerol). The EGF receptor is eluted batchwise with HTNG buffer containing 0.5 M N-acetyl-D-glucosamine (200 mL per 2 X 10^ cells,). The eluted material is stored in aliquots at -70*^C and diluted before use with TMTNG buffer (50 mmol Tris-Mes buffer, pH 7.6, 0.1% Triton X-100. 150 mmol NaCL 10% glycerol). 5. Inhibition of EGF-R Autophosphorylation A43 1 cells are grown to continence on human fibronectin coated tissue culture dishes. After washing 2 times with ice-cold PBS, cells are lysed by the addition of 500 mL/dish of lysis buffer (50 mmol Hepes, pH 7.5, 150 mmol NaCL 1.5 mmol MgCl2, 1 mmol EGTA. 10% glycerol, 1% triton X-100, I mmol PMSF, 1 mg/mL aprotinin, 1 mg/mL leupeptin) and incubating 5 minutes at 4'C, After EGF stimulation (500 mg/mL 10 minutes at 37°C) immunoprecipitation is performed with ami EGF-R (Ab 108) and the autophosphorylation reaction (50 mL aliquots, 3 mCi [g--^-P]ATP) sample is carried out in the presence of 2 or 10 mM of compound of the present invention, for 2 minutes at 4°C. The reaction is stopped by adding hot electrophoresis sample buffer. SDA-PAGE analysis (7.5% els) is followed by autoradiography and the reaction is quantitated by densitometry scanning of the x-ray films, a. Cell Culture Cells termed HER 14 and K721A are prepared by //'a/7.sfeeling N1H3T3 cells (clone 2.2) (From C. Fryling. NCI, NIH), which lack f;/^f^genous EGF-receptors, with cDNA constructs of wild-type EGF- receptor or mutant EGF-receptor lacking tyrosine kinase activity (in which Lys 721 at the ATP-binding site is replace by an Ala residue, respectively). All cells are grown in DMEM with 10% calf serum (Hyclone, Logan, Utah). 6. Selectivity vs. PKA and PKC is determined usina commercial kits: a. Pierce Colorimetric PICA Assay Kit, Spinzyme Format Brief Protocol: PKA enzyme (bovine heart) lU/assay tube Kemptide peptide (dye labeled) substrate 45 minutes @ 30°C Absorbance at 570 nm b. Pierce Colorimetric PKC Assay kit, Spinzyme Formal Brief Protocol: PKC enzyme (rai brain) 0.025U/as-say tube Neurogranin peptide (dye labeled) substrate 30 minutes @ 30^C Absorbance at 570 nm 7. p56^'* Tyrosine Kinase Inhibition Activity Measurements p56'* Tyrosine kinase inhibition activity is determined according to a procedure disclosed in United Slates Patent No. 5,714,493, incorporated herein by reference. In the alternative, the tyrosine kinase inhibition activity is determined according to the following method. A substrate (tyrosine-containing substrate. Biot-(p Ala)-Lys-Val-GIu-LyS'IIe-Giy-Glu-Gly-Thr-Tyr-GIu-Val-VaI-Tyr-Lys-(NH2) recognized by P56*''. I [iM) is first phosphorylated in presence or absence of a given concentration of the test compound, by a given amount of enzyme (enzyme is produced by expression of P56'*'*' gene in a yeast construct) purified from a cloned yeast (purification of the enzyme is done by following classical methods) in the presence of ATP (lO^M) MgCI2( 2,5mM), MnC12 (2.5mM), NaCl (25mM), DTT (0.4mM) in Hepes 50mM. pH 7.5, over 10 min at ambient temperature. The total reaction volume is 50^1, and the reactions are performed in a black 96-we!l fluoroplate. The reaction is stopped by addition of I50pl of slopping buffer (lOOmM Hepes pH7,5, KF 400mM, EDTA 133 mM, BSA Ig/1.) containing