Modulators of Protein Tyrosine Phosphatases FIELD OF INVENTION The present invention provides novel compounds, novel compositions, methods of their use, and methods of their identification, where such compounds are pharmacologically useful inhibitors of Protein Tyrosine Phosphatases (PTPases, PTPs) such as PTP1B, TC-PTP, CD45. SHP-I, SHP-2, PTPa, PTPs, PTP". PTPS, PTPa. PTP", PTPp, PTPD1, PTPD2, PTPH1, PTP-MEG1, PTP-LAR. and HePTP or ligands of phosphotyrosine units. These compounds are indicated in the management or treatment of a broad range of diseases such as autoimmune diseases, acute and chronic inflammation, osteoporosis, various forms of cancer and malignant diseases, and type I diabetes and type II diabetes. BACKGROUND OF THE INVENTION In accordance with the definition of iojdyQ activity of protein tyrosine phosphatases (PTPases) such as the following non-limiting examples PTPa, LAR, TC-PTP. SHP-1, SHP-2, PTPp. CD45, PTP1B, HePTP, it has been found that their unique activity plays a major role in the intracellular modulation and regulation of fundamental cellular signalling mechanisms involved in metabolism, growth, proliferation and differentiation (Flint et al., The EMBO J. 12:1937"6,1993; Fischer et al, Science 253:401-6,1991). Overexpression or altered activity of tyrosine phosphatases can also contribute to the symptoms and progression of various diseases (Wiener, et al., J. Natl. cancer Inst. 86:372-8. 1994; Hunter and Cooper. Ann. Rev. Biochem, 54:897-930. 1985). Furthermore, there is increasing evidence which suggests that inhibition of these PTPases may help treat certain types of diseases such as diabetes, autoimmune disease, acute and chronic inflammation and various forms of cancer. Protein phosphorylation is now well recognized as an important mechanism utilized by cells to transduce signals during different stages of cellular function (Fischer et al, Science 253:401-6 (1991); Flint et al., The EMBO J. 12:1937-46 (1993)). There are at least two major classes of phosphatases: (1) those that dephosphorylate proteins (or peptides) that contain a phosphate group(s) on a serine or threonine moiety (termed Ser/Thr phosphatases) and (2) those that remove a phosphate group(s) from the amino acid tyrosine (termed protein tyrosine phosphatases or PTPases). The PTPases are a family of enzymes that can be classified into two groups: a) intracellular or nontransmembrane PTPases and b) receptor-type or transmembrane PTPases. Intracellular PTPases: Most known intracellular type PTPases contain a single conserved catalytic phosphatase domain consisting of 220-240 amino acid residues. The regions outside the PTPase domains are believed to play important roles in localizing the intracellular PTPases subceliularly (Mauro, LJ. and Dixon, J.E. TIBS 19:151-155 (1994)). The first intracellular PTPase to be purified and characterized was PTP1B which was isolated from human placenta (Tonks e" a/., 1 Biol. Chem, 263: 6722-6730 (1988)). Shortly after, PTP1B was cloned (Charbonneau et a/., Proc, Natl. Acad Sci. USA 86: 5252-5256 (1989); Chemoff e" a/., Proc. Natl. Acad, ScL USA 87: 2735-2789 (1989)). Other examples of intracellular PTPases include (1) T-cell PTPase (Cool et al. Proc. Natl. Acad Sci, USA 86: 5257-5261 (1989)), (2) rat brain PTPase (Guan etal., Proa Natl, Acad, Sci, USA 87:1501-1502 (1990)). (3) neuronal phosphatase STEP (Lombroso etaL Proc. NatL Acad, ScL USA 88: 7242-7246 (1991)). (4) ezrin-domain containing PTPases: PTPMEG1 {Guetal,, Proc, Natl, Acad. Sci. USA 88: 5867-57871 (1991)), PTPH1 (Yang and Tonks, Proc. NatL Acad ScL USA 88: 5949-5953 (1991)), PTPD1 and PTPD2 {MoWer etal., Proc. NatL Acad ScL USA 91: 7477-7481 (1994)), FAP-1/BAS (Sato et aL, Science 268: 411-415 (1995); Banviile et aL, J. BioL Chem. 269: 22320-22327 (1994); Maekawa et al,, FEBS Letters 337: 200-206 (1994)), and SH2 domain containing PTPases: PTP1C/SH-PTP1/SHP-1 (Plutzky e" a/.. Proc, NatL Acad. ScL USA 89:1123-1127 (1992); Shen etal,, Nature Lond 352: 736-739 (1991)) and PTP1D/Syp/SH-PTP2/SHP-2 (Voget etal,, Science 259:1611-1614(1993); fengetaL, Science259:1607-1611 (1993); Basteine"a/., Biochem. Biophys, Res. Comm. 196:124-133 (1993)). Low molecular weight phosphotyrosine-protein phosphatase (LMW-PTPase) shows very little sequence identity to the intracellular PTPases described above. However, this enzyme belongs to the PTPase family due to the following characteristics: (i) it possesses the PTPase active site motif: Cys-Xxx-Xxx-Xxx-Xxx-Xxx-Arg (Cirri et aL, Eur 1 Biochem. 214: 647-657 (1993)); (ii) this Cys residue forms a phospho-intermediate during the catalytic reaction similar to the situation with "classical' PTPases (Cini et aL, supra] Chiarugi et ai, FEBS Lett. 310: 9-12 (1992)); (iii) the overall folding of the molecule shows a surprising degree of similarity to that of PTP1B and Yersinia PTP (Su e" al., Nature 370: 575-578 (1994)). Receptor-type PTPases consist of a) a putative ligand-binding extracellular domain, b) a transmembrane segment, and c) an intracellular catalytic region. The structures and sizes of the putative ligand-binding extracellular domains of receptor-type PTPases are quite divergent. In contrast, the intracellular catalytic regions of receptor-type PTPases are very homologous to each other and to the intracellular PTPases. Most receptor-type PTPases have two tandemly duplicated catalytic PTPase domains. The first receptor-type PTPases to be identified were (1) CD45/LCA (Ralph, SJ., EI\"BO 1 6:1251-1257 (1987)) and (2) LAR (Streuli et a!., 1 Exp. Med, 168:1523-1530 (1988)) that were recognized to belong to this class of enzymes based on homology to PTP1B (Charbonneau et al., Proc, NatL Acad ScL USA 86: 5252-5256 (1989)). CD45 is a family of high molecular weight glycoproteins and is one of the most abundant leukocyte cell surface glycoproteins and appears to be exclusively expressed upon cells of the hematopoietic system (Trowbridge and Thomas, Ann. Rev. ImmunoL "2:85-116(1994)). The identification of CD45 and lAR as members of the PTPase family was quickly followed by identification and cloning of several different members of the receptor-type PTPase group. Thus, 5 different PTPases, (3) PTPa, (4) PTPp, (5) PTP5, (6) PTPs. and (7) PTP", were identified in one eariy study (Kmeger et al., EMBO J. 9: 3241-3252 (1990)). Other examples of receptor-type PTPases include (8) PTPy (Bamea et al., Mol. Cell. Biol. 13:1497-1506 (1995)) which, like PTPC, (Krueger and Saito. Proc. Natl. Acad. ScL USA 89: 7417-7421 (1992)) contains a cariDonic anhydrase-iike domain in the extracellular region, (9) PTP" (Gebbink et ai, FEBS Letters 290:123-130 (1991)), (10) PTPK (Jiang et al., Mol. Cell. Biol. 13: 2942-2951 (1993)). Based on structural differences the receptor-type PTPases may be classified into subtypes (Fischer et ai, Science 253: 401-406 (1991)): (I) CD45; (II) U\R. PTP5, (11) PTPa ; (III) PTPp, (12) SAP-1 (Matozaki et aL, J. Biol. Chem. 269: 2075-2081 (1994)), (13) PTP-U2/GLEPP1 (Seimiya etal., Oncogene 10:1731-1738 (1995); Thomas etaL, J. BioL Chem, 269:19953-19962 (1994)), and (14) DEP-I; (IV) PTPa,_PTPe. All receptor-type PTPases except Type III contain two PTPase domains. Novel PTPases are continuously identified, and it is anticipated that more than 500 different species will be found in the human genome, i.e. dose to the predicted size of the protein tyrosine kinase superfamiiy (Hanks and Hunter, FASEB J. 9: 576-596 (1995)), PTPases are the biological counterparts to protein tyrosine kinases (PTKs). Therefore, one important function of PTPases is to control, down-regulate, the activity of PTKs. However, a more complex picture of the function of PTPases now emerges. Several studies have shown that some PTPases may actually act as positive mediators of cellular signalling. As an example, the SH2 domain-containing SHP-2 seems to act as a positive mediator in insulin-stimulated Ras activation (Noguchi e" a/., MoL Cell. Biol. 14: 6674-6682 (1994)) and of grov\rth factor-induced mitogenic signal transduction (Xiao et ai, J. BioL Chem, 269: 21244-21248 (1994)), whereas the homologous SHP-1 seems to act as a negative regulator of growth factor-stimulated proliferation (Bignon and Siminovitch, ClinJmmunol. Immunopathol. 73:168-179 (1994)). Another example of PTPases as positive regulators has been provided by studies designed to define the activation of the Src-famiiy of tyrosine kinases. In particular, several lines of evidence indicate that CD45 is positively regulating the activation of hematopoietic cells, possibly through dephosphorylation of the C-terminal tyrosine of Fyn and Lck (Chan et ai, Anna. Rev. Immunol. 12: 555-592 (1994)). Dual specificity protein tyrosine phosphatases (dsPTPases) define a subclass within the PTPases family that can hydroiyze phosphate from phosphortyrosine as well as from phosphor-serine/threonine. dsPTPases contain the signature sequence of PTPases: Cys-Xxx-Xxx-Xxx-Xxx-Xxx-Arg. At least three dsPTPases have been shown to dephosphorylate and inactivate extracellular signal-regulated kinase (ERKs)/mitogen-activated protein kinase (MAPK); MAPK phosphatase (CL100, 3CH134) (Charles etal., Proc. Natl. Acad, Sci. USA 90: 5292-5296 (1993)); PAC-1 (Ward etal., Nature 367: 651-654 (1994)); rVHS (Mourey etal., J. BioL Chem. 271: 3795-3802 (1996)). Transcription of dsPTPases are induced by different stimuli, e.g. oxidative stress or heat shock (Ishibashi et aL, J. BioL Chem. 269: 29897-29902 (1994); Keyse and Emslie. Nature 359: 644-647 (1992)). Further, they may be in- volved in regulation of the cell cycle: caczs (Millar and Russell, cell 6d: 407-410 (1992)); KAP (Hannon etal., Proc. NatL Acad. ScL USA 91:1731-1735 (1994)). Interestingly, tyrosine dephosphorylation of cdc2 by a dual specific phosphatase, cdc25, is required for induction of mitosis in yeast (review by Walton and Dixon. Annu. Rev, Biochem. 62: 101-120 (1993)). PTPases were originally identified and purified from cell and tissue lysates using a variety of artificial substrates and therefore their natural function of dephosphorylation was not well known. Since tyrosine phosphorylation by tyrosine kinases is usually associated with cell proliferation, cell transformation and cell differentiation, it was assumed that PTPases were also associated with these events. This association has now been proven to be the case with many PTPases. PTP1B, a phosphatase whose stnjcture was recently elucidated (Barford et al., Science 263:1397-1404 (1994)) has been shown to be involved in insulin-induced oocyte maturation (Flint et al.. The EMBO J. 12:1937-46 (1993)) and recently it has been suggested that the overexpression of this enzyme may be involved in pi 85 -associated breast and ovarian cancers (Wiener, et al., J. Natl, cancer Inst. 86:372-8 (1994); Weineret al.. Am. J. Obstet. Gynecol. 170:1177-883 (1994)). The insulin-induced oocyte maturation mechanism has been correlated with the ability of PTP1B to block activation of S6 kinase. The association with cancer is recent evidence which suggests that overexpression of PTP1B is statistically correlated with increased levels of p"35c-ert)B2 j" Qvarian and breast cancer. The role of PTP1B in the etiology and progression of the disease has not yet been elucidated. Inhibitors of PTP1B may therefore help clarify the role of PTP1B in cancer and in some cases provide therapeutic treatment for certain forms of cancer. The activity of a number of other newly discussed phosphatases are currently under investigation. Two of these: SHP-1 and Syp/PTP1D/SHPTP2/PTP2C/SHP-2 have recently been implicated in the activation of Platelet Derived Growth Factor and Epidermal Growth Factor induced responses (Li et al.. Mole. Cell. Biol. 14:509-17 (1994)). Since both growth factors are involved in nomnal cell processing as well as disease states such as cancer and arteriosclerosis, it is hypothesized that inhibitors of these phosphatases would also show therapeutic efficacy. Accordingly, the com- pounds of the present invention, which exhibit inhibitory activity against various PTPases, are indicated in the treatment or management of the foregoing diseases. PTPases: the insulin receptor signalling pathway/diabetes Insulin is an important regulator of different metabolic processes and plays a key role in the control of blood glucose. Defects related to its synthesis or signalling lead to diabetes mellitus. Binding of insulin to its receptor causes rapid (auto)phosphorylation of several tyrosine residues in the intracellular part of the b-subunit. Three closely positioned tyrosine residues (the tyrosine-1150 domain) must ail be phosphorylated to obtain full activity of the insulin receptor tyrosine kinase (IRTK) which transmits the signal further downstream by tyrosine phosphorylation of other cellular substrates, including insulin receptor substrate-1 (IRS-1) (Wilden etaL, J. Biol. Chem. 267:16660-16668 (1992); Myers and White, Diabetes 42: 643-650 (1993); Lee and Pilch, Am. 1 Physiol. 266: C319-C334 (1994); White et al., J. Biol. Chem. 263: 2969-2980 (1988)). The structural basis for the function of the tyrosine-triplet has been provided by recent X-ray crystallographic studies of IRTK that showed tyrosine-1150 to be autoinhibitory in its unphosphorylated state (Hubbard e" a/., A/a/are 372: 746-754 (1994)). Several studies clearly indicate that the activity of the auto-phosphorylated IRTK can be reversed by dephosphorylation in vitro (reviewed in Goldstein, Receptor 3: 1-15 (1993); Mooney and Anderson, J. Biol. Chem. 264: 6850-6857 (1989)), with the tri-phosphorylated tyrosine-1150 domain being the most sensitive target for protein-tyrosine phosphatases (PTPases) as compared to the di- and mono- phosphorylated fornis (King et al., Biochem. J. 275: 413-418 (1991)). It is, therefore, tempting to speculate that this tyrosine-triplet functions as a control switch of IRTK activity. Indeed, the IRTK appears to be tightly regulated by PTP-mediated dephosphorylation in vivo (Khan et al., J. Biol. Chem. 264:12931-12940 (1989); Faure e" a/., J. Biol. Chem. 267: 11215-11221 (1992); Rothenberg etai, J. Biol. Chem. 266: 8302-8311 (1991)). The intimate coupling of PTPases to the insulin signalling pathway is further evidenced by the finding that insulin differentially regulates PTPase activity in rat hepatoma cells (Meyerovitch et al., Biochemistry 31: " 0338-10344 (1992)) and in livers from alloxan diabetic rats (Boylan e" a/.. J. Clin. Invest 90:174-179 (1992)). Relatively little is known about the identity of the PTPases involved in IRTK regulation. However, the existence of PTPases with activity towards the insulin receptor can be demonstrated as indicated above. Further, when the strong PTPase-inhibitor perva-nadate is added to whole cells an almost full insulin response can be obtained in adipocytes (Fantus et aL, Biochemistry 28: 8864-8871 (1989); Eriksson e" a/., Diabetolo-gia 39: 235-242 (1995)) and skeletal muscle (Leighton et a/., Bioctiem, J. 276: 289-292 (1991)). In addition, recent studies show that a new class of peroxovanadium compounds act as potent hypoglycemic compounds in vivo (Posner et aL.supra), Two of these compounds were demonstrated to be more potent inhibitors of dephospho-rylation of the insulin receptor than of the EGF-receptor. It was recently found that the ubiquitously expressed SH2 domain containing PTPase, SHP-2 (Vogel et a/., 1993, supra), associates with and dephosphorylates IRS-1, but apparently not the IR itself (Kuhne et at., 1 Biol. Chem, 268:11479-11481 (1993); (Kuhne eta!., J. BioL Ctiem. 269:15833-15837 (1994)). Previous studies suggest that the PTPases responsible for IRTK regulation belong to the class of membrane-associated (Faure etal., J. BioL Chem. 267: 11215-11221 (1992)) and glycosylated molecules (Haring etal,, Biocliemistry 23: 3298-3306 (1984); Sale, Adv, Prot Phosphatases 6:159-186 (1991)). Hashimoto et at. have proposed that LAR might play a role in the physiological regulation of insulin receptors in intact ceils (Hashimoto et a!., J. Biol. Chem. 267: 13811-13814 (1992)). Their conclusion was reached by comparing the rate of dephosphorylation/inactivation of purified IR using recombinant PTP1B as well as the cytoplasmic domains of LAR and PTPa. Antisense inhibition was recently used to study the effect of LAR on insulin signalling in a rat hepatoma cell line (Kulas et aL J- BioL Chem. 270: 2435-2438 (1995)). A suppression of LAR protein levels by about 60 percent was paralleled by an approximately 150 percent increase in insulin-induced auto-phosphorylation. However, only a modest 35 percent increase in IRTK activity was observed, whereas the insulin-dependent phosphatidyiinositol 3-kinase (PI 3-kinase) activity was significantly increased by 350 percent. Reduced LAR levels did not alter the basal level of IRTK tyrosine phosphorylation or activity. The authors speculate that LAR could specifically dephosphorylate tyrosine residues that are critical for PI 3-kinase activation either on the insulin receptor itself or on a downstream substrate. While previous reports indicate a role of PTPa in signal transduction through src activation (Zheng et ai, Nature 359: 336-339 (1992); den Hertog e" a/., EMBO1 12: 3789-3798 (1993)) and interaction with GRB-2 (den Hertog et a/., EMBO J. 73: 3020-3032 (1994); Su ef a/., J. Biol. Chem. 269: 18731-18734 (1994)), a recent study suggests a function for this phosphatase and its close relative PTPE as negative regulators of the insulin receptor signal (Moiler et ai, 1995 supra). This study also indicates that receptor-like PTPases play a significant role in regulating the IRTK, whereas intracellular PTPases seem to have little, if any, activity towards the insulin receptor. While it appears that the target of the negative regulatory activity of PTPases a and z is the receptor itself, the downmodulating effect of the intracellular TC-PTP seems to be due to a downstream function in the IR-activated signal. Although PTP1B and TC-PTP are closely related, PTP1B had only little influence on the phosphorylation pattern of insulin-treated cells. Both PTPases have distinct stmctural features that determine their subcellular localization and thereby their access to defined cellular substrates (Frangione et ai, Cell 68: 545-560 (1992); Faure and Posner, Glia 9: 311-314 (1993)). Therefore, the lack of activity of PTP1B and TC-PTP towards the IRTK may, at least in part, be explained by the fact that they do not co-locaiize with the activated insulin receptor. In support of this view, PTP1B and TC-PTP have been excluded as candidates for the IR-associated PTPases in hepatocytes based on subcellular localization studies (Faure eta!., 1 Biol. Chem, 267: 11215-11221 (1992)). The transmembrane PTPase CD45, which is believed to be hematopoietic cell-specific, was in a recent study found to negatively regulate the insulin receptor tyrosine kinase in the human multiple myeloma cell line U266 (Kulas et al., J. Biol. Chem. 271:755-760(1996)). Knock-out (K.O.) mice have been useful in elucidating the importance of specific genes in a number of cases. From the results presented above, it would be expected that in particular LAR K.O. mice, PTPa K.O. mice and PTP1B K.O. mice, respectively, could provide important information in relation to insulin signaling. Two groups have generated LAR K.O. mice (Schaapveld at al., Developmental Biology 188:134-146 (1997); Skames et al., Proc.NatLAcad.Sci.U.S.A. 92:6592-6596 (1995)). Goldstein and coworkers analyzed the LAR K.O. mice from Skarnes et al. (supra) and claimed that these mice exhibited profound defects in glucose-homeostasis and (Ren et at.. Diabe- tes 47:493-497 (1998)). However, the control mice in this study were of a different genetic background than the K.O. mice. Other studies - using the LAR K.O. mice generated by Schaapveld et al. (supra) - did not confirm the results obtained by Ren et al. (supra) (A. R. Sorensen et al., Diabetologia 40 (Supp11):556-556 (1997)). In a recent thorough study, PTP1B K.O. mice (i.e. PTP1B -/- mice) were compared with +/+ and +/- mice of the same genetic background (Elchebly et al., Science 283:1544-1548 (1999)). In this latter study (Elcheby et a!., supra), it was found that disruption of the gene encoding the PTP1B yielded healthy mice that - in the fed state - had blood glucose levels that were slightly lower and concentrations of insulin that were about V% of those found in their PTP1B+/+ littermates. Further, both insulin and glucose tolerance tests showed enhanced insulin sensitivity in the PTP K.O. mice. On a high-fat diet, PTP1B-/- and PTP1B-/+ mice were resistant to weight gain and remained insulin sensitive - in contrast to the PTP1B +/+ mice that rapidly gained weight and became insulin resistant. Analysis of the levels of tyrosine phosphorylation of the insulin receptor and insulin receptor substrate-1 (IRS-1) showed increased phosphorylation of these proteins in PTP1B -/- mice (liver and muscle) in comparison with the.PTPI B +/+' mice. All of these findings are in accordance with the notion that PTP1B is likely to play a major role as negative regulator of the insulin receptor signaling pathway - and in contrast to the above-mentioned in vitro studies. The authors conclude that 'these results make PTP-1B a potential therapeutic target for treatment of type 2 diabetes and obesity' (Elcheby et al., supra). PTPases: somatostatin Somatostatin inhibits several biological functions including cellular proliferation (Lamberts et a/., Mo/ec. EndocrinoL 8:1289-1297 (1994)). While part of the antiproliferative activities of somatostatin are secondary to its inhibition of hormone and growth factor secretion (e.g. growth honrtone and epidermal growth factor), other antiproliferative effects of somatostatin are due to a direct effect on the target cells. As an example, somatostatin analogs inhibit the growth of pancreatic cancer presumably via stimulation of a single PTPase, or a subset of PTPases, rather than a general activation of PTPase levels in the ceils (Liebow ejf al., Proa Nati Acad ScL USA 86: 2003-2007 (1989); Colas et al., Eur. J. Biochem. 