a selected anti tyrosine antibody labeled with the Europium cryptatc (PY20-K) at 0.8pg/ml and allophycocyanine-labelled streptavidin (XL665) at 4ng/mL The labeling of Streptavidin and anti-tyrosine antibodies were performed by Cis-Bio International (France). The mixture is counted using a Packard Discovery counter which is able to measure time-resolved homogeneous fluorescence transfer (excitation at 337 nm. readout at 620 nm and 665 nm). The ratio of the 665 nm signal / 620nm signal is a measure of the phosphorylated tyrosine concentration. The blank is obtained by replacing enzyme by buffer The specific signal is the difference between the ratio obtained without inhibitor and the ratio with the blank. The percentage of specific signal is calculated. The ICso is calculated with 10 concentrations of inhibitor in duplicate using Xlfit soft. The reference compound is staurosporine (Sigma) and it exhibits an Id, ol 30± 6 nM (n=20). 8. Measurement of Tumor Inhibition In Vitro The inhibition of tumor growth in vitro by the compounds of this invention is determined as follows; C6 rat glioma cell line (provided by ATCC) is grown as monolayers in Dubelcco's Modified Eagle Medium containing 2 mM L-glutamine, 200 U/ml penicillin, 200 fig/ml streptomycin and supplemented with 10% (v/v) heat inactivated foetal calf serum. Cells in exponential phase of growth are trypsinized, washed with PBS and diluted to a fmal concentration of 6500 cells/ml in complete medium. Drug to be tested or control solvent are added to the cell suspension (2.5 ml) under a-volume of 50 fil and 0.4 ml of 2.4% Noble Difco agar maintained at 45 °C are added and mixed. The mixture is immediately poured into Petri dishes and left standing for 5 minutes at 4 °C. The number of cellular clones (>60 cells) are measured after 12 days of incubation at 31 °C under 5% CO7 atmosphere. Each drug is tested at 10, 1, 0.1, and 0.01 pg/'ml (fmal concentration in the agar) in duplicate. Results are expressed in percent inhibition of clonogenicity relatively to untreated controls. IC^o's are determined graphically from semi-logarithmic plots of the mean value determined for each drug concentration. 9. Measurement of Tumor Inhibition In Vivo The inhibition of tumor growth in vivo by the compounds of this invention is determined using a subucatenous xenograft model as described in U.S. Pat, Nos. 5,700,823 and 5,760,066, in which mice are implanted with C6 glioma cells and tumor growth is measured using venier calipers. The results obtained by the above experimental methods evidence that the compounds within the scope of the present invention possess useful PDGF receptor protein tyrosine kinase inhibition properties or p56'^ tyrosine kinase inhibition properties, and thus possess therapeutic value. The above pharmacological test results may be used to determine the dosage and mode of administration for the particular therapy sought. The present invention may be embodied in other specific forms without departing from the spirit or essential attributes thereof. WE CLAIM: 1. A stent device characterized in that it has a polymeric coating into which is incorporated a compound of formula (I) wherein X is L2Z2; L2 is (CR3aR3b)p-Z4 (i) a non-aromatic monocyclic or multicycHc ring system of 3 to 10 carbon atoms (hereinafter referred to as "cycloalkyl"); (ii) a non-aromatic monocyclic or multlcyclic ring system containing a carbon-carbon double bond and having 3 to 10 carbon atoms (hereinafter referred to as "cycloalkenyl"); (iii) a 4- to 10-member monocyclic or multicycHc ring system wherein one or more of the atoms in the ring system is chosen from amongst nitrogen, oxygen and sulfur (hereinafter referred to as "heterocyclyl"); or (iv) a 4- to 10-member monocyclic or multicycHc ring system which is partially saturated and wherein one or more of the atoms in the ring system is chosen from amongst nitrogen, oxygen or sulfur (hereinafter referred to as "heterocyclenyl"); any of which is substituted or unsubstituted by Si; Z4 is O, NR4, S, SO, SO2, or a bond; p and q are independently 0,1,2, 3 or 4, and p + q ~ 1, 2, 3, or 4 when Z4 is a bond, and p + q = 0,1,2, or 3 when Z4 is other than a bond; Ria and Rib are, independently: (i) an aliphatic hydrocarbon group which may be branched- or straight-chained, having 1 to 10 carbon atoms, and substituted or unsubstituted by S2 (hereinafter referred to as "alkyl"); (ii) an aromatic carbocyclic radical containing 6 to 10 carbon atoms and substituted or unsubstituted by S3 (hereinafter referred to as "aryl"); (iii) a 5- to 10-membered aromatic monocyclic or multicyclic hydrocarbon ring system in which one or more of the carbon atoms in the ring system is nitrogen, oxygen or sulfur, substituted or unsubstituted by S3 (hereinafter referred to as "heteroaryl") (iv) hydroxy; (v) H-CO-0- or aIkyl-CO-0- (hereinafter referred to as "acyloxy"); (vi) an alkyI-0- group substituted or unsubstituted by S4 (hereinafter referred to as "aJkoxy"); (vii) a cycloalkyl-O" group substituted or unsubstituted by Sj (hereinafter referred to as "cycloalkyloxy"); (viii) a heterocyclyl-0- group substituted or unsubstituted by Si (hereinafter referred to as "heterocyclyloxy"); (ix) a heterocycIyl-C(0)-0" group substituted or unsubstituted by S| (hereinafter referred to as "heterocyclylcarbonyloxy"); (x) an aryl-O- group substituted or unsubstituted by S3 (hereinafter referred to as "aryloxy"); (xi) a heteroaryl-O- group substituted or unsubstituted by S3 (hereinafter referred to as "heteroaryloxy"); (xii) cyano; (xiii) R5R6N-; or (xiv) acylRsN-; or one of Rja and R(b is hydrogen or halo and the other is alkyl, aryl, heteroaryl, hydroxy, acyloxy, alkoxy, cycloalkyloxy, heterocyclyloxy, heterocyclylcarbonyloxy, aryloxy, heteroaryloxy, cyano, RsRaN- or acylRjN-; Ric is hydrogen, alkyl, aryl, heteroaryl, hydroxy, acyloxy, alkoxy, cycloalkyloxy, heterocyclyloxy, aryloxy, heteroaryloxy, halo, cyano, RsR^N- or acylR5N"; Si is alkyl, hydroxy, acyloxy, alkoxy, halo, R5R6N-, acylRsN-, carboxy or R5R6NCO-or a bivalent oxygen (-0-) on two adjacent carbon atoms to form an epoxide; S2 is alkoxy, halo, carboxy, hydroxy, or R5R6N-; Sgishydrogen, hydroxy, halo, alkyl, alkoxy, carboxy, alkoxycarbonyl or Y(Y2NC0", wherein Yi and Y2 are independently hydrogen or alkyl; S4 is amino, alkoxy, carboxy, alkoxycarbonyl, carboxyaryl, carbamoyl or heterocyclyl; Rsa. Rsb, R3a' and Rsb' - are independently hydrogen or alkyl; R4 is hydrogen, alkyl or acyl; and R5 and R6 are