207: 1017-1024 (1992)). In a recent study it was found that somatostatin stimulation of somatostatin receptors SSTR1, but not SSTR2, stably expressed in CH0-K1 cells can stimulate PTPase activity and that this stimulation is pertussis toxin-sensitive. Whether the inhibitory effect of somatostatin on hormone and growth factor secretion is caused by a similar stimulation of PTPase activity in honnone producing cells remains to be determined. PTPases: the immune svstem/autoimmunitv Several studies suggest that the receptor-type PTPase CD45 plays a critical role not only for initiation of T cell activation, but also for maintaining the T cell receptor-mediated signalling cascade. These studies are reviewed in: (Weiss A., Ann. Rev. Genet 25: 487-510 (1991); Chan e" a/., Annu, Rev. Immunol. 12: 555-592 (1994); Trowbridge and Thomas, Annu. Rev. Immunol. 12: 85-116 (1994)). CD45 is one of the most abundant of the cell surface glycoproteins and is expressed exclusively on hemopoetic cells. In T cells, it has been shown that CD45 is one of the critical components of the signal transduction machinery of lymphocytes. In particular, evidence has suggested that CD45 phosphatase plays a pivotal role in antigen-stimulated proliferation of T lymphocytes after an antigen has bound to the T cell receptor (Trowbridge, Ann. Rev. Immunol, 12:85-116 (1994)). Several studies suggest that the PTPase activity of CD45 plays a role in the activation of Lck, a lymphocyte-specific member of the Src family protein-tyrosine kinase (Mustelin etal., Proc. Natl. Acad. Sci. USA 86: 6302-6306 (1989); Ostergaard et al., Proc. Natl. Acad. Sci. USA 86: 8959-8963 (1989)). These authors hypothesized that the phosphatase activity of CD45 activates Lck by dephosphorylation of a C-terminal tyrosine residue, which may, in turn, be related to T-cell activation. In a recent study it was found that recombinant p56lck specifically associates with recombinant CD45 cytoplasmic domain protein, but not to the cytoplasmic domain of the related PTPaa (Ng et al., J. BioL Chem. 271: 1295-1300 (1996)). The p56lck-CD45 interaction seems to be mediated via a nonconventional SH2 domain interaction not requiring phosphotyrosine. In immature B cells, another member of the Src family protein-tyrosine kinases, Fyn, seems to be a selective substrate for CD45 compared to Lck and Syk (Katagiri et al., J. Biol. Chem. 270; 27987-27990 (1995)). Studies using transgenic mice with a mutation for the CD45-exon6 exhibited lacked mature T cells. These mice did not respond to an antigenic challenge with the typi- cal T cell mediated response (Kishihara et al., Ce//74:143-56 (1993)). Inhibitors of CD45 phosphatase would therefore be very effective therapeutic agents in conditions that are associated with autoimmune disease. CD45 has also been shown to be essential for the antibody mediated degranulation of mast cells (Berger et al., J. Exp. Med 180:471-6 (1994)). These studies were also done with mice that were CD45-deficient. In this case, an IgE-mediated de-granulation was demonstrated in wild type but not CD45-deflcient T cells from mice. These data suggest that CD45 inhibitors could also play a role in the symptomatic or therapeutic treatment of allergic disorders. Another recently discovered PTPase, an inducible lymphoid-specific protein tyrosine phosphatase (HePTP) has also been implicated in the immune response. This phosphatase is expressed in both resting T and B lymphocytes, but not non-hemopoetic cells. Upon stimulation of these cells, mRNA levels from the HePTP gene increase 10-15 fold (Zanke et ai, Eur J. ImmunoL 22:235-239 (1992)). In both T and B cells HePTP may function during sustained stimulation to modulate the immune response through dephosphorylation of specific residues. Its exact role, however remains to be defined. Likewise, the hematopoietic cell specific SHP-1 seems to act as a negative regulator and play an essential role in hematopoietic cell development. Thus, SHP-1 plays a significant role in regulating the erythropoietin signalling pathway, which is enhanced in mice lacking intact SHP-1 (Schultz et al. Cell 73:1445-1454. In accordance with the above-mentioned important function of CD45, HePTP and SHP-1, selective PTPase inhibitors may be attractive drug candidates both as immunosup-pressors and as immunostimulants as well as inhibitors and stimulants of the hematopoietic system. One recent study illustrates the potential of PTPase inhibitors as immunmodulators by demonstrating the capacity of the vanadium-based PTPase inhibitor, BMLOV, to induce apparent B cell selective apoptosis compared to T ceils (Schieven et al., J. BioL Chem, 270: 20824-20831 (1995)). PTPases: cell-neli interactions/cancer Focal adhesion plaques, an in vitro phenomenon in which specific contact points are formed when fibroblasts grow on appropriate substrates, seem to mimic, at least in part, cells and their natural sun"oundings. Several focal adhesion proteins are phos-phorylated on tyrosine residues when fibroblasts adhere to and spread on extracellular matrix (Gumbiner, Neuron 11, 551-564 (1993)). However, aberrant tyrosine phosphorylation of these proteins can lead to cellular transformation. The intimate association between PTPases and focal adhesions is supported by the finding of several intracellular PTPases with ezrin-like N-terminal domains, e.g. PTPMEG1 (Gu etaL, Proc. Natl. Acad ScL USA 88: 5867-5871 (1991)), PTPH1 (Yang and Tonks, Proc. Natl, Acad Sa\ USA 88: 5949-5953 (1991)) and PTPD1 (MQWeretaL, Proc. Natl. Acad Sci, USA 91: 7477-7481 (1994)). The ezrin-like domain show similarity to several proteins that are believed to act as links between the ceil membrane and the cy-toskeieton. PTPD1 was found to be phosphorylated by and associated with c-src in vitro and is hypothesized to be involved in the regulation of phosphorylation of focal adhesions (Moller at a/., supra). PTPases may oppose the action of tyrosine kinases, including those responsible for phosphorylation of focal adhesion proteins, and may therefore function as natural inhibitors of transformation. TC-PTP, and especially the truncated form of this enzyme (Cool et al., Proc. Natl. Acad ScL USA 87:7280-7284 (1990)), can inhibit the trans-fonning activity of y-erb and w-fms (Lammers et aL, J. BioL Chem. 268:22456-22462 (1993); Zander et aL, Oncogene 8:1175-1182 (1993)). Moreover, it was found that transformation by the oncogenic form of the HER2/neu gene was suppressed in NIH 3T3 fribroblasts overexpressing PTP1B (Brown-Shimer et aL, Cancer Res, 52:478-482(1992)). The expression level of PTP1B was found to be increased in a mammary cell line transformed with neu (Zhay et aL, Cancer Res. 53:2272-2278 (1993)), The intimate relationship between tyrosine kinases and PTPases in the development of cancer is further evidenced by the recent finding that PTPs is highly expressed in murine mammary tumors in transgenic mice over-expressing c-neu and v-Ha-ras, but not c-myc or int-2 (Elson and Leder, 1 BioL Chem. 270:26116-26122 (1995)). Further, the human gene encoding PTPg was mapped to 3p21, a chromosomal region which is frequently deleted in renal and lung carcinomas (LaForgia e" aL, Proc. NatL Acad. Sci. USA 88: 5036-5040(1991)). In this context, it seems significant that PTPases appear to be involved in controlling the growth of fibroblasts. In a recent study it was found that Swiss 3T3 cells harvested at high density contain a membrane-associated PTPase whose activity on an average is 8-fold higher than that of cells harvested at low or medium density (Pallen and Tong, Proc. NatL Acad Sci. USA 88: 6996-7000 (1991)). It was hypothesized by the authors that density-dependent inhibition of cell growth involves the regulated elevation of the activity of the PTPase(s) in question. In accordance with this view, a novel membrane-bound, receptor-type PTPase, DEP-1, showed enhanced (>=10-fold) expression levels with increasing cell density of WI-38 human embryonic lung fibroblasts and in the AG1518 fibroblast cell line (Ostman et a/., Proc. Natl. Acad. Sci. USA 91: 9680-9684(1994)). Two closely related receptor-type PTPases. PTPK and PTPp, can mediate hemophilic cell-cell interaction when expressed in non-adherent insect cells, suggesting that these PTPases might have a normal physiological function in cell-to-cell signalling (Gebbink et ai, J. Bioi Chem. 268: 16101-16104 (1993); Brady-Kalnay et ai, 1 Cell Biol. 122: 961-972 (1993); Sap et ai, MoL Cell. Biol. 14:1-9 (1994)). Interestingly, PTPk and PTPp do not interact with each other, despite their staictural similarity (Zondag e" a!., J. Biol. Chem. 270:14247-14250 (1995)). From the studies described above it is apparent that PTPases may play an important role in regulating normal cell growth. However, as pointed out above, recent studies indicate that PTPases may also function as positive mediators of intracellular signalling and thereby induce or enhance mitogenic responses. Increased activity of certain PTPases might therefore result in cellular transformation and tumor fonnation. Indeed, in one study over-expression of PTPa was found to lead to transformation of rat embryo fibroblasts (Zheng, supra). In addition, a novel PTP, SAP-1, was found to be highly expressed in pancreatic and colorectal cancer cells. SAP-1 is mapped to chromosome 19 region q13.4 and might be related to carcinoembryonic antigen mapped to 19q13.2 (Uchida et al., J. Biol. Chem. 269:12220-12228 (1994)). Further, the dsPTPase, cdc25. dephosphorylates cdc2 at Thr14yTyr-15 and thereby functions as positive regulator of mitosis (reviewed by Hunter, Cell 80: 225-236 (1995)). Inhibitors of specific PTPases are therefore likely to be of significant therapeutic value in the treatment of certain forms of cancer. PTPases: platelet aggregation Recent studies indicate that PTPases are centrally involved in platelet aggregation. Agonist-induced platelet activation results in calpain-catalyzed cleavage of PTP1B with a concomitant 2-fold stimulation of PTPase activity (Frangioni et ai, EMBO J. 12: 4843-4856 (1993)). The cleavage of PTP1B leads to subcellular relocation of the enzyme and correlates with the transition from reversible to irreversible platelet aggregation in platelet-rich plasma. In addition, the SH2 domain containing PTPase, SHP-1/SH-PTP1, was found to translocate to the cytoskeleton in platelets after thrombin stimulation in an aggregation-dependent manner (Li et a/., FEES Lett, 343:89-93 (1994)). Although some details in the above two studies were recently questioned there is over-ail agreement that PTP1B and SHP-1 play significant functional roles in platelet aggregation (Ezumi etal., J. Biol. Chem. 270:11927-11934 (1995)). In accordance with these observations, treatment of platelets with the PTPase inhibitor pervanadate leads to significant increase in tyrosine phosphorylation, secretion and aggregation (Pumiglia et al., Biochem. J. 286:441-449 (1992)). PTPases: osteoporosis The rate of bone fonnation is determined by the number and the activity of osteoblasts, which in tenn are detennined by the rate of proliferation and differentiation of osteoblast progenitor cells, respectively. Histomorphometric studies indicate that the osteoblast number is the primary determinant of the rate of bone formation in humans (Gruber et ai, Mineral Eectrolyte Metab. 12: 246-254 (1987); reviewed in Lau et a/., Biochem. 1 257: 23-36 (1989)). Acid phosphatases/PTPases may be involved in negative regulation of osteoblast proliferation. Thus, fluoride, which has phosphatase inhibitory activity, has been found to increase spinal bone density in osteoporotics by increasing osteoblast proliferation (Lau e" ai, supra). Consistent with this ob- servation, an osteoblastic acid phosphatase with PTPase activity was found to be highly sensitive to mitogenic concentrations of fluoride (Lau etaL, J. Biol. Cham. 260: 4653-4660 (1985); Lau et a/., J. BioL Chem, 262:1389-1397 (1987); Lau et ai, Adv. Protein Phosphatases 4: 165-198 (1987)). Interestingly, it was recently found that the level of membrane-bound PTPase activity was increased dramatically when the os-teoblast-like cell line UMR 106.06 was grown on collagen type-1 matrix compared to uncoated tissue culture plates. Since a significant increase in PTPase activity was observed in density-dependent growth arrested fibroblasts (Pallen and Tong, Proc. Natl. Acad. Sci. 88: 6996-7000 (1991)), it might be speculated that the increased PTPase activity directly inhibits cell growth. The mitogenic action of fluoride and other phosphatase inhibitors (molybdate and vanadate) may thus be explained by their inhibition of acid phosphatases/PTPases that negatively regulate the cell proliferation of osteoblasts. The complex nature of the involvement of PTPases in bone fonmation is further suggested by the recent identification of a novel parathyroid regulated, receptor-like PTPase, OST-PTP, expressed in bone and testis (Mauro et ai, J. Biol. Chew. 269: 30659-30667 (1994)). OST-PTP is up-regulated following differentiation and matrix formation of primary osteoblasts and subsequently down-regulated in the osteoblasts which are actively mineralizing bone in culture. It may be hypothesized that PTPase inhibitors may prevent differentiation via inhibition of OST-PTP or other PTPases thereby leading to continued proliferation. This would be in agreement with the above-mentioned effects of fluoride and the observation that the tyrosine phosphatase inhibitor orthovanadate appears to enhance osteoblast proliferation and matrix formation (Lau et aL Endocrinology 116: 2463-2468 (1988)). In addition, it was recently observed that vanadate, vanadyl and pervanadate ail increased the growth of the osteobiast-like cell line UMR106. Vanadyl and pervanadate were stronger stimulators of cell growth than vanadate. Only vanadate was able to regulate the cell differentiation as measured by cell alkaline phosphatase activity (Cortizo et al., Mol. Cell. Biochem. 745:97-102(1995)). PTPases: microoroanisms Dixon and cowori2000 psi) in a Parr cell disruption bomb. Triton X-100 (0.1 %) was added to the lysate and stirring continued for 1 h prior to centrifugation at 40000 g for 30 min. The supernatant was applied to a Glutathione Sepharose column (Pharmacia) equilibrated with GST-equilibration buffer (50 mM imidazole, 1 mM EDTA, 150 mM NaCI and 10 % glycerol; pH 7.2) and initially washed with the same buffer. The flow direction was changed and washing was continued with a washing buffer (50 mM Tris, 1 mM EDTA and 10 % glycerol; pH 8). Finally, the bound protein was eluted with 10 mM glutathione in the washing buffer. The CD45 fusion protein was further purified on G25 and Mono Q columns (Pharmacia). The purified PTP domains are stored at -80 **C until use. Immediately prior to use the enzyme preparations are diluted appropriately. It should be noted that similar methods - well known to those skilled in the art - could be used to obtain the catalytic domains of the molecules shown in Table I. Said GST-PTPase fusion proteins are used to assess the potency and selectivity of PTPase inhibitor essentially as described for PTP1B above. To further illustrate these assays, a non-limiting example using PTPa domain 1 will be given. Similar procedures may be used for other PTPase domains. Half of a 96-well plate was used for this experiment, p-nitrophenyl phosphate (pNPP) was used as substrate. The following final assay concentrations of pNPP were used: 20 mM, 10 mM, 5 mM, 2.5 mM, 1.25 mM, 0.63 mM. 0.31 mM. The compound, 5-(1,3-dioxo-1,3-dihydro-isoindoi-2-ylmethyl)-2-(oxalyl-amino)-4,7-dihydro-5H-thieno[2,3-c]pyran-3-carboxylicacid, dissolved in dimethyisulfoxide (DMSO) was used as inhibitor and used at the following final assay concentrations: 200 "M, 66.6 |iM; 22,2 fxM; 7.4 jiM. Assay buffer instead of enzyme, and/or substrate was added to appropriate control wells as described in detail for PTP1B above. Assay buffer (final assay concentration): 100 mM sodium acetate pH 5.5, 50 mM NaCI, 5 mM glutathione, 1 mM EDTA, and 0.1 % bovine serum albumin. The reaction was started by addition of the enzyme, GST-PTPa domain 1 (final dilution 1:10000). The assay total volume in each well was 100 |il, including 10 "l of inhibitor dissolved in DMSO or 10 |il DMSO added to the control wells that did not receive inhibitor. The temperature was 25 °C. After 60 minutes, 10 "1 of a 0.5 M sodium hydroxide solution (in 50 percent (vol/vol) ethanol) was added to each well and the absorbance was read at 405 nm. The results are shown in Figure 6A. The calculated K" value is 4 |j.M (median value). Figure 6B shows the results when the same compound (5-(1,3-dioxo-1,3-dihydro-isoindol-2-ylmethyl)-2-(oxalyl-amino)-4 J-dihydro-5H-thieno[2,3-c]pyran-3-carboxylic acid) is tested against PTPa (final dilution 1:2000) in the following buffer 50 mM HEPES pH 7.0, 100 mM NaCI, 5 mM glutathione, 1 mM EDTA, and 0.1 % bovine serum albumin. After 60 minutes, 20 jil of a 0.5 M sodium hydroxide solution (in 50 percent (vol/vol) ethanol) was added to each well and the absorbance was read at 405 nm. Otherwise, the conditions are as described for Figure 6A. The calculated Kj value under these conditions is about 70 mM (median value). A selective inhibitor is defined as.an inhibitor that shows selectivity. A non-selective inhibitor is defined as an inhibitor that does not show selectivity. A selective modulator is defined as a modulator that shows selectivity. To further illustrate the concept of selective and non-selective PTPase inhibitors an example of a non-selective and a selective inhibitor, respectively, is provided in Tabl6 10. It should emphasized that the examples in Table 10 are not intended in any way to limit the scope of the invention. Table 10 Analysis of selectivity of PTPase inhibitors. Assay conditions are essentially the same as those used in Figure 4. The numbers given are K, values (pM). it appears from Table 10 that the compound of example 82 is an example of a non-selective inhibitor, whereas the compound of example 83 behaves like a selective inhibitor. It should be noted that the compound in example 83 when tested against other PTPases might be inhibitory against these. Yet, according to the present definition, the compound in example 83 is a selective inhibitor due to the fact that it inhibits PTP1B with little effect on the other PTPases tested in Table .10. Also, according to the present definition, the compound in example 82 is a non-selective inhibitor due to its inhibitory capacity against several PTPases, even though it has weak activity, if any, against PTP-LAR. A chemical group is defined as any single atom or any group of covalently linked atoms or any molecule, including any radical thereof. The tenns "halogen" or "halo" include fluorine, chlorine, bromine, and iodine. The term "alkyl" includes C"-Ce straight chain saturated and Cj-Ce unsaturated aliphatic hydrocarbon groups, Ci-Cebranched saturated and Cj-Ce unsaturated aliphatic hydrocarbon groups, C3-C6 cyclic saturated and Cs-Cg unsaturated aliphatic hydrocarbon groups, and C,-Cg straight chain or branched saturated and Ca-Cg straight chain or branched unsaturated aliphatic hydrocarbon groups substituted with Ca-Cg cyclic saturated and unsaturated aliphatic hydrocarbon groups having the specified number of carbon atoms. For example, this definition shall include but is not limited to methyl (Me), ethyl (Et), propyl (Pr), butyl (Bu), pentyl, hexyl, heptyl, ethenyl, propenyl, butenyl, penentyl, hexenyi, isopropyl (i-Pr), isobutyl (i-Bu), "ert-butyl (NBu), sec-butyl (s-Bu), isopentyl, neopentyl, cyclopropyl, cydobutyl, cy-ctopentyl. cyciohexyl, cyclopentenyl, cyclohexenyl, methylcyclopropyl, ethylcyclohexenyl, butenylcyclopentyl, and the like. The term "substituted alkyl" represents an alkyl group as defined above wherein the substi-tutents are independently selected from halo, cyano, nitro, trihalomethyl, carbamoyl, hydroxy, COR5. Ct-Cgalkyl, CrCealkyloxy, aryloxy, arylCrCgalkyloxy, thio, CrCealkylthio, arylthio, arylCi-Cgalkylthio, NRyRg, CrCealkylamino, arylamino, arylCi-Cgalkylamino, di(arylCi-C6alkyl)amino, CrCgalkylcarbonyl, arylC"Cealkylcarbonyl, Ct-Cgalkyl-carboxy, aryiCrCealkylcarboxy, Ci-Cealkylcarbonylamino, -Ci-Cealkyl-aminoCORn, arylC,-Cgalkylcarbonylamino, tetrahydrofuranyl, morpholinyl, piperazinyl, -CONRyRs, -Ci-CealkylCONRyRfl, or a saturated or partial saturated cyclic 5, 6 or 7 membered amine or lactam; wherein R,, is hydroxy, Ci-CealkyI, aryl, arylCi-Cealkyl, CrCgalkyioxy, aryloxy, arylC,-Cgalkyloxy and R5 is defined as above or NRyR", wherein R7, Rg are defined as above. The tenri "alkyloxy" (e.g. methoxy, ethoxy, propyloxy, allyioxy, cyclohexyloxy) represents an "alkyl" group as defined above having the indicated number of carbon atoms attached through an oxygen bridge. The term "aikyloxyalkyl" represents an "alkyloxy" group attached through an alkyl group as defined above having the indicated number of carbon atoms. The term "aryloxy" (e.g. phenoxy. naphthyloxy and the like) represents an aryl group as defined below attached through an oxygen bridge. The term "arylalkyloxy" (e.g. phenethyloxy, naphthylmethyloxy and the like) represents an "arylalkyr group as defined below attached through an oxygen bridge. The term "arylalkyloxyalkyl" represents an "arylalkyloxy" group as defined above attached through an "alkyl" group defined above having the indicated number of carbon atoms. The term "arylthio" (e.g. phenylthio, naphthylthio and the like) represents an*"aryr group as defined below attached through an sulfur bridge. The temi "alkyloxycarbonyl" (e.g. methylfonniat, ethylfonniat and the like) represents an "alkyloxy" group as defined above attached through a cariDonyl group. The term "aryloxycarbonyl" (e.g. phenyifonniat, 2-thia2olylfonniat and the like) represents an "aryloxy" group as defined above attached through a carbonyl group. The term "arylalkyloxycarbonyl" (e.g. benzylformiat, phenyletylformiat and the like) represents an "arylalkyloxy" group as defined above attached through a carbonyl group. The term "alkyloxycarbonylalkyl" represents an "alkyloxycarbonyl" group as defined above attached through an "alkyl" group as defined above having the indicated number of carbon atoms. The term "arylalkyloxycarbonylaikyi" represents an "arylalkyioxycariDonyi" group as defined above attached through an "alkyP group as defined above having the indicated number of carbon atoms. The term "alkylthio" (e.g. methylthio, ethylthio, propylthio, cyclohexenylthio and the like) represents an "alkyl" group as defined above having the indicated number of carbon atoms attached through a sulfur bridge. The term "arylalkylthio" (e.g. phenylmethylthio, phenylethylthio, and the like) represents an "arylalkyl" group as defined above having the indicated number of carbon atoms attached through a sulfur bridge. The term "alkylthioalkyl" represents an "alkylthio" group attached through an alkyl group as defined above having the indicated number of carbon atoms. The term "arylalkylthioalkyi" represents an "arylalkylthio" group attached through an alkyl group as defined above having the indicated number of carbon atoms. The term "alkylamino" (e.g. methylamino, diethylamino, butylamino, N-propyl-N-hexylamino, (2-cyclopentyl)propylamino, hexenylamino, pyn-olidinyl, piperidinyl and the like) represents one or two "alkyl" groups as defined above having the indicated number of carbon atoms attached through an amine bridge. The two alkyl groups may be taken together with the nitrogen to which they are attached forming a saturated, partially saturated or aromatic cyclic, bicyclic or tricyclic ring system containing 3 to 14 carbon atoms and 0 to 3 additional het-eroatoms selected from nitrogen, oxygen or sulfur, the ring system can optionally be substituted with at least one CrCealkyl, aryl. arylCi-Cgalkyl, hydroxy, oxo, Ci-Cealkyloxy. C"-Cealkyloxyd-Cealkyl, NRgRio, CrCealkyiaminoCrCgalkyl substituent wherein the alkyl and aryl groups are optionally substituted as defined in the definition section and R9 and Rio are defined as above. The term "arylalkylamino" (e.g. benzylamino, diphenylethylamino and the like) represents one or two "arylalkyl" groups as defined above having the indicated number of carbon atoms attached through an amine bridge. The two "arylalkyl" groups may be taken together with the nitrogen to which they are attached forming a saturated, partially saturated or aromatic cyclic, bicyclic or tricyclic ring system containing 3 to 14 carbon atoms and 0 to 3 additional heteroatoms selected from nitrogen, oxygen or sulfur, the ring system can optionally be substituted with at least one CrCealkyI, aryl, arylCrCealkyi, hydroxy, 0x0, Ct-Cgalkyloxy, C"-CgalkyloxyCi-Cealkyl, NR9R10, CrCgalkylaminoCi-Cealkyl substituent wherein the alkyl and aryl groups are optionally substituted as defined in the definition section and Rg and R"o are defined as above. The tenri "alkylaminoalkyl" represents an "alkylamino" group attached through an alkyl group as defined above having the indicated number of carbon atoms. The term "arylalkylaminoalkyi" represents an "arylalkylamino" group attached through an al-kyl group as defined above having the indicated number of carbon atoms. The tenn "arylalkyi" (e.g. benzyl, phenylethyl) represents an "aryl" group as defined below attached through an alkyl having the indicated number of carbon atoms or substituted alky! group as defined above. The tenn "alkylcarbonyl" (e.g. cyclooctylcarbonyl. pentylcarbonyl, 3-hexenylcarbonyl) represents an "alkyl" group as defined above having the indicated number of carbon atoms attached through a carbonyl group. The term "aryjalkylcarbonyl" (e.g. phenylcyclopropylcarbonyl, phenylethylcarbonyl and the like) represents an "arylalkyi" group as defined above having the indicated number of carbon atoms attached through a carbonyl group. The term "alkylcarbonylalkyl" represents an "alkylcarbonyl" group attached through an "alkyl" group as defined above having the indicated number of carbon atoms. The term "arylalkylcarbonylalkyl" represents an "arylalkylcarbonyl" group attached through an alkyl group as defined above having the indicated number of carbon atoms. The term "alkylcarboxy" (e.g. heptylcarboxy. cyclopropyicarboxy, 3-pentenylcarboxy) represents an "alkylcarbonyl" group as defined above wherein the carbonyl is in turn attached through an oxygen bridge. The term "arylalkylcarboxy" (e.g. benzylcarboxy. phenyicyclopropylcarboxy and the like) represents an "arylalkylcarbonyl" group as defined above wherein the carbonyl is in turn attached through an oxygen bridge. The term "alkylcarboxyalkyl" represents an "alkylcarboxy" group attached through an "alkyl" group as defined above having the indicated number of carbon atoms. The term "arylalkylcarboxyaikyi" represents an "arylalkylcarboxy" group attached through an "alkyl" group as defined above having the indicated number of carbon atoms. The tenn "alkylcarbonylamino" (e.g. hexylcarbonylamino, cyclopentylcarbonyl-aminomethyl, methylcarbonylaminophenyi) represents an "alkylcarbonyl" group as defined above wherein the carbonyl is in turn attached through the nitrogen atom of an amino group. The nitrogen atom may itself be substituted with an alky! or aryl group. The term "arylalkylcarbonylamino" (e.g. benzylcarbonylamino and the like) represents an "arylalkylcarbonyl" group as defined above wherein the carbonyl is in turn attached through the nitrogen atom of an amino group. The nitrogen atom may itself be substituted with an alkyl or aryl group. The term "alkylcarbonylaminoalkyl" represents an "alkylcarbonylamino" group attached through an "alkyl" group as defined above having the indicated number of carbon atoms. The nitrogen atom may itself be substituted with an alkyl or aryl group. The terni "arylalkyicarbonylaminoalkyl" represents an "arylalkylcarbonylamino" group attached through an "alkyl" group as defined above having the indicated number of carbon atoms. The nitrogen atom may itself be substituted with an alkyl or aryl group. The term "alkylcarbonylaminoaikylcarbonyl" represents an alkylcarbonylaminoalkyl group attached through a carbonyl group. The nitrogen atom may be further substituted with an "alkyl" or "aryl" group. The term "aryl" represents an unsubstituted, mono-, di- or trisubstituted monocyclic, polycy-clic, biaryl and heterocyclic aromatic groups covalently attached at any ring position capable of forming a stable covalent bond, certain preferred points of attachment being apparent to those skilled in the art (e.g., 3-indolyl. 4-imidazolyl). The aryl substituents are independently selected from the group consisting of halo, nitro. cyano, trihalomethyl, CrCgalkyl, aryl, arylCi-Cgalkyl, hydroxy, COR5, CrCealkyloxy. Ci-CgalkyloxyCi-Cealkyl. aryloxy, arylCi-Cealkyloxy. arylCt-CsalkyloxyCrCealkyl, thio, CrCgalkylthio, Ci-CealkylthioCi-CealkyI, arylthio, arylCi-Cfialkylthio, arylCrCealkylthioCrCealkyl. NRsRg. CrCg-alkylamino, CrCealkylaminoCi-Cfialkyj, arylamino, arylCt-Cealkylamino, arylCi-CsaikyiaminoCrCealkyI, di(arylC,-C6alkyl)-aminoCrCgalkyl, Ci-Cgalkylcarbonyl, Ci-CealkylcarbonylCi-Cgalkyi, arylCi-Cealkyl-carbonyl, arylCrCealkylcarbonylCrCgalkyl, CrCealkylcarboxy, Ci-CealkylcarboxyCi-CealkyI, arylC" Cealkylcarboxy, arylCrCealkylcarboxyCi-CealkyI, carboxyCrCealkyloxy, C,-Csalkylcarbonylamino, CrCealkylcarbonylaminoCrCealkyI,-carbonylNRyCrCealkylCORn, arylCi-Csalkylcarbonyl-amino, arylCrCgalkylcarbonylaminoCrCealkyl, -CONRgRs, or -Cr Cealkyl-CONRgRe; wherein R7, RQ, R9, and R" are defined as above and the alkyl and aryl groups are optionally substituted as defined in the definition section; The definition of aryl includes but is not limited to phenyl, biphenyl. indenyl, fluorenyl, naphthyl (1-naphthyl, 2-naphthyl). pynrolyi (2-pyn-olyl), pyrazolyl (3-pyrazolyl), imidazolyl (1-imidazolyl, 2-imidazolyl. 4-imidazolyl, 5-imidazolyl), triazolyl (1,2,3-triazol-1-yl. 1,2,3-triazol-2-yl 1,2,3-triazol-4-yl. 1,2.4-triazol-3-yl). oxazolyl (2-oxazolyl, 4-oxazolyl. 5-oxazolyl), isoxazolyl (3-isoxazolyl, 4-isoxazoiyl, 5-isoxazolyl), thiazolyl (2-thiazolyl, 4-thiazolyi, 5-thiazolyl), thio-phenyl, (2-thiophenyl, 3-thiophenyl, 4-thiophenyl, 5-thiophenyi), furanyl (2-furanyl, 3-furanyl, 4-furanyl, 5-furanyl), pyridyl (2-pyridyi, 3-pyridyl, 4-pyridyl, 5-pyridyl). pyrimidinyl (2-pyrimidinyl, 4-pyrimidinyl, 5-pyrimidinyl, 6-pyrimidinyl), pyrazinyl, pyridazinyl (3-pyridazinyl, 4-pyridazinyl, 5-pyridazinyl). quinolyl (2-quinolyl, 3-quinolyl, 4-quinolyl, 5-quinolyl, 6-quinolyl, 7-quinolyl, 8-quinolyl). isoquinolyl (1-isoquinolyi, 3-isoquinolyl, 4-isoquinolyl. 5-isoquinolyl, 6-isoquinolyl. 7-isoquinolyl, 8-isoquinolyl), benzo[b]furanyl (2-benzo[b]furanyl, 3-benzo[b]furanyl, 4-benzo[b]furanyl, 5-benzo[b]furanyl, 6-benzo[b]furanyl, 7-benzo(b]furanyl), 2,3-dihydro-benzo[b]furanyl (2-(2,3-dihydro-benzo[b]furanyl), 3-(2.3-dihydro-benzo[b]furanyl). 4-(2,3-dihydro-benzo[b]furanyl), 5-(2,3-dihydro-benzo[b]furanyl), 6-(2,3-dihydro-benzo[b]furanyl), 7-(2,3-dihydro-benzo{b]furanyl)). benzo[b]thiophenyl (2-benzo[b]thiophenyl, 3-benzo[b]thiophenyl, 4-benzo[b]thiophenyl, 5-benzo[b]thiophenyl, 6-benzo[b]thiophenyl, 7-benzo[b]thiophenyl), 2,3-dihydro-benzo[b]-thiophenyl (2-(2,3-dihydro-benzo[b]thiophenyl), 3-(2,3-dihydro-benzo[b]-thiophenyl), 4-(2.3-dihydro-benzo[b]thiophenyl), 5-{2,3-dihydro-benzo[b]-thiophenyl), 6-(2,3-dihydro-benzo[b]thiophenyl), 7-(2.3-dihydro-benzo[b]-thiophenyt)), 4.5,6,7-tetrahydro-benzo[b]thiophenyl(2-(4,5,6,7-tetrahydro-benzo[b]thiophenyl), 3-(4,5,6,7-tetrahydro-benzo-[b]thiophenyl), 4-(4,5,6.7-tetrahydro-benzo[b]thiophenyl). 5-(4,5,6,7-tetrahydro-benzo-[b]thiophenyl), 6-(4,5,6,7-tetrahydro-benzo[b]thiophenyl), 7-(4,5,6,7-tetrahydro-benzo[b]thiophenyl)), 4,5,6.7-tetrahydro-thieno[2,3-c]pyridyl(4-(4,5,6,7-tetrahydro-thieno[2,3-c]pyridyl), 5-4,5,6,7-tetrahydro-thieno[2,3-clpyridyl), 6-(4,5,6.7-tetrahydro-thieno[2,3-c]pyridyl), 7-(4,5,6.7-tetra-hydro-thieno[2,3-c]pyridyl)), indolyl (1-indolyl, 2-Jndolyl, 3-indolyl, 4-indolyl, 5-indolyl, 6-indolyl, 7-indolyl), indazole (1-indazolyl, 3Hndazolyl, 4-indazolyl, 5-indazolyl, 6-indazolyl, 7-indazolyl), benzimidazolyl (1-benzimidazolyl. 2-benzimidazolyl, 4-benzimidazolyl, 5-benzimidazolyl. 6- benzimidazolyi, 7-benzimidazolyl, 8-benzimidazolyl), benzoxazoiyl (1-benzoxazolyl, 2-benzoxazoiyl), benzothiazolyl (1-benzothiazolyl, 2-benzothiazolyl, 4-benzothiazolyl, 5-benzothiazolyl, 6-benzothiazolyl. 7-benzothiazolyl), carbazolyl (1-carbazolyl, 2-carbazolyl, 3-carbazoiyl, 4-carbazolyl). 5H-diben2[b,f]azepine (5H-dibenz[b,f]azepin-1-yl, 5H-dibenz[b,f]azepine-2-yl, 5H-dibenz[b,f]azepine-3-yl, 5H-dibenz-[b,f]azepine-4-yl, 5H-dibenz[b.f]-azepine-5-yl), 10,11 -dihydro-5H-dibenz[b,f]azepine (10,11 -dihydro-5H-dibenz(b.f]azepine-1-yl, 10J1-dihydro-5H-dibenz[b,f]azepine-2-yl, 10,11-dihydro-5H-dibenz[b.f]azepine-3-yl, 10,11-dihydro-5H-dibenz[b,f]azepine-4-yl, 10,11-dihydro-5H-dibenz[b,f|azepine-5-yl). piperidinyl (2-piperidinyl, 3-piperidinyl, 4-piperidinyi), pyrolidinyl (1-pyn'olidinyl, 2-pyn-olidinyl, 3-pyn-olidinyl), phenylpyridyl (2-phenyl-pyridyl, 3-phenylpyridyl, 4-phenylpyridyl), phenylpyrimidinyl (2-phenylpyrimidinyl, 4-phenylpyrimidinyl, 5-phenyipyrimidinyl, 6-phenylpyrimidinyl), phenyipyrazinyl, phenylpyridazinyl (3-phenylpyridazinyl, 4-phenylpyridazinyl, 5-phenyl-pyridazinyl). The term "arylcarbonyi" (e.g. 2-thiophenylcarbonyl, 3-methoxy-anthrylcarbonyl, oxazolylcar-bonyl) represents an "aryl" group as defined above attached through a carbonyi group. The term "arylalkylcarbonyl" (e.g. (2,3Hdimethoxyphenyl)-propylcarbonyl. (2-chloronaphthyOpentenylcarbonyl, imidazolylcyclo-pentylcarbonyl) represents an "arylalkyl" group as defined above wherein the "alkyl" group is in turn attached through a carbonyi. The compounds of the present invention which have asymmetric centers may occur as ra-cemates, racemic mixtures, and as individual enantiomers or diastereoisomers, with all isomeric forms being included in the present invention as well as mixtures thereof. Pharmaceutically acceptable salts of the compounds of the invention, where a basic or acidic group is present in the structure, are also included within the scope of this invention. V\flnen an acidic substituent is present, such as -COOH, 5-tetrazolyl and P(0)(OH)2, there can be formed the ammonium, sodium, potassium, calcium salt, and the like, for use as the dosage form. When a basic group is present, such as amino or a basic heteroaryl radical, such as pyridyl, an acidic salt, such as hydrochloride, hydrobromide, acetate, maleate, palmoate, methanesulfonate, p-toluenesulfonate, and the like, can be used as the dosage form. Also, in the case of the -COOH or -P(0)(0H)2 being present, phamiaceutically acceptable esters can be employed, e.g., methyl, tert-butyl, pivaloyloxymethyl, and the like, and those esters known in the art for modifying solubility or hydrolysis characteristics for use as sustained release or prodrug formulations. In addition, some of the compounds of the instant invention may form solvates with water or common organic solvents. Such solvates are encompassed within the scope of the invention. The tenn "therapeutically effective amount" shall mean that amount of drug or pharmaceutical agent that will elicit the biological or medical response of a tissue, system, animal, or human that is being sought by a researcher, veterinarian, medical doctor or other. DESCRIPTION OF THE INVENTION It has surprisingly been shown that compounds comprising a certain stmctural fragment show inhibitory or modulatory capacity against one or more PTPases or other molecules with phosphotyrosine recognition unit(s). Accordingly, the present invention relates to compounds that fulfills ail of the following 3 criteria: (1) has a structure represented by Fonnula I: Formula I wherein R, R2 and R4 are any chemical group or combination of chemical groups; (2) acts as a phosphotyrosine