independently hydrogen or alkyl, or R5 and R6 taken together with the nitrogen atom to which they are attached form a heteroaryl group in which at least one nitrogen atom is present as a ring atom (hereinafter referred to as "azaheterocyclyl"); or an N-oxide thereof, hydrate thereof, solvate thereof, prodrug thereof, or a pharmaceuticaily acceptable salt thereof 2. The stent device as claimed in claim 1 wherein U is (CR3aR3bVZ4-(CR3^CR3b)q; Z2 is substituted or unsubstituted cyclohexyl, substituted or unsubstituted norbomyl, or substituted or unsubstituted heterocyclenyl; p is 0; q is 0 or 1; Ria and Rib are independently substituted or unsubstituted alkyl, substituted or unsubstituted alkoxy, substituted or unsubstituted cycloalkyloxy or substituted or unsubstituted heterocyclyloxy, or one of Ria and Rib is hydrogen or halo; Ric is hydrogen; R3'a and Ry\y are independently hydrogen; and R4 is hydrogen, or an N-oxide thereof, hydrate thereof, solvate thereof, prodrug thereof, or pharmaceuticaily acceptable salt thereof. 3. The stent device as claimed in claim 1 wherein Z2 is methylcyclopentyl, methylcyclohexyl, [2.2.1]bicycloheptanyl, [2.2.2]bicyclooctanyl, cyclopentenyl, cyclohexenyl, [2.2.1]bicycloheptenyl or [2,2.2]bicyclooctenyL 4. The stent device as claimed in claim 1 wherein Z4 is O. 5. The stent device as claimed in claim 1 wherein Z4 is NR4. 6. The stent device as claimed in claim 1 wherein Z4 is S. 7. The stent device as claimed in claim 1 wherein the compound of formula I is: 2-cyclohexyIamino-6,7-dimethoxyquinoxaline; exo-bicyclo [22.1 ]hept-2-yl-(6-chloro-7-methoxyquinoxalin-2-yl)amine; exo-bicycio [2.2.1 ]hept-2-yl-(7-chloro-6-memoxyquinoxaIin-2-yl)amine; Bicyclo[2.2.1]hept-2-yl-(6,7-dimemyl-qumoxalin-2-yl)-amine; 2-cycloheptylamino-6,7-'dimethoxyquinoxaline; 2"Cyclopentylamino-6,7-dimethoxyquinoxaline; 2"Cyclohexylamino-6-methoxyquinoxaline; 2-Cyclohexylamino-6-methoxy-7-bromo-quinoxaline hydrochloride; 2,7-Bis-cyclohexyloxy-6-methoxy-quinoxaline; Cyclohexyl-(6,7-dimethoxyquinoxalin-2-ylmethyl)-amine; Cyclohexyl-(6-methoxy*7-morpholin-4-yl-quinoxalin-2-yl)-amine; (±)-Bicyclo[2.2.1 ]hept-2-yl-(6,7-dimethoxyquinoxalin-2-yl)-amine; exo-bicyclo[2.2,l]hept-5-en-2-yl-(6,7-dimethoxyquinoxaIin-2"yI)-amine; Cyclohexyl-(6,8-dimethyl-qninoxalin-2-yl)"amine; Endo-bicyclo[2.2.I ]hept-2-yl-(6,7-dimethoxyquinoxalm-2-yl)-amine; (6,7-Dimethoxyquinoxalin-2-yl)-(4-methoxy-cyclohexyl)-amine; ExO"bicyclo[2.2,1 ]hept-2-yl-(6-methoxyquinoxalin-2-y])-amine; exo-2-(Bicyclo[2.2.1 ]hept-2-yloxy)-6,7-dimethoxyquinoxaline; (Bicyclo[2.2.2]oct-2-yloxy)-6,7-dimethoxy-2-quinoxaline; Endo-2"(bicyclo[2.2.1 ]hept-2-yloxy)-6,7-dimethoxy-quinoxaline; exo-2-(Bicyclo[2.2.1]hept-5-en-2-yloxy)-6,7-dimethoxy-2-quinoxaline; (BicycIo[2.2.1 ]hept-5-en-2-yloxy)-6,7-dimethoxyquinoxaline; 2-Cyclohexyloxy-6,7-dimethoxyquinoxaline; 2-cyclopentyIthio-6,7-dimethoxy-quinoxaline; 6,7-dimethoxy-2-cyclopentyloxy-quinoxaline; 2-cyclopentylmethy]oxy-6,7-dimethoxy-quinoxaline; 6,7-dimethoxy-2-tetrahydropyran-4-oxy-quinoxaline; exo,exo-6,7-dimethoxy-2-(5,6-epoxy"bicyclo[2.2. l]heptan-2-yloxy)-quinoxaline; cis/trans-4-(6,7-Dimethoxyquinoxalin-2-yloxy)-cyclohexanecarboxylicacid; 6,7-Dirnethoxy-2-(4-rnethoxy-cyclohexyloxy)-quinoxaline; (1 