recognition unit ligand, preferably an inhibitor or modulator of one or more PTPases or proteins that contain SH2 domains; and (3) has a molecular weight below or equal to 2500 daltons; In a preferred embodiment the compounds of the invention has a structure represented by Formula II Formula II where R, R"and R4 are any chemical group or combination of chemical groups, and R" preferably is H. In another preferred embodiment the compounds that fulfills all of the following 3 criteria: (1) has a structure represented by Formula III: Formula III wherein Ri, R2. R3. R4 and R5 are any chemical group or combination of chemical groups, and R3 and R5 may be covalently linked to each other; (2) acts as a phosphotyrosine recognition unit ligand, preferably an inhibitor or modulator of one or more PTPases or proteins that contain SH2 domains; and (3) has a molecular weight below or equal to 2500 daltons. In another preferred embodiment the compounds of the invention has a structure represented by Formula IV Formula IV where R", R3, R4 and R5 are any chemical group or combination of chemical groups, and R3 and R5 may be covalently linked to each 6ther, and R preferably is H. In another prefen-ed embodiment the compounds of the invention has a structure represented by Formula V Formula V where R,, R3, R4 and R5 are any chemical group or combination of chemical groups" and R3 and R5 may be covalently linked to each other, and R is preferably H. In another preferred embodiment the compounds of the invention has a structure represented by Formula VI where R3, R4 and R5 are any chemical group or combination of chemical groups, and R3 and R5 may be covalently linked to each other, and R is preferably H. In another preferred embodiment the compounds of the invention has a structure represented by Formula VII wherein A together with the double bond in formula VII represents any aryl as defined above, and R", Rj, R3 and R4 are any chemical group or combination of chemical groups. In another preferred embodiment the compounds of the invention has a stmcture represented by Formula VIII wherein A together with the double bond in formula VIII represents any aryl as defined above, and R, R", R3 and R4 are any chemical group or combination of chemical groups, and R preferably is H. In another preferred embodiment the compounds of the invention has a structure represented by Formula IX wherein A together with the double bond in formula IX represents any aryl as defined above, and Ri, R2, R3 and R4 are any chemical group or combination of chemical groups. In another preferred embodiment the compounds of the invention has a structure represented by Formula X wherein A together with the double bond in formula X represents any aryl as defined above, and R2, R3 and R4 are any chemical group or combination of chemical groups. In another preferred embodiment the compounds of the invention has a structure represented by Formula XI Formula XI wherein A together with the double bond in formula XI represents any aryl as defined above, and R, R3 and R4 are any chemical group or combination of chemical groups, and R preferably is H. In another preferred embodiment the compounds of the invention has a structure represented by Formula XII wherein R, is a chemical group capable of being a proton donor and/or a proton acceptor, preferably -COOH, S-tetrazolyl, -NH2, -CONH2, and R, R2. R3 and R4 are any chemical group or combination of chemical groups. In another preferred embodiment the structure of the compounds of the invention is represented by the following Formula XX wherein: A is together with the double bond in Fonnula 1 phenyl, biphenyl, indenyl, fluorenyl, fluo-renyl-9-one, naphthyl. pyridyl, pyridazinyl. pyrimidyl or pyrazinyl; or A is together with the double bond in Formula 1 indolyl, benzo[b]thiophenyl, benzo[b]furanyl, indazoiyl, benzo[b]isoxazolyl. benzimidazolyl, benzthiazolyl, benzoxazolyl, 9H-thieno[2,3-c]chromenyl, 4,5,6,7-tetrahydro-benzo[b]thiophenyl, 4,5,6,7-tetrahydro- thieno[2,3-b]pyridyl, 4,5.6J-tetrahydro-thieno[2,3-c]pyridyl, 4,5,67-tetrahydro-thieno[3.2-c]pyridyl. 4,5,6,7-tetrahydro-thieno[3,2-b]pyridyl, 4,7-dihydro-5H-thieno[2,3-c]pyranyl, 4,7-dihydrO"5H-thieno[2,3-c]thiopyranylor4,5,6,7-tetrahydro-4.7-ethanon-thieno[2,3-b]pyridyl; or A is together with the double bond in Formula 1 furanyl, thiophenyl, pyrrojyl, oxazolyl, thi-azolyl, imidazoiyi, pyrazolyl. isoxazolyl, isothiazolyl, 1,2,3-oxadiazolyl, furazanyl or 1,2,3-thazolyl; or A is together with the double bond in Fomiula 1 furo[2,3-b]pyridyl, thieno[2,3-b]pyridyl, pyrrolo[2,3-b]pyridyl, furo[2,3-c]pyridyl, thieno(2,3-c]pyridyl, pyn-olop.S-cjpyridyi, furo[3,2-c]pyridyi, thieno[3,2-c]pyridyl, pyrrolo[3,2-c]pyridyl, furo[3,2-d]pyridyl, thieno[3,2-d]pyridyl, pyrrolo[3,2-d]pyridyl, furo(2,3-d]pyrimidyl, thieno[2,3-d]pyrimidyl, pyrroio[2,3-d]pyrimidyl, furo[2,3-b]pyrazinyl, thieno[2,3-b]pyrazinyl, pyrrolo[2,3-b]pyrazinyl, furo(2,3-c]pyridazinyl, thieno[2,3-c]pyridazinyi, pyn-olo[2,3-c]pyridazinyl, furo[2,3-d]pyridazinyl. thieno[2,3-d]pyridazinyl, pyrrolo[2,3-d]pyridazinyl, furo(3,2-c]pyridazinyl, thieno[3,2-c]pyridazinyl, pyr-rolo[3,2-c]pyridazinyl, quinolizinyl, quinolinyl. isoquinolinyl. cinnolinyl, phthalazinyl, quinazoli-nyl, quinoxalinyl, 1,8-naphthyridinyl. chromanyl. thiochromanyl. isochromanyl, isothio-chromanyl. 2,3-dihydro-thieno[2,3-b]furanyl, 4.6-dihydro-thieno[2,3-c]furanyl, 2.3-dihydro-thieno(3.2-b]furanyl, 4,5-dihydro-thieno[2,3-b]thiophenyl, 4,6-dihydro-thieno[3,4-b]thiophenyl. 5,6-dihydro-thieno[3,2-b]thiophenyl, 4,5-dihydro-thieno[2,3-b]pyrrolyl. thieno[3,2-d]isothiazolyl, thieno[3,2-d]thiazolyl, thieno[2,3-d]thiazolyl, thieno[2.3-c]pyrrolyl-4,6-dione, 1H-thieno[2,3-d]imidazolyl, 6H-thieno[2,3-b]pyn-olyl, 5,6-dihydro-4H-thieno[2,3-c]pyn-olyl or 4H-thieno[3,2-b]pyn-oiyl; Ri and R2 are independently selected from the group consisting of COR5, ORg, CF3, nitro, cyano. SO3H, SO2NR7R8. P0(0H)2, CH2pO(OH)2, CHFP0(0H)2. CF2PO(OH)2, C(=NH)NH2, NRyRs. and the following 5-membered heterocycles Ra, Ri6 and R"are hydrogen, halo, nitro, cyano, trihalomethyl, Ci-Cgalkyl, aryl, arylCrCg-alkyl, hydroxy, carboxy, carboxyCrCealkyl. Ci-Cfialkyloxycarbonyl, aryloxycarbonyi, arylC"-Cgalkyloxycarbonyi, CrCealkyioxy, Ci-CealkyloxyCi-Cgalkyl, aryloxy, arylCi-Cealkyloxy, arylCi-CealkyloxyCrCgalkyl, thio, CrCealkylthio. CrCealkylthioCi-CealkyI, arylthio, arylCr Cgalkylthio, arylCrCealkylthioCrCealkyl, NRyRg, Ci-Cealkyl-aminoCrCealkyl. arylC,-CealkylaminoCrCealkyl, di(arylCrC6alkyl)aminoCi-Cealkyl, CrCealkylcarbonyl, Cr CfialkylcarbonylCrCsalkyl, arylCrCealkylcarbonyl, arylC"-CealkylcarbonylCi-Cealkyl. Ci-Cgalkytcarboxy, CrCealkyicarboxyCi-Ce-alkyl, arylcarboxy, arylCi-Cealkylcarboxy, arylC" CsalkylcarboxyCt-Cfialkyl, CrCgalkylcarbonyl-amino, Ci-CealkylcarbonylaminoCrCealkyl. -carbonylNRyd-CealkylCORn, arylCi-Cgalkylcarbonyiamino, arylCrCealkylcarbonylaminoCi-Cgalkyl, CONRyRfl, or CrCsalkylCONRyRg wherein the alkyl and aryl groups are optionally substituted and R"" is NRyRg. or Ci-CealkyJNRyRg; or, when Ri6 and R"/are hydrogen, R3 is A-B-C-D-Ci-Cfialkyl, wherein A is CrCsalkyi, aryl or aryiCi-Cgalkyl; B is amino, thio, SO, SO2 or 0x0; C is Ci-Cgalkyl, amino; D is a chemical bond, amino or Ci-Cgalkyl wherein the alkyl and aryl groups are optionally substituted; or wherein R12, R13, and R14 are independently hydrogen, Ci-Cgalkyl, aryl, arylCrCgalkyl and the alkyl and aryl groups are optionally substituted; R4 is hydrogen, hydroxy. CrCgalkyl, aryl, arylCi-CeaikyI, NRyRs. Ci-Cealkyloxy; wherein the alkyl and aryt groups are optionally substituted; R5 is hydroxy, Ci-Cgalkyl. aryl, arylCi-Cgalkyl, CFj, NRyRg; wherein the alkyl and aryl groups are optionally substituted; Rg is hydrogen, d-Cealkyl. aryl, arylCrCgalkyl; wherein the alkyl and aryl groups are optionally substituted; R7 and Rfi are independently selected from hydrogen, CrCsalkyl. aryl, arylCrCealkyI, C" Cealkylcarbonyl, arylcarbonyl, arylCi-Cealkyicarbonyl, Ci-Cealkyl-carboxy orarylCr Csalkylcarboxy wherein the alkyl and aryl groups are optionally substituted; or R7 and Rg are together with the nitrogen to which they are attached forming a saturated, partially saturated or aromatic cyclic, bicyclic or tricyclic ring system containing from 3 to 14 carbon atoms and from 0 to 3 additional heteroatoms selected from nitrogen, oxygen or sulfur, the ring system can optionally be substituted with at least one Ci-CealkyI, aryl, arylCi-CealkyI, hydroxy. 0x0, CrCealkyloxy, arylCrCgalkyloxy, CrCsalkyloxyCi-Cealkyl. NRgRioOrC,-CgalkylaminoCrCealkyl, wherein R9 and R"o are independently selected from hydrogen, C"-Cgalkyl, aryl, arylCi-CealkyI, CrCealkylcarbonyl.-arylcartDonyl, arylCrCealkylcarbonyi, C,-Cgalkylcarboxy or arylCrCealkylcarboxy; wherein the alkyl and aryl groups are optionally substituted; or R7 and Rfl are independently a saturated or partial saturated cyclic 5, 6 or 7 membered amine, imide or lactam; Compounds of the invention may modulate or inhibit the activity of protein tyrosine phosphatases or other molecules with phosphotyrosine recognition unit(s) via different mechanisms of action. Examples of such mechanism of actions, which are not intended in any way to limit the scope of the invention, are (a) classical competitive inhibition; (b) uncompetitive inhibition; (c) mixed-type inhibition as defined above. The invention furthermore relates to compounds which after uptake in cells or mammals has a stnjcture as defined above. In one preferred embodiment, the compounds of the invention act as dassical,competitive inhibitors of one or more PTPases. In another preferred embodiment, the compounds of the invention act as mixed-type inhibitors of one or more PTPases. In one prefenred embodiment, the compounds of the invention substantially act as an inhibitor of one or more PTPases involved in regulation of tyrosine Wnase signalling pathways. In another preferred embodiment, the compounds of the invention substantially inhibit or modulate receptor-tyrosine kinase signalling pathways via interaction with one or more regulatory PTPases, preferably the signalling pathways of the insulin receptor, the IGF-1 receptor and/or other members of the insulin receptor family, the EGF-receptor family, the platelet-derived growth factor receptor family, the nerve growth factor receptor family, the hepatocyte growth factor receptor family, the growth homnone receptor family and/or members of other receptor-type tyrosine kinase families. In another prefen-ed embodiment, the compounds of the invention substantially inhibit or modulate non-receptor tyrosine kinase signalling through modulation of one or more regulatory PTPases, preferably modulation of members of the Src kinase family or other intracellular kinases. In another preferred embodiment, the compounds of the invention substantially inhibit or modulate the activity of one or more PTPases that negatively regulate signal transduction pathways. In another preferred embodiment, the compounds of the invention inhibit or modulate the activity of one or more PTPases that positively regulate signal transduction pathways, preferably CD45. In another preferred embodiment, the compounds of the invention inhibit or modulate the activity of one or more PTPases that positively regulate signal transduction pathways in immune cells. In another preferred embodiment, the compounds of the invention inhibit or modulate the activity of one or more PTPases that negatively regulate signal transduction pathway. In another preferred embodiment, the compounds of the invention inhibit one or more PTPases via binding to the active site of said PTPase(s) or to other sites that negatively influences the binding of substrate to said PTPase(s), an allosteric modulator. In another preferred embodiment, the compounds of the invention modulate the activity of one or more PTPases via interaction with structures positioned outside of the active sites of the enzymes, preferably SH2 domains. In another preferred embodiment, the compounds of the invention modulate the signal transduction pathways via binding of the compounds of the invention to SH2 domains or PTB domains of non-PTPase signalling molecules. In one embodiment, the compounds of the invention are characterized by being selective PTPase inhibitors or compounds that are selective phosphotyrosine recognition unit ligands. The compound of the invention can e.g. be selective for a PTPase not described herein or, preferably, a PTPase listed in Table 1. In another prefen-ed embodiment, the compounds of the invention are characterized by being non-selective PTPase inhibitors such as inhibitors or modulators of at least 4 PTPases or 4 PTPase families. In one preferred embodiment, the compounds of the invention are selective for the PTPa family. In another prefen'ed embodiment, the compounds of the invention are selective for PTPa. In another preferred embodiment, the compounds of the invention are selective for PTPE. In another preferred embodiment, the compounds of the invention are selective for CD45. In one preferred embodiment, the compounds of the invention are selective for PTPp family. In another prefen'ed embodiment, the compounds of the invention are selective for PTPp. In another preferred embodiment, the compounds of the invention are selective for PTP-DEP1. In one preferred embodiment, the compounds of the invention are selective for PTP-LAR family. In one prefen"ed embodiment, the compounds of the invention are selective for PTP-LAR. In one preferred embodiment, the compounds of the invention are selective for PTPa. In one preferred embodiment, the compounds of the invention are selective for PTP5. In one preferred embodiment, the compounds of the invention are selective for PTP"i family. In one preferred embodiment, the compounds of the invention are selective for PTP", in one prefenred embodiment, the compounds of the invention are selective for PTPK. In one preferred embodiment, the compounds of the invention are selective for PTP1B family. In one preferred embodiment, the compounds of the invention are selective for PTP1B. In one preferred embodiment, the compounds of the invention are selective forTC-PTP. In one preferred embodiment, the compounds of the invention are selective for SHP-PTP family. In one preferred embodiment, the compounds of the invention are selective for SHP-1. In one preferred embodiment, the compounds of the invention are selective for SHP-2. In one preferred embodiment, the compounds of the invention are selective for PTP<:; family. In another preferred embodiment, the compounds of the invention are selective for PTPy. In one prefen-ed embodiment, the compounds of the invention are selective for PTP-PEST family. In one preferred embodiment, the compounds of the invention are selective for PTPH1 family. In one preferred embodiment, the compounds of the invention are selective for PTPH1. In one preferred embodiment, the compounds of the invention are selective for PTPD1. In one preferred embodiment, the compounds of the invention are selective for PTPD2. In one prefeaed embodiment, the compounds of the invention are selective for PTPMEG1. In one prefen-ed embodiment, the compounds of the invention are selective for IA-2 family. In one preferred embodiment, the compounds of the invention are selective for IA-2. In one preferred embodiment, the compounds of the invention are selective for IA-23. In one preferred embodiment, the compounds of the invention are selective for the PTPi); family. In another preferred embodiment, the compounds of the invention are selective for PTPv|/. In another preferred embodiment, the compounds of the invention are selective for PTPp. In another prefen-ed embodiment, the compounds of the invention are selective for PTPf In another preferred embodiment, the compounds of the invention have a molecular weight of less than 1000 Daitons, and preferably of more than 100 Daitons. In one preferred embodiment, the compounds of the invention have Kj values of less than 200 "M against one or more PTPases. In another preferred embodiment, the compounds of the invention have K| values of less than 2 "M against one or more PTPases. In another preferred embodiment, the compounds of the invention have Kj values of less than 100 nM against one or more PTPases. In another preferred embodiment, the compounds of the invention have a Kj value of < 2 \iM against one or two PTPase or PTPase families and a Kj value of > 50 \M against at least two other PTPases or PTPase families. In another preferred embodiment, the compounds of the invention have a K; value of < 100 nM against one or two PTPase or PTPase families and a Kj value of > 10 |J.M against at least two other PTPases or PTPase families. In one preferred embodiment, the compounds of the invention have a IC50 value of less than 200 M against one or more molecules with phosphotyrosine recognition unit(s). In another preferred embodiment, the compounds of the invention have a IC50 value of less than 2 M against one or more molecules with phosphotyrosine recognition unit(s). In another preferred embodiment, the compounds of the invention have a IC50 value of less than 100 nM against one or more molecules with phosphotyrosine recognition unit(s). In one preferred embodiment, the compounds of the invention act as inhibitors of one or more PTPases, e.g. protein tyrosine phosphatases involved in regulation of tyrosine kinase signalling pathways. Preferred embodiments include modulation of receptor-tyrosine kinase signalling pathways via interaction with regulatory PTPases, e.g. the signalling pathways of the insulin receptor, the IGF-I receptor and other members of the insulin receptor family, the EGF-receptor family, the platelet-derived growth factor receptor family, the nerve growth factor receptor family, the hepatocyte growth factor receptor family, the growth hormone receptor family and members of other receptor-type tyrosine kinase families. Further preferred embodiments of the inventions is modulation of nonreceptor tyrosine kinase signalling through modulation of regulatory PTPases, e.g. modulation of members of the Src kinase family and other non-receptor tyrosine kinases. One type of preferred embodiment of the inventions relates to modulation of the activity of PTPases that negatively regulate signal transduction pathways. An example, which is not intended in any way to limit the scope of the invention, is SHP-1 that negatively regulates the eiTthropoietin signalling pathway. Another type of prefen"ed embodiments of the inventions relate to modulation of the activity of PTPases that positively regulate signal transduction pathways. An example of the latter, which is not intended in any way to limit the scope of the invention, is CD45 which dephosphorylates tyrosine kinase of the Src family and thereby plays a positive role in signalling in ceils from the hematopoietic system. One type of prefen-ed CD45 inhibitor can be used to regulate the activity of lymphocytes, including T- and/or B-lymphocytes. In a prefen-ed embodiment the compounds of the invention act as modulators or inhibitors of the active site of one or more PTPases. In another preferred embodiment the compounds of the invention modulate the activity of one or more PTPases via interaction with structures positioned outside of the active sites of the