R,2R,4S)-(+)-Bicyclo[2.2.1]hept-2-yl-(6,7-dimethoxyquinoxaIin-2-yl)-amine; (lS,2S,4R)-(-)-Bicyclo[2.2.1]hept-2'yl-(6,7-dimethoxyquinoxalin-2-yl)-amine; Cis/trans-4-(6,7-Dimethoxy-quinoxalin-2-ylamino)-cyclohexanecarboxylic acid methyl ester; Cis/trans-4-(6,7-dimethoxy-quinoxalln-2-ylamino)-cyclohexanecarboxylic acid; Cis-4-(6,7-dimethoxy-qumoxalm-2-ylamino)-cyclohexanecarboxylic acid methyl ester; Trans-4'(6,7-dimemoxy-qumoxaIin-2-ylamino)-cyc!ohexanecarboxylic acid methyl ester; (6,7-dimemoxy-qxunoxaline-2-yl)-c:/V-rraA7^-(3-(R)-methylcyclohexyl) amine; (6,7-dimethoxy-quinoxaline-2-yl)-/raAiy-(3-(R)-methylcyclohexyl) amine; (6,7-dimethoxy-quinoxaline-2-yl)-c/5-(3 -(R)-methylcyclohexyl) amine; or Methyl c/^//raw5-4-(6,7-Dimethoxyquinoxalin-2-yloxy)-cyclohexanecarboxylate, or an N-oxide thereof, hydrate thereof, solvate thereof, prodrug thereof, or pharmaceutically acceptable salt thereof 8. The stent device as claimed in claim 1, wherein the coating comprises one or more polymers selected from the group consisting of polycaprolactone, poly(ethylene-co-vinyl acetate),poly(vinyl acetate) and silicone gum rubber. 9. The stent device as claimed in claim 1, wherein the coating comprises one or more polymers selected from the group consisting of latexes, urethanes, polysiloxanes and styrene-ethylene/butylene-styrene block copolymers. 10. The stent device as claimed in claim 1, wherein the coating comprises one or more polymers selected from the group consisting of poly-DL-lactic acid, poly-L-lactic acid, polyorthoesters, polyiminocarbonates, aliphatic polycarbonates and polyphosphazenes. 11. The stent device as claimed in claim 1, wherein the coating further comprises a porosigen, 12. The stent device as claimed in claim 11, wherein the porosigen is selected from the group consisting of microgranules of sodium chloride, lactose or sodium heparin. 13. The stent device as claimed in claim 11, wherein the porosigen is selected from the group consisting of polyethylene glycol and polyethylene oxide/polypropylene oxide copolymers. 14. The stent device as claimed in claim 1, wherein a rate-controlling membrane is applied over the coating, to limit the release rate of the compound of formula I from the coating. 15. The stent device as claimed in claim 14, wherein the rate-controlling membrane comprises a porosigen selected from the group consisting of sodium chloride, lactose, sodium heparin, polyethylene glycol, polyethylene oxide/polypropylene oxide copolymers, and mixtures thereof 16. The stent device as claimed in claim 1, wherein the compound of formula I is incorporated into the coating by applying the compound of formula I to at least one surface of the stent device to form a bioactive layer and then applying one or more coats of porous polymeric material over the bioactive layer. 17. The stent device as claimed in claim 16, wherein the porous polymeric material comprises a polyamide, parylene or parylene derivative* 18. The stent device as claimed in claim 16, wherein the porous polymeric material is applied by plasma deposition. 19. The stent device as claimed in claim 18, wherein the porous polymeric material is selected from the group consisting of poly(ethylene oxide), poly(ethylene glycol), poly(propylene oxide), and polymers of methane, silicone and tetrafluoroethylene tetramethyldisiloxane. 