enzymes, preferably SH2 domains. Further preferred embodiments include modulation of signal transduction pathways via binding of the compounds of the invention to SH2 domains or PTB domains of non-PTPase signalling molecules. In preferred embodiments the compounds of the invention are selective inhibitors that are more than 10-fold potent against one PTPase family than against another PTP family. In one embodiment, the compounds of the invention can be used for managing, treating or preventing type I diabetes, type II diabetes, impaired glucose tolerance, insulin resistance, obesity, immune dysfunctions including autoimmunity and AIDS, diseases with dysfunctions of the coagulation system, allergic diseases, osteoporosis, proliferative disorders including cancer and psoriasis, diseases with decreased or increased synthesis or effects of growth hormone, diseases with decreased or increased synthesis of hormones or cytokines that regulate the release of/or response to growth hormone, diseases of the brain including Alzheimer's disease and schizophrenia, and infectious diseases. In another embodiment, the compounds of the invention can be used for In another embodiment, the compounds of the invention can be used for managing, treating or preventing type I diabetes, type II diabetes, impaired glucose tolerance, insulin resistance, and/or obesity. In another embodiment, the compounds of the invention can be used for managing, treating or preventing conditions with immune dysfunctions, including autoimmunity such as rheumatoid arthritis, systemic lupus erythematosus. In another embodiment, the compounds of the invention can be used as immunosuppressants. In another embodiment, the compounds of the invention can be used for managing or treating conditions with immune dysfunctions including AIDS. In another embodiment, the compounds of the invention can be used for managing, treating or preventing allergic diseases, including asthma and allergic skin diseases. In another embodiment, the compounds of the invention can be used for managing, treating or preventing proliferative disorders, including cancer. In another embodiment, the compounds of the invention can be used for managing, treating or preventing osteoporosis. In another embodiment, the compounds of the invention can be used for managing, treating or preventing psoriasis. in another embodiment, the compounds of the invention can be used for managing, treating or preventing diseases with decreased or increased synthesis or effects of growth hormone, diseases with decreased or increased synthesis of hormones or cytokines that regulate the release of/or response to growth hormone. In another embodiment, the compounds of the invention can be used for managing, treating or preventing diseases with dysfunctions of the coagulation system. In another embodiment, the compounds of the invention can be used for managing, treating or preventing diseases of the brain including Alzheimer's disease and schizophrenia. In another embodiment, the compounds of the invention can be used for managing, treating or preventing infectious diseases. The compounds of the invention can furthemiore be used to manufacture of medicaments for managing, treating or preventing the above-mentioned diseases and disorders. Other preferred embodiments include use of the compounds of the invention for modulation of cell-cell interactions as well as cell-matrix interactions. The present invention is furthermore concerned with pharmaceutical compositions comprising, as an active ingredient, at least one of the compounds of the present invention in association with a pharmaceutical carrier or diluent. Optionally, the pharmaceutical composition can comprise at least one of the compounds of the invention combined with compounds exhibiting a different activity, e.g. an antibiotic or other pharmacologically active material. As a preferred embodiment, the compounds of the invention may be used as therapeutical to inhibit or modulate one or more PTPases involved in regulation of the insulin receptor tyrosine kinase signalling pathway in patients with type I diabetes, type II diabetes, impaired glucose tolerance, insulin resistance, and obesity. Further preferred embodiments include use of the compounds of the invention for management of disorders with general or specific dysfunctions of PTPase activity, e.g. proliferarive disorders such as psoriasis and neoplastic diseases. As another embodiment, the compounds of the invention may be used in pharmaceutical preparations for management of osteoporosis. Preferred embodiments of the invention further include use of compound of the invention in pharmaceutical preparations to increase the secretion or action of growth hormone and its analogous or somatomedins including IGF-1 and IGF-2 by modulating the activity of one or more PTPases or other signal transduction molecules with affinity for phosphotyro-sine involved controlling or inducing the action of these hormones or any regulating molecule. The compounds of the invention may be used in pharmaceutical preparations for management of various disorders of the immune system, either as a stimulant or suppressor of normal or perturbed immune functions, including autoimmune reactions. Further embodiments of the invention include use of the compounds of the invention for management of allergic reactions, e.g. asthma, demial reactions, conjunctivitis. In another embodiment, the compounds of the invention may be used in phamiaceutlcal preparations used for immunosuppression. A non-limiting example of such use is in connection with management of organ and/or tissue transplantation. In another embodiment, compounds of the invention may be used in pharmaceutical preparations for prevention or induction of platelet aggregation. In yet another embodiment, compounds of the invention may be used in pharmaceutical preparations for management of infectious disorders. In particular, the compounds of the invention may be used for management of infectious disorders caused by Yersinia and other bacteria as well as disorders caused by viruses or other micro-organisms. Compounds of the invention may additionally be used for management or prevention of diseases in animals, including commercially important animals. Also included in the present invention is a process for isolation of PTPases via affinity purification procedures based on the use of immobilized compounds of the invention using procedures well-known to those skilled in the art. Such methods, well-known to those skilled in the arts, may be used to identify novel PTPases or other molecules with phos-photyrosine recognition units. As a non-limiting example, compounds of the invention may be immobilized by coupling to a solid-phase. A tissue sample or a sample from a cell line prepared as a lysate by methods well-known to those skilled in the art may be passed over said solid-phase coupled with a compound of the invention. After appropriate washing procedures designed to remove material that binds unspecifically to said solid-phase, using standard procedures well known to those skilled in the art, mostly PTPases or other molecules with phosphotyrosine recognition units will be bound to the compounds of the invention coupled to the solid phase. Said PTPases or other molecules with phosphotyrosine recognition units may in tum be released by procedures well-known in the art and further subjected to amino acid sequence analysis according to standard procedures well-known to those skilled in the art. By back-translation of said amino acid sequence into a nucleotide sequence of the corresponding cDNA can be deduced using the appropriate genetic code. Said nucleotide sequence can be used to design and produce an equivalent oligonucleotide, which in turn can be used to identify partial or fulMength cDNA clones from appropriate cDNA libraries encoding a protein or glycoprotein corresponding to or similar to the isolated PTPase or molecule with pTyr recognition units. Said oligonucleotide or isolated cDNA clone(s) can similarly be used to isolate genomic clones corresponding to said cDNA clones. Said partial or fulMength cDNA can be inserted into appropriate vectors and expressed and purified proteins with procedures well known to those skilled in the arts. Said purified proteins, in particular PTPases, may be used to further analyze the inhibitory capacity and selectivity of compounds of the invention as described. The invention is further directed to compounds of the invention coupled to a suitable solid-phase matrix such as a Wang-resin or a Rink-resin The invention is further diected to a method for isolating a protein or a glycoprotein with affinity for a compound according to the invention from a biological sample, comprising: • contacting a compound of the invention immobilized by coupling to a suitable solid-phase matrix with said biological sample in order for said immobilized compound to form a complex by binding said protein or glycoprotein, • removing unbound material from said biological sample and isolating said complex, and • extracting said protein or glycoprotein from said complex. The invention is further directed to a method for isolating a protein-tyrosine phosphatase with affinity for a compound according to the invention from a biological sample, comprising • contacting a compound of the invention immobilized by coupling to a suitable solid- • phase matrix with said biological sample in order for said immobilized compound to forni a complex by binding said protein-tyrosine phosphatase • removing unbound material from said biological sample and isolating said complex • extracting said protein-tyrosine phosphatase. The invention is further directed to a method for isolating a Src-homology 2 domain containing protein or a phosphotyrosine binding domain containing protein with affinity for a compound of the present invention from a biological sample, comprising • contacting a compound of the invention immobilized by coupling to a suitable solid-phase matrix with said biological sample in order for said immobilized compound to form a complex by binding said Src-homology 2 domain containing protein or a phos-photyrosine binding domain containing protein • removing unbound material from said biological sample and isolating said complex • extracting said Src-homology 2 domain containing protein or a phosphotyrosine binding domain containing protein from said complex. The present invention also relates to a compound of the invention coupled to a fluorescent or radioactive molecule. The invention furthennore relates to a method for coupling a fluorescent or radioactive molecule to a compound of the invention comprising • contacting said compound with said fluorescent or radioactive molecule in a reaction mixture to produce a complex • removing uncomplexed material and isolating said complex from said reaction mixture. The invention is further directed to a method for detecting protein-tyrosine phosphatase or other molecules with phosphotyrosine recognition unit(s) in a cell or in a subject using a compound of the invention coupled to a fluorescent or radioactive molecule comprising • contacting said cell or an extract thereof or a biological sample from said subject or by injecting said compound into said subject in order for said compound to produce a complex with said protein-tyrosine phosphatase or said molecules with phosphotyrosine recognition unit(s) • detecting said complex, thereby detecting the presence of said protein tyrosine phosphatase or said other molecules with phosphotyrosine recognition unit(s). The invention is further directed to a method for quantifying the amount of protein-tyrosine phosphatases or other molecules with phosphotyrosine recognition unit(s) in a cell or in a subject using a compound of the invention coupled to a fluorescent or radioactive molecule comprising • contacting said cell or an extract thereof or a biological sample from said subject or by injecting said compound into said subject in order for said compound to produce a complex with said protein-tyrosine phosphatase or said molecules with phosphotyrosine recognition unit(s) • measuring the amount of said complex, thereby detecting the presence of said protein tyrosine phosphatase or said molecules with phosphotyrosine recognition unit(s). The invention is also concerned with a method for detemiining the function of a given protein-tyrosine phosphatase or group of protein-tyrosine phosphatases or said molecules with phosphotyrosine recognition unit(s) in a cell or a subject using a compound of the invention coupled to a fluorescent or radioactive molecule comprising • contacting said cell or an extract thereof or a biological sample from said subject or by injecting said compound into said subject in order for said compound to produce a complex with said protein-tyrosine phosphatase or said molecules with phosphotyrosine recognition unit(s) • measuring the biological effects induced by said complex. Pharmacological Methods For the above indications the dosage will vary depending on the compound of the invention employed, on the mode of administration and on the therapy desired. However, in general, satisfactory results are obtained with a dosage of from about 0.5 mg to about 1000 mg, preferably from about 1 mg to about 500 mg of compounds of the invention, conveniently given from 1 to 5 times daily, optionally in sustained release form. Usually, dosage fomis suitable for oral administration comprise from about 0.5 mg to about 1000 mg, preferably from about 1 mg to about 500 mg of the compounds of the invention admixed with a pharmaceutical carrier or diluent. The compounds of the invention may be administered in a pharmaceuticaJly acceptable acid addition salt fomri or where possible as a metal or a Ci"-alkylammonium salt. Such salt fonns exhibit approximately the same order of activity as the free acid forms. This invention also relates to pharmaceutical compositions comprising a compound of the invention or a phanriaceuticaily acceptable salt thereof and, usually, such compositions also rnntpin a nharmaceuticai canrier or diluent Thp rnmnnsitions containinn thp rnm- CQatina: HPMC approx. 9 mg 'Mywacett* 9-40 T approx. 0,9 mg 'Acylated monogiyceride used as plasticiser for film coating. The route of administration may be any route which effectively transports the active compound to the appropriate or desired site of action, such as oral or parenteral e.g. rectal, transdermal, subcutaneous, intranasal, intramuscular, topical, intravenous, intraurethral, ophthalmic solution or an ointment, the oral route being prefeaed. The process for preparing compounds of the invemtion is further illustrated in the following examples, which, however, are not to be construed as limiting. EXAMPLES Hereinafter, TLC is thin layer chromatography, CDCI3 is deuterio chlorofonm, CD30D is tetradeuterio methanol and DMSO-dg is hexadeuterio dimethylsulfoxide. The structures of the compounds are confirmed by either elemental analysis or NMR, where peaks assigned to characteristic protons in the title compounds are presented where appropriate. "H NMR shifts (5H) are given in parts per million (ppm) downfield from tetramethylsitane as internal reference standard. M.p,: is melting point and is given in °C and is not corrected. Column chromatography was carried out using the technique described by W.C. Still et al., J. Org. Chem. 43: 2923 (1978) on Merck silica gel 60 (Art. 9385). HPLC analyses are peri'ormed using 5fxm C18 4 x 250 mm column eluted with various mixtures of water and acetonitrile, flow = 1 ml/min, as described in the experimental section. Compounds used as starting material are either known compounds or compounds which can readily be prepared by methods known per se. Wang-resin is polystyrene with a 4-hydroxymethylphenol ether linker. 2-Aminothiophenes are prepared according to Gewald ef a/., Chem. Ben 99:94 (1966). 3-Aminothiophenes are prepared according to H. Hartmann and J. Liebscher, Synthesis 275 (1984). 3-(Oxalvl-amino"naDhthalene-2-carboxvlicacid: M.p.; 227 - 228 °C: Calculated for C13H9NO5; C, 60.24 %; H, 3.50 %; N, 5.40 %. Found: C, 59.98 %; H, 3.46 %; N. 5.25 %. MS(ES):m/z = 326(M+1) Calculated for CgHeNIOs, 0.75 x H2O; C, 31.01 %; H, 2.17 %; N, 4.02 %. Found: C, 31.14 %; H, 2.33 %; N, 3.76 %. 4-"Qxalvl-aminQ"-biphenvl-3-carboxvlicacid: To a suspension of 5-bromo-2-amino-benzoic acid methyl ester (3.0 g, 13,04 mmol), tetral250°C; Calculated for CaHgNzOs; C, 45.72 %; H, 2.88 %; N, 13.33 %. Found: C, 45.62 %; H, 2.98 %; N, 13.04 %. EXAMPLE 34 5-rOyalvl-aminQl-2.6-dioxo-1.2.3.6-tetrahvdro-pvrimidine-4-carboxvlicacid; To a solution of 5-Aminoorotic acid (61.1nng, 0.36 mmol) in tetrahydrofuran (1 ml) was added jmidazoi-1-yl-oxo-acetic acid te/t-butyl ester (140 mg, 0.71 mmol) and triethyiamine (50 )il, 0.36 mmol). The mixture was stirred at room temperature for 20 h. The solvent was removed in vacuo and the residue was dissolved in ethyl acetate (5.0 ml) and washed with 1 % hydrochloric acid (2x2 mi) then water (2x2 ml). The organic phase was dried (MgSOO, filtered and the solvent evaporated in vacuo. The residue was purified by preparative TLC (Kieselgel 6OF254, 0.5 mm. hexane:ethyl acetate. 80:20) which afforded 30 mg (28 %) of 5-("ert-butoxyoxaiyl-amino)-2.6-dioxo-1.2,3,6-tetrahydro-pyrimidine-4-carboxylic acid as a solid. "H NMR (400 MHz. CDCI3) 5 1.80 (s. 9H), 7.56 (s. 2H), 8.96 (s. 1H). 5-(tert-Butoxyoxalyl-amino)-2,6-dioxo-1.2,3.6-tetrahydro-pyrimidine-4-carboxylic acid (28 mg. 0.094 mmol) was stirred in 20 % trifluoroacetic acid in dichloromethane (1.0 ml) at room temperature for 2 h. The reaction mixture was co-evaporated in vacuo with toluene to complete dryness which afforded 22.6 mg (100 %) of the title compound as a solid. "H NMR (400 MHz. CD3OD) 5 7.30 (s, 2H). 3-(Oxalvl-amino)-pvrazine-2-carboxylicacid; To a solution of 3-aminopyrazine-2-carboxylic acid (64.2 mg, 0.46 mmol) in tetrahydrofuran (1 ml) was added imidazol-1-yi-oxo-acetic acid te/t-butyl ester (181mg, 0.92 mmol) and triethyiamine (64.3 "1, 0.46 mmol). The mixture was stin-ed at room temperature for 20 h. The solvent was removed in vacuo and the residue was dissolved in ethyl acetate (5.0 ml) and washed with 1 % hydrochloric acid (2x2 ml) then water (2x2 ml). The organic phase was dried (MgS04), filtered and the solvent evaporated in yacufi. The residue was washed with diethyl ether (4 x 1.0 mi) affording 48 mg (39 %) of 3-(tert-butoxyoxalyl-amino)-pyra2ine- 2-carboxylic acid as a solid. "H NMR (CDCI3 + CD3OD) 5 1.70 (s, 9H), 8.02 (d. 1H, J = 1.5 Hz), 8.36 (d, 1H, J = 1.5 Hz). 3-(tert-Butoxyoxalyl-amino)-pyrazine-2-carboxyiic acid (31.7 mg. 0.12 mmol) was stirred in 20 % trifiuoroacetic acid in dichloromethane (1 ml) at room temperature for 2 h. The volatiles were evaporated in vacuo and the residue co-evaporated with toluene in yacuo affording 25 mg (100 %) of the title compound as a solid. "H NMR (400 MHz. CDCI3) 5 7.80 (d, 1H, J = 1.5 Hz), 8.15 (d, 1H, J = 1.5 Hz), 8.62 (s, 1H). To a solution of 2-aminonicotinic acid (61.4 mg, 0.45 mmol) in tetrahydrofuran (1 ml) was added imidazol-1-yl-oxo-acetic acid tert-hutyl ester (174.2mg, 0.89 mmol) and triethylamine (62 fil, 0.45 mmol). The mixture was stirred at room temperature for 2 h. The solvent was removed in vacuo and the residue was dissolved in ethyl acetate (5.0 ml) and washed with 1% hydrochloric acid (2x2 ml) then water (2x2 ml). The organic phase was dried (MgS04), filtered and the solvent evaporated in yaeuQ. The residue (125 mg) was purified by preparative TLC (Kieselgel 6OF254, 1 mm, CHzClj/MeOH. 80/20) affording 7.9 mg (7 %) of 2-(terf-butoxyoxalyl-amino)-nicotinic acid as a solid. "H NMR (400 MHz, CD3OD) 5 1.80 (s, 9H). 7.40 (m, 1H), 8.50 - 8.70 (m, 2H). 2-(tert-Butoxyoxalyl-amino)-nicotinic acid (7.1 mg, 0.03 mmol) was stin-ed in 20 % trifiuoroacetic acid in dichloromethane (0.5 ml) at room temperature for 2 h. The volatiles were evaporated to dryness in vacuo affording 5.6 mg (100 %) of the title compound as a solid. "H NMR (400 MHz, CD3OD) 5 7.40 (m, 1H), 8.50 - 8.70 (m. 2H). fi-QlliQrQ>5"isoproDvlamino-3-(oxalvl-aminoVpyra2ine-2-carboxvlic acid, dilithium salt: To a solution of 3-amino-6"Chloro-5-isopropyiamino-pyrazine-2-carboxylic acid (65.4 mg, 0.27 mmol) in tetrahydrofuran (1 ml) was added imidazol-1-yl-oxo-acetic acid fert-butyl ester (104.8 mg, 0.54 mmol) and triethylamine (37.4 "1, 0.27 mmol). The mixture was stinted at room temperature for 20 h followed by heating to 50 °C for 1.5 h. The solvent was removed in vacuo and the residue was dissolved in ethyl acetate (5.0 ml) and washed with 1 % hydrochloric acid (2x2 ml) then water (2x2 ml). The organic phase was dried (MgS04), filtered and the solvent evaporated in vacuo affording cmde 97 mg (97 %) of 3-(tert-butoxyoxalyl-amino)-6-chloro-5-isopropylamino-pyrazine-2-carboxylic acid as an oil. "H NMR (400 MHz, CDCI3) 5 1.50 (d, 6H), 1.80 (s. 9H). 4.10 (s, 3H). 4.40 (m, 1H). 3-(fert-Butoxyoxalyl-amino)-6-chloro-5-isopropyiamino-pyrazine-2-carboxylic acid (30 mg, 0.1 mmol) was dissolved in tetrahydrofuran (1 ml) and 1.0 N lithium hydroxide (1 mi, 1 mmol) was added at room temperature. The reaction mixture was stirred for 3 days at room temperature. After removing the solvent in vacuo, the residue was dissolved in ethyl acetate (20 ml) and washed with water (4 x 3.0 ml). The organic phase was dried (Na2S04), filtered and the solvent evaporation IQ vacuo affording 21 mg (82 %) of the title compound as a solid. "H NMR (400 MHz. CD3OD) 8 1.42 (d. 6H). 4.50 (m. 1H). MSm/z228(M.74). 5.6-DichlQro-3-fQxalvl-aminQ)-pvrazine-2-carboxvlic acid, dilithium salt: To a solution of 3-amino-5,6-dichloro-pyrazine-2-carboxylic acid (57 mg, 0.26 mmoi) in tetra-hydrofuran (0.5 ml) was added imidazol-l-yl-oxo-acetic acid tert-buty\ ester (100.6 mg, 0.513 mmoi) and triethylamine (35.8 |LLI, 0.26 mmoi). The mixture was stirred at room temperature for 20 h followed by heating at 40 °C for 4 h. The solvent was removed in vacuo and the residue was dissolved in ethyl acetate (5.0 ml) and washed with 1 % hydrochloric acid (2x2 ml) then water (2x2 ml). The organic phase was dried (MgS04), filtered and the solvent evaporated in vacuo. The residual oil was purified by preparative tic (Kieselgel 6OF254. 1 mm, hexane: ethyl acetate, 1:1) affording 23.6 mg (26 %) of 3-(fert-butoxyoxalyl-amino)-5,6-dichloro-pyra2ine-2-carboxylic acid as an oil. 'H NMR (400 MHz. CDCI3) 5 1.58 (s, 9H), 1.80 (s, 9H). 3.90 (s, 3H). To a solution of 3-(/ert-butoxyoxalyl-amino)-5,6-dichloro-pyrazine-2-carboxyiic acid (23 mg, 0.07 mmoi) in tetrahydrofuran (0.5 ml) was added al.O N aqueous solution of lithium hydroxide (0.5 ml) and the resulting mixture was stirred for 3 days. After removing the solvent in vacuo, the residue was dissolved in ethyl acetate (20 ml) and washed with water (4 x 3.0 ml). The organic phase was dried (NajSO"), filtered and the solvent evaporation in vacuo affording 14 mg (80 %) of the title compound as a solid. MS m/z 290.3 (M-74). 2-MethvM-(oxalvl-aminoV1 H-Dvrrole-3-carbQxvlic acid: To a stirred solution of 4-(methoxyoxalyl-amino)-2-methyl-1H-pyn'ole-3-carboxylic acid tert-butyl ester (2.0 g, 7.09 mmoi) in dichioromethane (20 ml) was added trifluoro acetic acid (10 ml). The resulting reaction mixture was stin-ed at room temperature for 2 h. The volatiles were evaporated in yaeuQ affording 1.6 g (100 %) of 4-(methoxyoxalyl-amino)-2-methyl-1H-pyrrole-3-carbpxylic acid as a solid. To a solution of the above pyrrole-3-carboxylic acid (1.2 g. 5.31 mmol) in ethanol (100 ml) was added a solution of sodium hydroxide (0.47 g. 11.7 mmol) in water (50 ml). The resulting reaction mixture was stirred at room temperature for 18 h. The volatiles were evaporated in vacuo and the residue dissolved in water (100 ml). To the aqueous phase was added concentrated hydrochloric acid to pH = 1. The suspension was washed with ethyl acetate (50 ml) and dichloromethane (50 ml) and the precipitate was filtered off and dried in vacuo at 50 ""C for 2 h. The solid was dissolved in isopropanol (100 ml), filtered and evaporated in vacgo affording 0.4 g (36%) of the title compound as a solid. Calculated for CgHaNsOg, 0.1 x HjO ; C, 44.91 %; H, 3.86 %: N. 12.98 %. Found: C, 45.06 %; H, 3.89 %; N. 12.72 %. 1-Benzyl-3-(Qxalvl-aminoV1 H-pvrazQle-4-carboxylic acid: To a stin-ed solution of 3-amino-1H-pyra2ole-4-carboxylic acid ethyl ester (5,0 g. 0.032 mol) and triethylamine (9 ml) in dry tetrahydrofuran (150 ml) at 0 ''C was added dropwise ethyl oxalyl chloride (5.3 g, 0.039 mol). The resulting reaction mixture was stinted at room temperature for 18 h. An additional portion of ethyl oxalyl chloride (5.3 g, 0.039 mol) was added dropwise and the reaction mixture was stin-ed at room temperature for an additional 18 h. The volatiles were evaporated in vacuo and the residue dissolved in a mixture of water (200 ml) and ethyl acetate (200 ml). Undissolved matter was filtered off and dried in vacuo at 50 °C for 18 h affording 4.0 g (49 %) of 3"(ethoxyoxalyi-amino)-1H-pyrazole-4-carboxylic acid ethyl ester as a solid. The organic phase separated and washed with saturated aqueous sodium chloride (100 ml), dried (MgS04), filtered and the solvent evaporated in vacuo affording 3,7 g (45%) of 3-(ethoxyoxalyl-amino)-1H-pyrazo(e-4-carboxylic acid ethyl ester as a solid. A total yield of 7,7 g (94 %) was obtained. To a solution of the above pyra20le-4-carboxyiic acid ethyl ester (3.7 g, 0.015 mol) in dry N,N-dimethylformamide (75 ml) was added sodium hydride (640 mg, 0.016 moi, 60 % in mineral oil). The resulting reaction mixture was stirred at room temperature for 0.5 h. To the reaction mixture was added benzyl bromide (2.7 g, 0.016 mol) and the mixture was stirred at 50 °C for 4 h. Water (100 ml) was added and the reaction mixture was extracted with diethyl ether (2 x 100 ml). The combined organic extracts were washed with water (100 ml) saturated aqueous sodium chloride (2 x 50 ml), dried (MgS04), filtered and the solvent evaporated in yasuo. The residue (3,8 g) was purified on silicagel (800 ml) using a mixture of ethyl acetate and heptane (1:1) as eluent. Pure fractions were collected and the solvent evaporated in vacua affording 0.9 g (18 %) of 1-benzoyl-3-(ethoxyoxaiyl-amino)-1H-pyra20le-4-carboxylic acid ethyl ester as a solid. Unpure fraction were collected and the solvent evaporated in \/a£uo. The residue (1.0 g) was crystallised from diethyl ether (30 mi), filtered off and dried in vacuo at 50 °C for 2 h affording 0.9 g (18 %) of 1-benzoyl-3-(ethoxyoxaiyl-amino)-1H-pyrazole-4-carboxylic acid ethyl ester as a solid. A total yield of 1.8 g (36 %) were collected. To a solution of the above 1 H-pyrazole-4-carboxylic acid ethyl ester (0.9 g, 2.61 mmol) in ethanoi (50 ml) was added a solution of sodium hydroxide (0.26 g, 6.51 mmol) in water (25 ml). The resulting reaction mixture was stirred at room temperature for 60 h. The volatiles were evaporated in vacuo and the residue dissolved in water (100 ml). To the aqueous phase was added concentrated hydrochloric acid to pH = 1. The precipitate was filtered off and dried in ygcuo at 50 °C for 18 h. affording 0.55 g (73 %) of the title compound as a solid. M.p.: 189-191 °C: Calculated for C13H11N3O5, 1.75 x H2O; C, 48.68 %; H, 4.56 %; N. 13.10 %. Found: C, 48.81 %; H. 4.17 %; N, 12.84 %. 4-CvclQhexvl-2-(oxalvl-aminoVthiophene-3-carboxvlicacid: To a solution of 4-cyclohexyi-2-(ethoxyoxalyl-amino)-thiophene-3-carboxylic acid (60 mg, 0.18 mmol) in ethanol (10 ml) was added a solution of 1N sodium hydroxide (0.5 ml) in water (5 ml). The resulting reaction mixture was stirred at room temperature for 18 h. To the reaction mixture was added concentrated hydrochloric acid to pH = 1. The precipitate was filtered off and dried in vacuo at 50 °C for 18 h. affording 30 mg (55 %) of the tilig compound as a solid. M.p.: > 250 °C: Calculated for C13H15NO5S, 1.5 x H2O; C. 48.14 %; H, 5.59 %; N. 4.32 %. Found: C, 47.84 %; H. 9.92 %; N, 4.21 %. 2-(Oxalvl-amJnQM-Dh6nvl-thioDhene-3-carboyvlicacid- To a solution of 4-phenyl-2-{ethoxyoxalyl-amino)-thiophene-3-carboxyiic acid etinyt ester (2.2 g, 6.33 mmol) in ethanol (50 ml) was added sodium liydroxide (630 mg, 15.83 mmoi) in water (25 ml). The resulting reaction mixture was stirred at room temperature for 18 h., the volatiles were evaporated in vacuo and the residue was dissolved in water (100 mi) and washed with diethyl ether (2 x 100 ml). To the aqueous phase was added concentrated hydrochloric acid to pH = 1 and the resulting mixture was extracted with diethyl ether (2 x 100 ml). The combined organic phases were washed with saturated aqueous sodium chloride (100 ml), dried (MgS04), filtered and evaporated in vacuo affording 0.8 g of a mixture of mono ethyl ester and title compound according to NMR. The product mixture was dissolved in a mixture of ethanol (40 ml), water (20 ml) and sodium hydroxide (400 mg) and the resulting mixture was stirred at room temperature for 18 h, the volatiles were evaporated in vacuo and the residue was dissolved in water (50 ml) and washed with diethyl ether (50 ml). To the aqueous phase was added concentrated hydrochloric acid to pH = 1 and the precipitate was filtered off, washed with diethyl ether and dissolved in 2-propanol (25 ml). Undissolved matter was filtered off and the organic phase evaporated in vacuo affording 180 mg (10 %) of the title compound as a solid. M.p.: 196-198"0: Calculated for C13H9NO5S, 0.5 H2O; C, 52.00 %; H, 3.36 %; N. 4.66 %. Found: C, 52.21 %; H, 3.44 %; N, 4.50 %. 5-(4-Fluoro-DhenylV3-(oxalyl-aminoVthiophene-2-carboxyiic acid: A solution of 5-{4-fluorophenyl)-3-aminothiophene-2-carboxylic acid methyl ester (1.0 g, 4.0 mmol) and triethytamine (11.1, 80 mmol) in dry tetrahydrofuran (40 ml) was cooled on ice and dropwise added ethyl oxalyl chloride (1.2 g, 9.0 mmol). After stirring for 2h, the reaction mixture was filtered and the solvent evaporated in vacuo. The residue was dissolved in di-chloromethane, washed with 0.1 N hydrochloric acid (2 x-dicared). The organic phase was dried (MgS04), filtered and the solvent evaporated in vacuo. The residue was submitted to flash chromatography using toluene/ethyl acetate (19:1) as eiuent, to give 1.19 g (85 %) of 5-(4-fluorophenyl)-3-(ethoxyoxalyiamino)-thiophene-2-carboxylic acid ethyl ester. To a solution of 5-(4-fluorophenyl)-3-(ethoxyoxalylamino)-thiophene-2-carboxylic acid ethyl ester (1.19 g, 3,4 mmol) in methanol (150 ml) was added 2 N sodium hydroxide (20 ml). The reaction mixture was stirred at 60 °C for 18 h. The voiatiles were evaporated in vacuo. The residue was added water and IN hydrochloric acid (pH = 1), and the product extracted with a mixture of dichloromethane/2-propanol. The organic phases were dried (MgS04), filtered and the solvent evaporated in vacuo. The product was recrystallised from methanol/water to give 619 mg (67 %) of the title compound as a solid. Calculated for C13H8FNO5S, 0.5 HjO; C. 49.06 %; H, 2.83%; N, 4.40 %. Found: C, 49.06 %; H. 2.72%; N. 4.31%. In a similar way as described in Example 43 the following compounds were prepared. 5-(4-lsobutvl-Dhenvn-3-(Qxalvl-amino"thiQphene-2-carbQxvlicacid: Calculated for CiyH"NOsS, 0.33 x HjO; C, 57.79 %; H, 5.00 %; N, 3.96 %. Found: C, 57.79 %; H, 5.08 %; N. 3.89 %. EXAMPLE 45 5-f4-Chloro-Dhenvl')-3-(oxalvl-amino)-thiophene-2-carboxylic acid, mono sodium salt: M.p.:>250°C; Calculated for CaHrCINOsSNa, 1x HjO; C, 42.63 %; H, 2.52 %; N, 3.55 %. Found: C, 42.69 %; H, 2.48 %; N, 3.83 %. 4-(Oxalvl-amino)-[2.3]-bitliiophenyl-5-carboxviicacid; M.p.: 220 - 222 °C: Calculated for CHrNOsSz; C. 44.44 %; H, 2.37 %; N. 4.71 %. Found: C, 44.17 %; H, 2.43 %; N, 4.54 %. EXAMPLE 47 3-fOxalvl-aminoV5-Dhenvl-thioDhene-2-carboxylic acid, mono sodium salt; M.p.:>250°C: Calculated for CiaHaNOgSNa, 1.6 x H2O; C. 45.64 %; H, 3.30 %; N, 4.09 %. Found: C, 45.25 %; H, 2.93 %; N, 3.92 %. 3-(Oxalvl-aminoMhioDhene-2-carboxviic acid, mono sodium salt: M.p.: > 250 °C: Calculated for CyHyNOsSNa, 1.5 x H2O; C, 31.83 %; H, 2.67 %; N, 5.30 %. Found: C, 32.23 %; H. 3.14 %; N, 5.15 %. EXAMPLE 49 4-Methvl-3-(oxalvl-amino"thioDhene-2-carboxylic acid, mono sodium salt: M.p.: 232 - 234 °C: Calculated for CsHgNOsSNa, 1.5 x H2O; C, 34.54 %; H, 3.26 %; N, 5.03 %. Found: C. 34.58 %; H, 3.30 %; N, 4.81 %. 3-(Oxalyl-amino)-5-('4-phenoxv-phenvn-thiODhene-2-carfaoxvlicacid M.p.: 230 °C (decomp.) Calculated for CigHiaNOsS, 1.25 x HjO C, 56.22 %; H, 3.85 %; N, 3.45 %. Found: C, 56.00 %; H, 3.57 %; N, 3.39 %. 5-"4-Ben2vloxv-ohenvlV3-(oxalyl-aminoMhiophene-2-carboxvlicacid M.p.: 210 °C (decomp.) Calculated for CzoHisNOeS C, 60.45 %; H, 3.80 %; N, 3.52 %. Found: C, 59.94 %; H, 3.79 %; N, 4.45 %. 5-"4-(4-Methoxv-Dhenoxv"-DhenvlV3-(oxalvl-amino"-thiophene-2-carboxvlicacid M.p.: 215 °C (decomp.) Calculated for C20H15NO7S, 1.5 H2O C, 54.54 %; H. 4.12 %; N, 3.18 %. Found: C, 54.80 %; H, 3.88 %; N, 3.15 %. 5-(4-Hvdroxv-phenvn-3-(oxalvl-amino)-thiophene-2-carboxvlic acid mono sodium salt M.p.: 205 - 206 °C Calculated for CiaHgNOsSNa,, 0.75 x HjO C. 45.42 %; H, 3.08 %; N, 4.07 %. Found: C, 45.11 %; H, 3.16 %; N, 3.98 %. To 3-nitrophenethyl alcohol (102 mg, 0.61 mmol) in dichloromethane (2.2 ml) at room temperature under nitrogen was added a solution of Dess-Martin periodinane reagent (285 mg, 0.67 mmol) in dichloromethane (2.7 ml). The reaction was stirred at room temperature under nitrogen for 45 minutes, at which time tic analysis (hexane/ethyl acetate, 50/50) indicated the reaction was complete. Diethyl ether (5.0 ml) was added followed by a solution of 10 % sodium sulfite/saturated sodium bicarbonate (1:1, 5.0 ml). The emulsion gradually turned to a clear heterogeneous solution after standing for 10 minutes. Additional dichloromethane was added and the organic phase was washed with water (5 ml), dried (MgS04), filtered and evaporated in yaeuo which afforded 100 mg (100 %) of 3-nitrophenyl-acetaldehyde as a clear oil. The aldehyde was used without further purification in the next step. 'H NMR (400 MHz. CDCI3) 5 3.90 (s. 2H), 7.65 (d, 2H), 8.20 (s, 1H), 8.25 (m, 1H). 9.90 (s. 1H). A mixture of fert-butyl cyanoacetate (67 mg, 0.48 mmol), 3-nitrophenyl acetaldehyde (86 mg, 0.52 mmol), triethylamine (73 )il, 0.52 mmol) and elemental sulfur (17 mg, 0.52 mmol) in N,N-dimethylformamide (0.5 ml) was stirred at 60 °C for 1.5 h. After cooling to room temperature, the dark solution was diluted with ethyl acetate and washed with water (3x5 mi). The organic layer was dried (MgS04), filtered and the solvent evaporated in vacuo which afforded crude 2-amino-5-(3-nitro-phenyl)-thiophene-3-carboxylic acid tert-butyl ester (191 mg). Purification by preparative TLC (hexane/ethyl acetate, 80/20) afforded 74 mg (49 %) of 2-amino-5-(3-nitro-phenyl)-'thiophene-3-carboxylic acid tert-butyl ester as a solid. "H NMR (400 MHz, CDCI3) 6 1.56 (s, 9H), 6.05 (s. 2H), 7.20 (s, 1H), 7.40 (t, 1H), 7.68 (d, 1H), 7.90(d, 1H), 8.25(s, 1H). A solution of 2-amino-5-(3-nitro-phenyl)-thiophene-3-carboxylic acid tert-buty\ ester (66 mg, 0.21 mmol), imidazol-1-yl-oxoacetic acid ferf-butyi ester (202 mg, 1.03 mmol) and triethy-lamine (40.4 )al, 0.21 mmol) in tetrahydrofuran (0.5 ml) was stirred at room temperature for 3 h. The volatiles were evaporated in vacuo and the residue was dissolved in ethyl acetate and washed successively with water (3x5 ml) and brine (5ml). The organic layer was dried (Na2S04), filtered and the solvent evaporated in vacuo affording crude product. Purification by preparative TLC gave 91 mg (98 %) of 2-(feAt"butoxyoxalyl-amino)-5-(3-nitrophenyl)-thiophene-3-carboxylic acid fert-butyl ester as a solid. "H NMR (400 MHz. CDCI3) 5 1.54 (s. 9H). 1.62 (s, 9H). 7.5 (s, 1H). 7.55 (t, 1H, J = 8.4 Hz), 7.84 (d. 2H, J = 8.4 Hz), 8.16 (d, 1H. J = 8.4 Hz). 8.45 (s, 1H). MSm/z:447(M-1). The above 3-nitrophenyl-thiophene (85 mg, 0.19 mmol) was dissolved in a 20 % solution of triftuoroacetic acid in dichloromethane (3.0 mi) and stirred at room temperature for 6 h. The solution was co-evaporated in vacuo with toluene affording 64 mg (100 %) of the tltig compound. 'H-NMR (400 MHz, CD3OD) 5 7.71 (t, 1H, J = 8,25 Hz), 7.8 (s, 1H). 8.1 (d, 1H, J = 7.5 Hz), 8.2 (d, 1H, J = 9Hz), 7.86(m, 1H). MSm/z: 335 (M-1). The following examples were prepared in a similar way as described in Example 54. C, 54.94 %; H, 3.63 %; N, 4.43 %. 5-<'Naphthalen-2-ylV2-(oxalyl-amino)-thiODhene-3-carboxylic acid: 'H NMR (400 MHz, CD3OD) 5 7.42 - 7.49 (m, 2H), 7.65 (d, 1H. J = 4.5 Hz), 7.75 (m, 1H). 7.8 - 7.9 (m, 3H), 8.04 (d, 1H ,J = 7.5 Hz). MSm/z:340(M-1). 'H NMR (400 MHz, CD3OD) 5 7.3 (t, 1H, J = 4.5 Hz), 7.38 (t, 1H, J = 4.5Hz), 7.54 (s, 1H), 7.61 (m, 3H). Calculated for C13H9NO5S, 1 x H2O; C, 47.13 %; H, 3.04 %; N, 4.23 %. Found: C, 47.34 %; H, 3.53 %; N, 4.20 %. 5-(?-Fkiorn-phenvlV2-(oxalvl-aminoVthiophene-3-carboxvlicacid: "H NMR (400 MHz, CD3OD) 6 7.18 - 7.23 (m, 2H). 7.30 (m, 1H), 7.63 -7.69 (m, 2H). MS/77/2:308(M-1). 5-(3-Chloro-phenyn-2-(oxalvl-aminoMhioDhene-3-carboxvlicacid: Yield: 99 %. 'H NMR (400 MHz, CD3OD) 5 7.28 (m, 1H), 7.38 (m, 1H), 7.52 - 7.61 (m, 3H). MSm/2:324(M-1). EXAMPLE 60 5-(2.4-Dichloro-phenvn-2-(oxalvl-amino)-thiophene-3-carboxylic acid: "H NMR (400 MHz, CD3OD) 5 7.37 (m, 1H), 7.39 (m, 1H), 7.52-7.58 (m, 3H). MSm/z: 358 (M-1). 5-(4-Bromo-phenvl)-2-(;oxalvl-amino)-thiophene-3-carboxylicacid: 'H NMR (400 MHz, CD3OD) 5 7.51 (s, 4H), 7.54 (s, 1H). MS/77/z:370(M-1). 5-Ethvl-2-(oxalvl-aminoVthioDhene-3-carboxvlicacid: 'H NMR (400 MHz, CD3OD) 5 1.35 (t, 3H, J = 3.75), 2.95 (q, 2H), 7.05 (s, 1H). MS m/z. 170.2 (M-73) (-COCOOH), 228.1 (M-1). 5-Methvl-2-foxalvl-amino)-thiODhene-3-carboxvlicacid: 'H NMR (400 MHz, CD3OD) 5 2.6 (s, 3H), 7.05 (s, 1H). MS m/z: 228 (M-1). 5-(3-Methyl-phenyn-2-(oxalvl-amino)-thiophene-3-carboxylic acid: 'H NMR (400 MHz, CD3OD) 5 2.39 (s, 3H), 7.12 (d, 1H, J = 8 Hz), 7.25 (t, 1H, J = 7.5 Hz), 7.4 (m, 2H), 7.5 (s, 1H). MS m/z 304, 232 (M-1). 'H NMR (400 MHz, CD3COCD3) 5 7.4 (t, 1H , J = 2 Hz), 7.52 (t, 1H, J = 2 Hz), 7.7 (m, 3H), 7.9 (t, 1H, J = 2 Hz), 8.25 (d, 1H, J = 2 Hz), 8.5 (s, 1H). MS m/z 380.5 (M-1). 5-(2-(4-Chloro-Dhenvi')-ethvl')-2-foxalyl-amino')-thiophene-3-carboxvlic acid, mono sodium salt M.p.: > 250 °C Calculated for CisHnNiCliOsSiNa,, 0.75 x H,0 C, 46.28 %; H, 3.24 %; N, 3.60 %. Found; C, 46.17 %; H, 3.38 %; N, 3.40 %. 2-<'Oxalyl-amino)-thiophene-3-carboxvlic acid: M.p.: 225 - 228 °C Calculated for C7H5N,OsSi, 1.25 x H2O C, 35.37 %; H, 3.18 %; N, 5.89 %. Found: brine (10 ml), dried (MgS04) and filtered. The solvent was evaporated in vacuo and the resi-due was washed with cold ethyl acetate (2 x 1 mi) affording 52 mg of 2-amino-5-(1,3-dioxo-1,3-dihydro-isoindol-2-ylmethyt)-thiophene-3-carboxylic acid fert-butyl ester as a solid. A total yield of 241 mg (91 %) was obtained. "H NMR (400 MHz. CDCI3) 5 7.86 (dd, 2H, J = 7.2, 4 Hz), 7.72 (dd, 2H, J = 7.2, 4 Hz). 