20. The stent device as claimed in claim 1, wherein the coating is derived from an addition-photopolymerizable, polyethylenically-unsaturated acrylic or methacrylic acid ester containing two or more acrylate or methacrylate groups per molecule, or mixtures thereof 21. The stent device as claimed in claim 20, wherein the monomer is selected from the group consisting of ethylene glycol diacrylate, ethylene glycol dimethacrylate, trimethylopropane triacrylate, trimethylopropane trimethacrylate, pantaerythritol tetraacrylate, pentaerythritol tetramethacrylate, 1,6-hexanediol dimethacrylate and diethyleneglycol dimethacrylate. 22. The stent device as claimed in claim 20, wiierein the monomer is selected from the group consisting of n-butyl acrylate, n-butyl methacrylate, 2-ethylhexyl acrylate, lauryl acrylate and 2-hydroxypropyl acrylate. 23. The stent device as claimed in claim 1, wherein the coating comprises a polymer selected from the group consisting of poly(L-lactic acid), polycaprolactone, poly(lactide-co- glycolide), poly(hydroxybutyrate), poly(hydroxybutyrate-co-valerate), polydioxanone, polyorthoester, polyanhydride, poIy(glycolic acid), poly(D,L-lactic acid), poly(glycolic acid- cotrimethylene carbonate), polyphosphoester, polyphosphoester urethane, poly(amino acids), cyanoacrylates, poly(trimethylene carbonate), poly(iminocarbonate), poly(ether-esters), polyalkylene oxalates, polyphosphazenes, fibrin, fibrinogen, cellulose, starch, collagen and hyaluronic acid. 24. The stent device as claimed in claim 1, wherein the coating comprises a polymer selected from the group consisting of polyurethanes, silicones, polyesters, polyolefins, polyisobutylene, and ethylene-alphaolefm copolymer; acrylic polymers and copolymers, vinyl halide polymers and copolymers, such as polyvinyl chloride; polyvinyl ethers, such as polyvinyl methyl ether; polyvinylidene halides, such as polyvinylidene fluoride and polyvinylidene chloride; polyacrylonitrile, polyvinyl ketones, polyvinyl aromatics, such as polystyrene, polyvinyl esters, such as polyvinyl acetate; copolymers of vinyl monomers with each other and olefins, such as ethylene-methyl methacrylate copolymers, acrylonitrile-styrene copolymers, ABS resins, and ethylene-vinyl acetate copolymers; polyamides, such as Nylon 66 and polycaprolactam; alkyl resins, polycarbonates; polyoxymethylenes; polyimides, polyethers; epoxy resins, polyurethanes; rayon; rayon-triacetate; cellulose, cellulose acetate, cellulose butyrate; cellulose acetate butyrate; cellophane, cellulose nitrate; cellulose propionate; cellulose ethers; and carboxymethylcellulose.

Documents:

in-pct-2001-880-che-abstract.pdf

in-pct-2001-880-che-assignement.pdf

in-pct-2001-880-che-claims filed.pdf

in-pct-2001-880-che-claims granted.pdf

in-pct-2001-880-che-correspondnece-others.pdf

in-pct-2001-880-che-correspondnece-po.pdf

in-pct-2001-880-che-description(complete)filed.pdf

in-pct-2001-880-che-description(complete)granted.pdf

in-pct-2001-880-che-form 1.pdf

in-pct-2001-880-che-form 13.pdf

in-pct-2001-880-che-form 26.pdf

in-pct-2001-880-che-form 3.pdf

in-pct-2001-880-che-form 5.pdf

in-pct-2001-880-che-pct.pdf