6.97 (s, 1H), 5.83 (s, 2H. NH2), 4.78 (s, 2H). 1.56 (s, 9H) To a stirred solution of the above thiophene (100 mg, 0.28 mmol) in tetrahydrofuran (2 ml) was added a solution of imidazol-1-yl-oxo-acetic acid fe/t-butyl ester (60 mg, 0.31 mmol) in tetrahydrofuran (1 ml). The mixture was stirred at room temperature for 3 h. The solvent was evaporated in vacuo. The residue was dissolved in ethyl acetate (50 ml), washed with 0.5 N hydrochloric acid (2x5 ml), saturated sodium bicarbonate (2x5 ml), brine (5 ml), dried (MgSOO and filtered. The solvent was evaporated in vacuo affording 130 mg (96 %) of 2-(fert-butoxyoxalyl-amino)-5-(1,3-dioxo-1,3-dihydro-isoindol-2-ylmethyi)-thiophene-3-carboxylic acid te/t-butyl ester as a solid. "H NMR (400 MHz, CDCI3) 5 12.23 (s, 1H), 7.87 (dd, 2H, J = 7.2, 4 Hz), 7.73 (dd, 2H, J = 7.2, 4 Hz), 7.24 (s, 1H), 4.93 (s, 2H), 1.60 (s, 9H), 1.57 (s, 9H). To a solution of trifluoroacetic acid (1 ml) in dichloromethane (1 ml) was added the above di-fe/t-butyl ester (100 mg, 0.21 mmol). The solution was stirred at room temperature for 1 h. The solvent was evaporated in vacuo. The residue was washed with dichloromethane (3 x 1 ml) which afforded 63 mg (82 %) of the title compound as a solid. "H NMR (400 MHz, DMSO-dg) 5 12.05 (s, 1H), 7.89 (m, 2H), 7.87 (m, 2H), 7.10 (s, 1H), 4.83 (s. 2H). MSm/2:373(M-1). In a similar way as described in Example 43 the following compounds were prepared, EXAMPLE 69 5-(3.4-Dimethoxv-phenvl'>-3-(oxalvl-amino)-thiophene-2-carboxylicacid M.p.:230-231 °C Calculated for CISHISNIOTSI, 1 x H2O C, 48.78 %; H, 4.09 %; N, 3.79 %. Found: C, 49.01 %; H, 3.75 %; N, 3.79 %. EXAMPLE 70 5-(3-Methoxv-Dhenyn-3-(oxalyl-aminoVthiophene-2-carboxylicacid M.p.:217-218°C Calculated for CuHnNiOgSi, 0.75 x HjO C, 50.22 %; H, 3.76 %; N. 4.18 %. Found: C, 50.02 %; H, 3.73 %; N, 4.16 %. EXAMPLE 71 5-(3.5-Dimethoxv-phenvlV3-(oxalyl-amino)-thiophene-2-carboxvlicacid M.p.:223-225°C Calculated for CsHiaNiOyS,, 1.25 x H2O C, 48.19 %; H, 4.18 %; N, 3.75 %. Found: C, 48.25 %; H, 4.10 %; N, 3.39 %. 5-(3-Nitro-phenyl)-3-(oxalvl-anninoVthiophene-2-carboxylicacid M.p.:>250°C Calculated for Ci3H7N,07SiNa,, 1.25 x HjO C, 41.01 %; H, 2.51 %; N, 7.36 %. Found: C, 41.03 %; H, 2.38 %; N, 7.17 %. EXAMPLE 73 5-C3-Amino-phenvn-3-Coxalyl-amino)-thiophene-2-carboxvlic acid M.p.: > 250 "C Calculated for C13H1QN2O5S,, 0.5 x H2O C, 49.52 %; H. 3.52 %; N, 8.88 %. Found: C, 49.48 %; H, 3.44 %; N, 8.71 %. M.p.: 220 - 221 °C Calculated for Ci4H,iNi06S„ 0.4 x HjO C, 51.19 %; H. 3.62 %; N, 4.62 %. Found: C, 51.29 %; H, 3.53 %; N, 3.96 %. Calculated for C13H10N2O5S,. 0.5 x H2O C, 49.52 %; H, 3.52 %; N, 8.88 %. Found: C. 49.40 %; H, 3.87 %; N. 8.23 %. 5-(4-(2-(2-Methoxv-phenyn-2'OXO-ethoxvVDhenvn-3-(oxalvl-arnino)-thiophene-2-carbQXVIic acid, dtsodium salt To a solution of 3-(ethoxyoxalylamino)-5-(4-hydroxyphenyi)thiophene-2-carboxylic acid methyl ester (524 mg, 1.5 mmol) and potassium carbonate (275 mg, 2.0 mmol) in N,N-dimethylformamide (35 ml) was under an nitrogen atmosphere added co-brom-2-methoxyacetophenon (460 mg, 2.0 mmol). After stirring for 3 h, the precipitate caide 3-(ethoxyoxalylamino)-5-(4-(2-(2-methoxyphenyl)-2-oxy-ethoxy)phenyl)-thiophene-2-carboxyiic acid methyl ester (1.0 g) was filtered off. To a solution of crude 3-(ethoxyoxalylamino)-5-(4-(2-(2-methoxyphenyl)-2-oxy-ethoxy)phenyl)-thiophene-2-carboxylic acid methyl ester (0.5 g) in methanol (15 ml) was added 1N sodium hydroxide (10 ml). After stirring at 65 °C for 3h, the product was isolated by filtration and washed with a mixture of water and ethanol (1:1) affording after drying 290 mg of the title compound as a solid. M.p.: 286 - 287 °C. Calculated for CssHigNiOgSiNas; C. 50.19 %; H, 3.42 %; N, 2.66 %. Found: C. 51.18 %; H, 3.42 %; N, 2.58 %. 5-(4-CarboxvmethQxv-phenylV3-foxalyl-aminoVthiophene-2-carboxylic acid, trisodium salt: To a solution of 3-(ethoxyoxalytamino)-5-(4-hydroxyphenyl)thiophene-2-carboxylic acid methyl ester (307 mg, 1.0 mmol) and potassium carbonate (166 mg, 1.2 mmol) in N,N-dimethylformamide (5 ml) was added 2-bromoacetamide (165 mg, 1.2 mmol). After stimng at 50 °C for 16 h, the reaction mixture was quenched by addition of water, and the precipitate 5-(4-carbamoylmethoxy-phenyl)-3-(ethoxyoxaiytamino)-thiophene-2-carboxylicacid methyl ester (70 mg) was isolated by filtration. The pH of the filtrate was adjusted to 1-2 with 1 N hydrochloric and the semi hydrolysed product, 5-(4-carbamoylmethoxy-phenyl)-3-(oxalylamino)-thiophene-2-carboxylic acid methyl ester (300 mg), was isolated by filtration. To a suspension of 5-(4-carbamoylmethoxy-phenyl)-3-(oxaiyiamino)-thiophene-2-carboxylJc acid methyl ester (295 mg, 0.78 mmol) in methanol (5 ml) and water (5 ml) was added 1 N sodium hydroxide (2 ml). After stirring for 5 days the precipitate was filtered of affording 105 mg (88 %) of the titlg compound as a solid. M.p.:>300"C. Calculated for CigHisNiOioSiNaa; C, 38.56 %; H, 2.59 %; N, 3.00 %. Found: C, 38.73 %; H. 2.74 %; N, 3.06 %. In a similar way as described in Example 77 the following compound was prepared: 5~(4-(4-FluorQ-ben2vloxv)-phenvn-3-(oxalyl-aminoVthiophene-2-carbQXvlic acid: 'H NMR (300 MHz, DMSO-de) 5 5.15 (s. 2H). 7.1 (d, 2H). 7.25 (t. 2H). 7.55 (q, 2H), 7.7 (d, 2H), 8.2(s, 1H). SP/MS: 415 (M+. 12%), 372, 353, 299. 218, 190, 162, 109 (100%). EXAMPUg 79 5-((2-(1.3-Dioxo-1.3-dihvdrQ-isoindQl-2-vn-acetylaminoVmethvlV2-""" 3-carboxvlic acid: To a solution of 2-(fert-butoxyoxalyl-amino)-5-(1.3-dioxo-1,3-dihydro-isoindol-2-yl-methyl)-thiophene-3-carboxylic acid te/t-butyl ester (0,4 g, 0.82 mmol, prepared as described in example 30) in dichloromethane (2 ml) was added aniiydrous hydrazine (28 ml, 0.9 mmol) and the mixture stirred at ambient temperature for 19 h under nitrogen. An additional portion of hydrazine (84 ml, 2.7 mmol) and dichloromethane (5.5 ml) was added and stirring was continued for an additional 88 h. Dichloromethane (50 ml) was added and the reaction mixture was placed in a sonicator for 20 min and filtered through Celite. The filtrate was evaporated iQ vacuo affording 0.24 g (82 %) of 5-aminomethyl-2-(fert-butoxyoxalyl"amino)-thiophene-3- carboxylic acid fe/t-butyl ester as a solid which was used without further purification in the next step. To a solution of (1,3-dioxo-1,3-dihydro-isoindol-2-yi)-acetic acid (0.17 g, 0.82 mmol), 1-hydroxybenzotriazole (0.133 g, 0.98 mmol) and 2,6 lutidine (0.4 mi) in dry acetonitrile (10 ml) under nitrogen cooled in an ice bath was added 1-(3-dimethylaminopropyl)-3-ethylcarbodiimide hydrochloride (0.21 g, 1.1 mmol) and the solution was stirred for 0.5 h. 5-Aminomethyl-2-(tert-butoxyoxalyl-amino)-thiophene-3-carboxylic acid fert-butyl ester (0.24 g, 0.68 mmol) was added, the cooling bath removed, and the solution stirred at ambient temperature for 20 h. The volatiles were evaporated in vacuo and the residue dissolved in di-chloromethane and washed with saturated aqueous sodium bicarbonate and 1N hydrochloric acid, dried (Na2S04) and the solvent evaporated in vacuo. The residue (0.18 g) was dissolved in dry tetrahydrofuran (6 ml) under nitrogen, imidazol-1-yl-oxo-acetic acid fe/t-butyl ester (0.25 g, 1.3 mmol) was added and the solution stirred at ambient temperature for 17 h, the solvent evaporated in vacuo and the residue dissolved in a mixture of dichloromethane and saturated aqueous sodium bicarbonate solution. The organic layer was dried (Na2S04) and the solvent evaporated in vacuo. The residue was subjected to chromatography on silica gel affording 0.1 g of 2-(tert-butoxyoxaiyl-amino)-5-((2-(1,3-dioxo-1,3-dihydro-isoindol-2-yl)-acetylamino)-methyl)-thiophene-3-carboxyiic acid tert-huty\ ester, 'H NMR (400 MHz, CDCI3) 5 12.3 (bs, 1H), 7.9 (m, 2H), 7.8 (m, 2H), 7.1 (s, 1H). 6.5 (m. 1H), 4.6 (m, 2H). 4.4 (s, 2H,), 1.8 (s, 9H). 1.6 (s, 9H). To 2-(fe/t-butoxyoxalyl-amino)-5-((2-(1,3-dioxo-1,3-dihydro-isoindol-2-yl)-acetyl-ami-no)- methyl)-thiophene-3-carboxylic acid fert-butyl ester (0.1 g, 0.18 mmol) was added 20 % trifiuoroacetic acid in dichloromethane (4 ml) and the reaction mixture was stirred at ambient temperature under nitrogen for 14 h. The volatiles were evaporated in vacuo and the residue chased with dichloromethane until a solid remained. The precipitate was filtered off and dried in vacuo for 18 h affording in quantitative yield the tille compound as a solid. Mp. 243-244°C(dec). MSm/z:430(M-1). "H NMR (400 MHz, DMSO-dg) 5 12.1 (s. 1H), 8.9 (s. 1H), 7.8 - 7.9 (m, 4H), 7.1 (s. 1H), 4.4 (m, 2H). 4.2 (s, 2H). 6-Benzovl-2-(oxalvl-aminoM.5.67-tetrahvdro4hienof2.3-c]pvridine-3-carboxylicacid. mono sodium salt: A mixture of N-benzoyl-4-piperidone (20.0 g, 0.1 mol), ethyl cyanoacetate (10.9 ml, 0.1 moi), ammonium acetate (2.0 g) and acetic acid (6 ml) in benzene (100 ml) was heated at reflux temperature in a 3-nacked reaction flask equipped with a Dean-Stark water trap for 1 h. The cooled reaction mixture was diluted with ethyl acetate (100 ml) washed with water (3 x 100 ml), saturated aqueous sodium chloride (80 ml), dried (MgSO" filtered and evaporated in vacuo affording quantitative yield of (1-benzoyl-piperidin-4-ylidene)-cyano-acetic acid ethyl ester as a slowly crystallising oil. A mixture of "the above benzoyl-piperidin-4-ylidene (10.0 g, 0.034 mol), sulphur (1.13 g, 0.035 mol), morpholin (6.5 ml) in ethanol (35 ml) was heated at 50 °C for 2 h and stirred at room temperature over night. The precipitate was filtered off and washed with 96 % ethanol (3 x 50 ml), diethyl ether (3 x 50 ml) and dried in vacuo which afforded 9.27 g (84 %) of 2-amino-6-benzoyl-4,5,6,7-tetrahydro-thieno[2,3"-c]pyridine-3-carboxylic acid ethyl ester as a solid. To a stirred solution of the above 4,5,6,7-tetrahydro-thieno[2,3-c]pyridine-3-carboxylic acid ethyl ester (5.0 g, 0.015 mol), triethylamine (4.21 ml, 0.03 mol) in dry tetrahydrofuran (30 ml) at 0 "C was added dropwise a solution of ethyl oxalyl chloride (1.9 ml, 0.017 moi) in dry tetrahydrofuran (20 ml). The resulting reaction mixture was stirred at room temperature for 18 h, pored into ice water (300 ml) and extracted with ethyl acetate (3 x 100 ml). The combined organic extracts were washed with saturated aqueous sodium chloride (100 ml), dried (MgSOd) filtered and evaporated in vacua affording 4.2 g (84 %) of 6-benzoyl-2-(ethoxyoxalyl-amino)-4,5,6 J-tetrahydro-thieno[2,3-c]pyridine-3-carboxylic acid ethyl ester as a crystallising oil. To a solution of the above thieno[2.3-c]pyridine-3-carboxylic acid ethyl ester (4.2 g, 9.76 mmol) in ethanoi (100 ml) was added a solution of sodium hydroxide (0.9 g, 21.46 mmoi) in water (100 ml). The resulting reaction mixture was stirred at room temperature for 18 h. The volatiles were evaporated in ya£UQ and the residue dissolved in water (100 ml) and washed with ethyl acetate (2 x 100 ml). To the aqueous phase was added concentrated hydrochloric acid to pH = 1 and the precipitate was filtered off and washed with water (2 x 50 ml), diethyl ether (2 x 30 ml) and dried in vacuo at 50 °C affording 2.9 g (79 %) of the tills compound as a solid. By a similar procedure as described in Example 81 the following compounds have been prepared. Calculated for Ci"H"iNOgS; C, 49.07 %; H. 4.12 %; N, 5.20%. Found: C. 49.87 %; H, 4.37 %; N. 5.06%. EXAMPLE 83 6-Ben2yl-2-(oxalvl-aminoM.5.6.7-tetrahvdro-thieno[2.3-c]pvridine-3-carboxvlicacici: Calculated for C17H16N2O5S, 1.75 HjO; C, 52.10 %; H, 5.01 %; N. 7.15 %. Found: C, 52.11 %; H, 4.81 %; N, 7.01 %. 6-Methvl-2-(oxalyl-aminoM.5.6.7-tetrahydro-thienof2.3-c]pyridine-3-carboxylJcacid: M.p.: > 250 °C Calculated for C11H12N2O5S, 0.6 H2O; C, 44.77 %; H, 4.51 %; N, 9.49 %. Found: C, 44.54 %; H, 4.17 %; N, 9.21 %. 2-(Oxalvl-aminoV4.7-dlhvdro-5H-thienof2.3-c1pvran-3-carbQxylic acid, mono sodium salt: M.p.: > 250 °C Calculated for CioHgNiOgSNa, 0.75 x HjO; To a solution of the above thieno[2,3-c]pyridine-3-carboxylic acid ethyl ester (4.2 g, 9.76 mmol) in ethanol (100 ml) was added a solution of sodium hydroxide (0.9 g, 21.46 mmol) in water (100 ml). The resulting reaction mixture was stirred at room temperature for 18 h. The volatiles were evaporated in vacuo and the residue dissolved in water (100 ml) and washed with ethyl acetate (2 x 100 ml). To the aqueous phase was added concentrated hydrochloric acid to pH = 1 and the precipitate was filtered off and washed with water (2 x 50 ml), diethyl ether (2 x 30 ml) and dried in vacuo at 50 °C affording 2.9 g (79 %) of the title CQmpound as a solid. M.p.: Amorph: Calculated for CuHiaNzOeSiNai. 1 x HjO ; C, 49.28 %; H. 3.65 %; N, 6.76%. Found: C, 49.31 %; H, 3.86 %; N, 6.53%. By a similar procedure as described in Example 81 the following compounds have been prepared. M.p.: 230-231 °C: Calculated for Ci,H,,N05S; C, 49.07 %; H, 4.12 %; N. 5.20%. Found: C. 49.87 %; H, 4.37 %; N, 5.06%. 2-<'Oxalvl-aminQM.5.6.7-tetrahvdro-thieno[2.3-c]pvridine-3-carboxvlic acid, hydrochloride: 4-0x0-1-piperidine carboxylic acid tert-butyl ester was used as starting material. The Boc-group was removed using 25 % trifluoroacetic acid in dichloromethane. M.p.:>250°C Calculated for C10H10N2O5S, 1 HCI, 0.5 x H2O; C, 38.35 %; H, 4.34 %; N, 8.64 %, Found: C. 38.04 %; H, 3.83 %; N, 8.87 %. 2-(Oxalvl-amino"-6-Dvridin-2-vlmethvl-4 5.6.7-tetrahydrQ-thienof2.3-c]Dvridine-3-carboxvlic acid; To a mixture of 2-{ethoxyoxaiyl-amino)-4,5,6J-tetrahydro-thieno[2,3-c]pyridine-3-carboxylic acid ethyl ester trifluoroacetic acid salt (1.5 g, 3.40 mmol), potassium carbonate (2.4 g, 17.1 mmol), potassium iodine (100 mg) in acetone (40 ml) was added 2-picolyl chloride hydrochloride (0.61 g, 3.7 mmol). The resulting mixture was stinted at reflux temperature for 18 h, filtered and evaporated in yasuQ. The residue was trituated with diethyl ether and the solid was filtered off and purified on silicagel (300 ml) using a mixture of ethyl ace- tate/ethanol/triethyl amine (3:1:0.4) as eluent. Pure fractions were collected and the eluent evaporated in yaeuQ affording 650 mg (39 %) of 2-(ethoxyoxalyl-amino)-6-pyridin-2-ylmethyl-4,5,6,7-tetraiiydrQ-thieno[2,3-c]pyridine-3-carboxy(ic acid triethyl ammonium salt as a solid. To a solution of the above triethyl ammonium salt (650 mg, 1.40 mmol) in ethanol (15 ml) was added 1 N aqueous sodium hydroxide (4.1 ml, 4.1 mmol) followed by water (15 ml). The resulting reaction mixture was stirred at room temperature for 18 h. The volatiles were evaporated in yafiufi and the residue dissolved in water (20 ml) and washed with diethyl ether (2x10 ml). To the aqueous phase was added 1N hydrochloric acid to pH = 1 and the aqueous phase was evaporated in vacuo. The residue was suspended in a mixture of 2-propanoi/water (1:1. 40 ml), stin-ed for 1 h., the solid filtered off and washed with 2-propanol (2x15 ml) and dried in vacuo at 50 °C affording 181 mg (38 %) of crude title compound. The crude product (181 mg) was dissolved in a mixture of water (10 ml) and5 N sodium hydroxide (10 ml) and washed with diethyl ether (2 x 10 ml). The aqueous phase was acidified to pH = 3 with 1 N hydrochloric acid and the precipitate filtered off and washed with water (3 x 20 mi), dried in vacuo at 50 °C for 18 h which afforded 51 mg (11%) of the title compound as a solid. M.p.:238-244°C Calculated for C16H15N3O5S, 2.5 x H2O; C, 47,29 %; H, 4,96 %; N, 10.34 %. Found: ■ C, 47.43 %; H. 4.84 %; N, 10.00 %. By a similar procedure as described in Example 89 the following compounds were prepared. 6-C3-Methoxv-benzvlV2-(oxalvl-amino)-4.5.6.7-tetrahvdro-thieno[2.3-c]pyridine-3-carboxvlic acid: M.p.: 233 - 237 °C Calculated for CigHiaNzOsS, 1 x H2O; C, 52.93 %; H, 4.94 %; N, 6.86 %. Found: C, 52.79 %; H, 4.99 %; N, 6.42 %. EXAMPLE 91 2-(Oxalvi-amino)-6-pvridin-3-vlmethvl-4.5.6.7-tetrahvdrQ-thienof2.3-c]Dvridine-3-carboxvlic acid, hydrochloride: M.p.: 234-238 °C Calculated for CigHisNaOsS, 1 x HCI, 0.5 x HjO; C, 47.24 %; H, 4.21 %; N, 10.33 %. Found: C, 47.35 %; H. 4.10 %; N, 10.35 %. 2-COxalvl-amino"6-quinolin-2-vlmethyl-4.5.6.7-tetrahydro-thienof2.3-c]pyridine-3-carboxylic 9Cid; M.p.:>250°C Calculated for CzoHiyNjOjS, 1 x H2O; C, 55.95 %; H, 4.22 %; N, 9.61 %. Found: C, 55.94 %; H, 4.46 %; N, 9.78 %. 2-(Oxalvl-aminoV6-pvridin-4-vlmethyl-4.5.6.7-tetrahvdro-thienof2.3-c]Pvridine-3-carboxvlic acid, hydrochloride: M.p.:230-235°C Calculated for CieHisNjOsS, 1 x HCI, 1 x H2O; C, 46.21 %; H, 4.36 %; N, 10.10 %. Found: C, 45.82 %; H, 4.42 %; N, 10.02 %. 6-(Qxalvl-aminQV1H-indole-7-carbQxvlic acid, mono sodium salt: To a stirred solution of 6-amino-1H-indoie-7-carboxylic acid ethyl ester (1.5 g, 7.3 mmol, prepared as described in J. Org. Chem. 61, 1155-1158 (1996)), triethy-lamine (1.55 mi, 11.0 mmol) in dry tetrahydrofuran (100 ml) at 0 ''C was added dropwise a solution of ethyl oxaiyi chloride (980 ul, 88.0 mmol) in dry tetrahydrofuran (10 mi). The re-suiting reaction mixture was stirred at room temperature for 2 h. pored into ice water (300 ml) and the precipitate filtered off and dried in vacuo at 50 '"C affording 2.25 g (100 %) of 6-(ethoxyoxalyl-amino)-1H-indole-7-carboxylic acid ethyl ester as an oil. To a solution of the above 1H-indole-7-carboxylic acid ethyl ester (2.0 g, 6.60 mmol) in etha-nol (30 ml) was added IN aqueous sodium hydroxide (16.4 ml, 16.4 mmoi) in water (30 ml). The resulting reaction mixture was stirred at room temperature for 18 h. The volatiles were evaporated in vacuo and to the residual aqueous phase was added 1N hydrochloric acid to pH = 1. The precipitate was filtered off and washed with water (2 x 50 ml), diethyl ether (2 x 30 ml) and dried in vacuo at 50 ""C affording 1.34 g (82 %) of the title compound as a solid. M.p.: > 250 X Calculated for C"HyNzOsNa, 1.5 x H2O; C, 44.46 %; H, 3.39 %; N, 9.43 %. Found: C. 44.31 %; H, 3.34 %; N, 9.00 %. By a similar procedure as described in Example 94 the following compound was prepared. 6-fOxalyl'aminoV1H-fndole-5-carboxylic acid, mono sodium salt: 6-amino-1H-indole-5-carboxylic add ethyl ester was prepared as described in J. Org. Chem. 61, 1155-1158(1996)). M,p.:>250"C Calculated for CnHyNsOgNa, 1.5 x HjO; C, 44.46 %; H, 3.39 %; N, 9.43 %. Found: C. 44.44 %; H, 3.68 %; N, 9.00 %. 3-[4-(3-Morpholin-4-vl-proDionvn-Diperazin-1-vlmethyl]-6-(oxalvl-amino"-1H-indole--5-carboxylic acid, mono sodium salt: To a ice cooled solution of 37 % aqueous formaldehyde (2.7 g, 33.0 mmol) in acetic acid (8 ml) was added dropwise a solution of piperazine-1-carboxylic acid tert-butyl ester (2.7 g, 15 mmol). After stirring for 15 min, a solution of 6-(ethQxyoxalyl-'amino)-1H-indole-5-carboxylic acid (4.0 g, 13.0 mmol) in a mixture of acetic acid (80 mi) and tetrahydrofuran (80 ml) was added and the resulting reaction mixture was stinted for 18 h. at room temperature. The votatiles were evaporated in vacuo and to the residue was added water (100 ml). The aqueous phase was extracted with ethyl acetate (2 x 100 ml), the combined organic extracts were washed with water (2 x 100 ml), saturated aqueous ammonium chloride (1 x 80 ml), dried (MgSOa), filtered and evaporated in vacuo. The residue was trituated with diethyl ether (50 ml) and the precipitate was filtered off and washed with diethyl ether, dried IQ vacuo at 50°C which afforded 3.4 g (51 %) of 3-(4-tert-butoxycarbonyl-piperazin-1-ylmethyl)-6-(ethoxyoxalyl-amino)-1H-indoie-5-carboxylic acid ethyl ester as a solid. To a solution of the above 6-(ethoxyoxalyl-amino)-1H-indole-5-carboxylic acid ethyl ester in dichloromethane (20 ml) was added trifluoroacetic acid (20 ml) at room temperature. The resulting mixture was stirred for 1 h., the volatiles were evaporated in vacuo and to the residue was added water (50 ml) and the resulting mixture was stirred for Vz h. The precipitate was filtered off and washed with water (50 ml), diethyl ether (50 ml) and in vacuo at 50 °C which afforded 3.6 g (100 %) of 6-(ethoxyoxalyl-amino)-3-piperazin-1-ylmethyl-1H-indole-5-carboxylic acid ethyl ester trifluoroacetic acid salt as a solid. To a ice cooled mixture of the above piperazin (3.0 g, 5.81 mmoi) in dichloromethane (100 ml) and triethylamine (2.5 ml) was added dropwise a mixture of chloropropionyl chloride (0.6 ml, 6.39 mmol) in dichloromethane (10 ml). The resulting mixture was stirred for 1 h. at room temperature, washed with water (50 ml), dried (MgS04), filtered and evaporated in vacuo affording 1.8 g (68 %) of 3-(4-acryloyl-piperazin-1-ylmethyl)-6-(ethoxyoxalyl-amino)-1H-indole-5-carboxylic acid ethyl ester as a oil. To a solution of the above acryloyi-piperazin (0.5 g, 1.1 mmol) in ethanol (50 ml) was added morphotin (0.24 g, 2.74 mmol). The resulting mixture was stirred at reflux temperature for 18 h. and the volatiles were evaporated in vacuo. The residue was dissolved in water (50 ml), pH was adjusted to 2 with IN hydrochloric acid and washed with ethyl acetate (2 x 50 ml). The aqueous phase was neutralised with IN sodium hydroxide, the precipitate was filtered off, washed with water and dried in vacuo at 50 °C for 3h which afforded 0.3 g (50 %) of 6-(ethoxyoxalyl-amino)-3-[4-(3-morpholin-4"yl-propionyl)-piperazin-1-ylmethyl]-1H-indole-5-carboxylic acid ethyl ester as a solid. To a solution of the above 1H-indole-5-carboxylic acid ethyl ester (0.2 g, 0.37 mmol) in ethanol (5 ml) was added sodium hydroxide (45 mg, 1.10 mmol) in water (15 ml). The resulting reaction mixture was stirred at room temperature for 18 h, pH adjusted to 1 by addition of IN . hydrochloric acid. The aqueous phase was washed with ethyl acetate (2 x 25 ml) and pH adjusted to 5 by addition of 1N sodium hydroxide, followed by addition of dichloromethane (25 ml). The precipitate was filtered off and washed with water (50 ml) and dried in vacuo at 50 ""C affording 30 mg (17 %) of the title compound as a solid. M.p.:>250°C LC-MS (E*) M/Z 488 1 -(3'Methoxy-ben2vlV6-(oxalvl-aminoV1 H-indole-S-carboxylic acid: To a solution of 6-amino-1H-indole-5-carboxylic acid ethyl ester (1.0 g. 3.3o mmol; prepared as described in J. Org. Chem. 61. 1155-1158 (1996)) in dry N,N-dimethylformamide (40 ml) was added sodium hydride (0.28 g, 7.3 mmol; 60 % in mineral oil). The reaction mixture was stirred for 1.5 h and a solution of 3-methoxyben2ylchloride (0.5 ml, 3.6 mmol) in dry N,N-dimethylformamide (2.5 ml) was added dropwise. The resulting reaction mixture was stirred for 1.5 h, poured into water (300 ml) and washed with diethyl ether (3 x 100 ml). Undissolved matter was filtered off and the aqueous phase was acidified to pH = 4 by addition of IN hydrochloric acid. The precipitate was filtered off and washed with water, dried in yasuQ at 50 °C affording 400 mg (29 %) of 6-(ethoxyoxalyl-amino)-1-(3-methoxy-benzyl)-1H-indole-5-carboxyiic acid ethyl ester as a solid. To a solution of the above 1H-indole-5-carboxylic acid ethyl ester (0.3 g, 0.7 mmol) in etha-nol (10 ml) was added 1N sodium hydroxide (2.1 mi, 2.1 mmol) and water (10 ml). The resulting reaction mixture was stirred at room temperature for 18 h. The volatiles were evaporated in vacuo, pH adjusted to 2 by addition of 1N hydrochloric acid, the precipitate filtered off and washed with water, dried in vacuo at 50 °C affording 230 mg (89 %) of the tillg compound as a solid. M.p.:222-226°C Calculated for CgHigNzOe, 0.4 x H2O; C, 60.77 %; H, 4.51 %; N, 7.46 %. Found: C, 60.96 %; H, 4.44 %; N. 7.28 %. By a similar procedure as described in Example 81 the following compound was prepared. 2-rQxaM-aminoM.7-dihvdro-5H-thienof2.3-clthioDvran-3-carboxvlicacid: Calculated for CoHgNOsSj; C, 41.80 %; H, 3.16 %; N, 4.88 %. Found: C, 41.97 %; H, 3.20 %; N, 4.69 %. 2-rQxalyi-aminoV9H-thienof2.3-c|chromen-3-carboxvlic acid, mono sodium salt To a solution of 4-cromanone (20 g, 0.14 mol), ethyl cyanoacetate (16.8 g, 0.15 mol) and ammonium acetate (11.4 g, 0.15 mol) in benzene (500 mi) was added acetic acid (5 ml), the resulting reaction mixture was heated at reflux temperature for 18 h and the formed water was collected in a Dean-Stark water trap. An additional portion of ammonium acetate (10 g, 0.13 mol) was added and heating at reflux temperature was continued for an additional 8 h. The volatiles were evaporated in vacuo, to the residue was added water (500 ml) and the aqueous phase was extracted with ethyl acetate (2 x 200 ml). The combined organic extracts were washed with water (2 x 100 ml), saturated aqueous sodium chloride (100 ml), dried (MgSOJ, filtered and evaporated in yasuo afforded 28 g of a 1:1 mixture of unchanged starting material and chroman-4-ylidene-cyano-acetic acid ethyl ester as an oil. To a solution of the crude product in ethanol (250 ml) was added sulphur (2.5 g. 0.08 mol) and morpholin (15 ml). The resulting reaction mixture was stirred at 50 °C for 4 h cooled to room temperature and filtered. The volatiles were evaporated in vacuo affording 30 g of crude product. The product was divided into two portions which was semi purified on silica gel (900 ml) using a mixture of ethyl acetate/heptane (1:3). Semi pure fractions were collected and the solvent evaporated in yacuQ affording a crude oil which was dissolved in diethyl ether (80 ml) and crystallised by addition of heptane (125 ml). The precipitated was filtered off, washed with heptane and dried in vacuo at 50 °C for 18 h affording 8.9 g (24 %) of 2-amino-9H-thieno[2,3-c]chromen-3-carboxylic acid ethyl ester as a solid. To a stirred solution of the above 2-amino-6H-thieno[2,3-c]chromen-3-carboxylic acid ethyl ester (2.9 g, 10.53 mmol), triethylamine (3 ml) in dry tetrahydrofuran (100 ml) at 0 °C was added dropwise a solution of ethyl oxalyl chloride (1.6 g, 11.6 mmol) in dry tetrahydrofuran (20 ml). The resulting reaction mixture was stirred at room temperature for 1.5 h. pored into ice water (200 ml) and the precipitate filtered off and dried in vacuo at 50 °C affording 2.6 g (66 %) of 2-(ethoxyoxalyl-amino)-9H-thieno[2,3-c]chromen-3-carboxyiic acid ethyl ester as a solid. To a solution of the above ethyl ester (1.5 g, 4.0 mmol) in ethanol (25 ml) was added sodium hydroxide (480 mg. 12 mmol) and water (50 ml). The resulting reaction mixture was stirred at room temperature for 42 h. Water (100 ml) was added and the mixture was washed with diethyl ether (100 ml). pH of the aqueous phase was adjusted to 1 by addition of concentrated hydrochloric acid, the precipitate was filtered off, washed with water and dried in vacuo at 50 "C for 6 h affording 0.6 g (47 %) of the title compound as a solid. M.p.: 227 - 228 X Calculated for Ci4H9N06SNa, 0.5 H2O; C. 48.01 %; H. 2.59 %; N. 4.00 %. Found; C, 48.39 %; H, 2.93 %; N, 3.93 %. 2-ff"-H-Tetrazol-5-carbonynaminoV4.7-dihydrO'5H-thienQ[2.3-c]pvran--3-carboxylicacid: To a mixture of N,N-dimethylformamide (1.6 ml) and acetonitrile (5 ml) cooled to -20 *C was added dropwise a mixture of oxalyl chloride (0.8 g, 6.31 mmol) in acetonitrile (1 ml). The resulting mixture was stirred for 15 min. and tetrazole-5-carboxylic acid dipotassium salt (1 g, 5.25 mmol, prepared as described in J. Med, Chem, 29, 538-549 (1986)) was added and the resulting mixture was stirred for an additional 20 min. To the mixture was added drop-wise a solution of 2-amino-4,5-dihydro-7H-thieno[2,3-c]pyran-3-carboxylic acid te/t-butyl ester (1.3 g, 5.25 mmol). pyridine (2.2 ml) and acetonitrile (2.5 ml) during 10 min. The reaction mixture was allowed to reach room temperature where after it was heated at reflux temperature for 0.5 h. The cooled reaction mixture was pored into water (100 ml) and pH was adjusted to 1 by addition of concentrated hydrochloric acid. The precipitate was filtered off, washed with heptane and dried in vacuo at 50 'C for 18 h affording 1.3 g (70 %) of 2-((1H-tetrazole-5-carbonyl)-amino)-4,7-dihydro-5H-thieno[2,3-c]pyran-3-carboxylicacid fert-butyl ester as a solid. The above fe/t-butyl ester (0.6 g, 1.71 mmol) was dissolved in dichloromethane (5 ml) and trifluoroacetic acid (5 ml) was added. The resulting mixture was stin-ed for 40 min. at room temperature. The volatiles were evaporated in vacuo and to the residue was added diethyl ether (50 ml), water (25 ml) and 1 N sodium hydroxide (2 ml). The phases were separated and the aqueous phase was washed with diethyl ether (50 ml) and pH was adjusted to 1 by addition of concentrated hydrochloric acid. The precipitate was filtered off, washed with water (25 ml) and dried in vacuo at 50 **C for 18 h which afforded 190 mg (38 %) of the title compound as a solid. M.p,: >250"C Calculated for C10H9N5O4S, 0.25 x H2O; C, 40.07 %; H, 3.19 %; N, 23.36 %. Found: C, 40.39 %; H, 3.18 %; N. 22.92 %. EXAMPLE 101 N-(3-r2H-TetrazQl-5-vlM.7-dihvdro-5H-thienof2.3-c]pyran-2-vnQxalamic acid, di sodium salt 2-Amino-4,5-dihydro-7H-thieno[2,3-c]pyran-3-carboxylic acid ethyl ester (26 g, 0.114 mol) was dissolved in formamide (200 mi) and the resulting mixture was heated at reflux temperature for 1.5 h. After cooling to room temperature the precipitate was filtered off, washed with water (2 x 60 ml) and dried in yasuQ at 50 "C for 18 h which afforded 10.0 g (42 %) of 5,6-dihydro-8H-pyrano[4',3':4,5]thieno(2,3-d]pyrimidin-4-one as a solid. To phosphorus oxychloride (70 ml) was added the above pyrimidin-4-one (7.0 g, 0.04 mol) and N.N-dimethylaniline (0.2 ml). The resulting mixture was heated at reflux temperature for 2 h, cooled and pored onto ice water (700 ml). The precipitate was filtered off, suspended in a mixture of ethyl acetate (400 ml) and water (250 ml) and stirred for 15 min. The aqueous phase was separated off and the organic phase was washed with saturated aqueous sodium chloride (100 ml), dried (MgS04), filtered and evaporated in vacuo which afforded 5.2 g (68 %) of 4-chloro-5,6-dihydro-8H-pyrano[4',3*:4,5]thieno[2,3-d]pyrimidine as a solid. To a warm solution of the above thieno-pyrimidine (4.5 g, 0.02 mol) in ethanol (40 mi) was added dropwise a solution of hydrazine hydrate (10.0 ml) in ethanol (20 ml). The resulting solution was heated at reflux temperature for 2 h, cooled to room temperature, the precipitate filtered off, washed with ethanol (20 ml) and dried in vacuo at 50 X for 1.5 h affording 3.2 g (73 %) of 5,6-dihydro-8H-pyrano(4',3':4,5]thieno[2,3-d]pyrimidin-4-yl hydrazine as a solid. To a solution of the above hydrazine (3.0 g, 0.014 mol) in 50 % aqueous acetic acid (100 ml) cooled in a ice bath was added dropwise a solution of sodium nitrite (1.0 g, 0.015 mol) in water (10 ml). The reaction mixture was stirred for 2 h, the precipitate filtered off, washed with water (25 ml) and dried in vacuo at 50 X for 1 h affording 3.0 g (95 %) of 10,11-dihydro-8H-pyrano[4\3*:4,5]thieno[3,2-e]tetrazolo[5,1-c]pyrimidine as a solid. To a solution of the above tetrazol (2.5 g, 0.011 mol) in dioxane (30 ml) wa§ added dropwise 1 N sodium hydroxide (25 ml). The reaction mixture was stirred for 3 h, pored into ice cooled water (100 ml) and pH was adjusted to 4 by addition of acetic acid. The precipitate was filtered off, washed with water (25 ml) and dried in vacuo at 50 *C for 18 h affording 2.2 g (82 %) of N-(3-(2H-tetrazol-5-yl)"4,7-dihydro-5H-thieno[2,3-c]pyran-2-yl)formamide as a solid. The above fomriamide (0.6 g, 2.7 mmol) was dissolved in dry tetrahydrofuran (50 ml) and triethylamine (1 ml) was added. To the resulting mixture cooled in a ice bath was added dropwise a solution of ethyl oxalylchloride (0.4 g. 2.96 mmol) in dry tetrahydrofuran (5 ml). The resulting reaction mixture was stirred for 2 h at room temperature, the volatiles were evaporated iQ vacuo. To the residue was added water (50 ml), diethyl ether (50 ml) and 1 N hydrochloric acid to pH = 2 and a small precipitate was filtered off. The organic phase was separated, dried (NasSOJ, filtered and evaporated in vacuo. The residue (0.4 g) was suspended in dichloromethane (20 ml) and stirred for 1 h, the solid matter was filtered off and dried in vacuo at 50 X affording 0.16 g (18 %) of N-(3-(2H-tetrazoi-5-yi)-4,7-dihydro-5H-thieno[2,3-c]pyran-2-yl)oxalamic acid ethyl ester as a solid. To a solution of the above oxalamic acid ethyl ester (0.16 g. 0.49 mmoi) in ethanol (15 ml) was added 1 N sodium hydroxide (1.0 ml, 1.01 mmol). The resulting reaction mixture was stirred at room temperature for 2 h. The precipitate was filtered off and washed with ethanot (10 ml), dried in vacuo at 50 "'C for 48 h affording 140 mg (83 %) of the tills compound as a solid. M.p.: > 250 "C Calculated for CioH9N504SNa2. 3 x HjO; C, 30.54 %; H, 3.33 %; N, 17.81 %. Found: C, 30.70 %; H, 3.35 %; N, 17.49 %. By a similar procedure as described in Example 81 the following compounds were prepared. EXAMPLE 102 2-fOxalvl-aminoV4.7-dihydro-5H-thieno[2.3-c]pvridine-3.6-dicarboxylic acid 6-benzvl ester M.p.: >250''C Calculated for CaHieNzOyS; C, 53.46 %; H, 3.99 %; N, 6.93 %. Found: C, 53.44 %; H, 4.15 %; N, 6.69 %. EXAMPLE 103 2-(Oxalvl-aminoM.7-dihvdro-5H-thieno[2.3-c]pvridine-3.6-dicarboxvlic acid 6-ethvi ester M.p.: 245 - 247 "C Calculated for C13H14N2O7S; C, 45.61 %; H, 4.12 %; N, 8.18 %. Found: C, 45.71 %; H, 4.31 %; N, 7.86 %. EXAMPLE 104 6-Acetvl-2-(oxalvl-aminoM.5.6.7-tetrahvdro-thieno[2.3-c]pvridine-3-carboxylicacid M.p.:242-244°C Calculated for CijHizNjOeS, 0.25 x H2O; C, 45.50 %; H, 3.98 %; N, 8.84 %. Found: C, 45.64 %; H, 3.97 %; N, 8.51 %. EXAMPLE 105 2-(Oxalvl-aminoV6-phenyicarbannoylmethyl-4.5.6.7-tetrahvdro-thieno[2.3-c]pyridine-3-carboxvlic acid M.p.: 244 - 246 "C Calculated for C18H17N3O6S, 1 x H2O; C, 51.30 %; H, 4.54 %; N, 9.97 %. Found: C, 51.08 %; H, 4.52 %; N, 9.63 %. EXAMPLE 106 5-M 3-DiQyo-1.3-dihvdrQHSoindol-2-vlmethvlV2-fQxalvl-amino)-47-di""" c]pyran-3-carboxvlic acid: To a mixture of benzyloxyacetaldehyde (8.3 g, 0.06 mol) in benzene (80 mL) was added 1-methoxy-3-trimethylsilyloxy-1,3-butadiene (10.6 g, 0.06 mol). The reaction mixture was stirred under nitrogen for 15 min., cooled to 0 °C and a solution of 0.5 M zinc chloride (55 ml, 0.03 mol) was added dropwise. The reaction mixture was allowed to warm to room temperature over 16 h and evaporated in vacuo. The resultant oil was diluted with ethyl acetate (100 ml), washed with 1N hydrochloric acid (3 x 50ml), saturated sodium bicarbonate (3 x 50 ml), brine (3 x 50 ml), dried (MgSOJ and evaporated in yacys. The resulting oil was subjected to flash chromatography using a mixture of ethyl acetate/hexanes (1:2) as eluent. Pure fractions were collected affording after evaporation in vacuo 7.1 g (60 %) of benzyloxy-methyl-2,3-dihydro-pyran-4-one as an oil. "H NMR (400 MHz, CDCI3) 5 7.39 - 7.31 (m, 6H), 5.42 (dd, J = 6.1 Hz, 1H), 4.61 (d, J = 3 Hz, 1H), 4,57 (m, 1H), 3.70 (m, 2H). 2.74 (dd, J = 17 Hz, 14 Hz, 1H). 2.41 (ddd. J = 17 Hz, 2 Hz, 1 Hz, 1H). The above 2,3-dihydro-pyran-4-one (7.1 g, 0.032 mol) and 10 % palladium on carbon (0.4 g) in ethyl acetate (50 ml) were placed in a Parr bomb shaker and hydrogenated at 30 psi. The reaction mixture was shaken for 2 h, at which time TLC analysis (methanol/dichloromethane 1:9) indicated the reaction was complete. The reaction mixture was filtered through a pad of Celite and the volatiles evaporated in vacuo. The residue was subjected to flash column chromatography using ethyl acetate as eluent. Pure fractions were collected affording after evaporation in vacuo 3.0 g (75 %) of 2-hydroxymethyi-tetrahydro-pyran"4-one as an oil. "H NMR (400 MHz, CDCI3) 5 4.36 - 4.29 (m, 1H), 3.77 - 3.66 (m, 3H). 3.61 - 3.54 (m, 1H), 2.65 - 2.43 (m, 2H), 2.34 - 2.27 (m, 2H), 2.04 (bs. 1H, CH2OH). The above tetrahydro-pyran-4-one (1.90 g, 0.015 mol), tert-butyl cyanoacetate (2.7 g, 0.019 mol). sulfur (0.51 g, 0.016 mol) and morpholine (2.55 ml, 0.03 mol) were dissolved in absolute ethanol (20 ml), and heated to 50 "C for 16 h. The reaction mixture was cooled, filtered and the filtrate evaporated inyaeuo. The resultant oil was dissolved in ethyl acetate (50 ml), washed with water (2 x 50 ml), brine (2 x 50 m) and dried (MgSO"). The solvent was evaporated in yasyQ and the residue was subjected to flash column chromatography using ethyl acetate/hexanes (1:1) as eluent. Pure fractions were collected affording after evaporation ID vacuo 3.7 g (90 %) of 2-amino-5-hydroxymethyl-4,7-dihydro-5H-thieno[2,3-c]pyran-3-carboxyiic acid fe/t-butyl ester as a solid. "H NMR (400 MHz, CDCy 5 4.64 (s, 2H), 3.80 - 3.67 (m, 3H), 2.77 - 2.72 (m, 1H), 2.57 -2.53 (m,1H), 1.54 (s,9H). The above carboxyiic acid tert-butyi ester (3.0 g, 0.015 mol), phthalimide (2.10 g, 0.014 mol) and triphenylphosphine (3.68 g, 0.014) were dissolved in dry tetrahydrofuran (60 ml) and cooled to 0 °C under a nitrogen atmosphere. Diisopropyl azodicarboxylate (DIAD) (2.71 ml, 0.014 mol) was added dropwise at 0 °C and the solution allowed to stir overnight, slowly warming to room temperature. The volatiies were evaporated in vacuo and the resultant solid dissolved in ethyl acetate (60 mi). The organic phase was washed with brine (2 x 50 ml), dried (MgSOJ and evaporated in YSSUQ. The residue was subjected to flash column chromatography initially eluted with a mixture of ethyl acetate/hexanes (1:3). Once the product began to elute, the eluent mixture was switched to ethyl acetate/hexanes (1:2). Pure fractions were collected affording after evaporation in vacuo 2.90 g (47 %) of 2-amino-5-(1,3-dioxo-1,3-dihydro-isoindol-2-ylmethyl)-4,7-dihydro-5H-thieno[2,3-c]pyran-3-carboxylicacid tert-butyl ester as a solid. "H NMR (400 MHz, CDCI3) 5 7.87 - 7.85 (m, 2H), 7.83 - 7.71 (m, 2H), 5.94 (bs, 2H), 4.59 (d, J = 14 Hz, 1H), 4.52 (d, J = 14 Hz. 1H), 4.0 - 3.98 (m, 2H), 3.83 - 3.79 (m. 1H). 2.87 (d, J = 17 Hz, 1H), 2.58 (dd, J = 17 Hz, 9 Hz, 1H), 1.50 (s, 9H). To the above 4,7-dihydro-5H-thieno[2,3-c]pyran-3-carboxylic acid tert butyl ester (0.5 g, 1.2 mmol) dissolved in dichioromethane (5 ml), was added triethylamine (0.33 ml, 2.4 mmol) and imidazol-1-yl-oxo-acetic acid tert butyl ester (0.47 g, 2.4 mmol) under nitrogen. The reaction mixture was allowed to stir at room temperature for 18 hours. The volatiies were evaporated in vacuo and the solid residue dissolved in ethyl acetate (20 ml). The organic phase was washed with 1% hydrochloric acid (2x10 ml), brine (2x10 ml), dried (MgSOJ. The organic phase was evaporated in yasuQ affording 0.64 g (99 %) of 2-(tert-butoxyoxalyl-amino)-5-(1,3-dioxo-1,3-dihydro-isoindol-2-ylmethyl)-4,7-dihydro-5H-thieno[2,3-c]pyran-3-carboxylic acid fe/t-butyl ester as a solid. "H NMR (400 MHz, CDCI3) 5 12.48 (s, 1H, NWCO). 7.88 - 7.86 (m, 2H), 7.74 - 7.72 (m, 2H). 4.78 (d. J = 19 Hz, 1H), 4.65 (d, J = 19 Hz, 1H), 4.07 -3.90 (m, 2H), 3.88 - 3.80 (m, 1H), 2.97 (d, J = 17 Hz, 1H), 2.68 (dd. J = 17 Hz, 9 Hz, 1H), 1.58 (s. 9H), 1.54 (s, 9H). The above di-terf-butyl ester (2.8 g, 5.16 mmol) was dissolved in a mixture of trifluoroacetic acid and dichloromethane (1:5) (36 ml). The reaction was stirred at room temperature for 6 hr. The precipitate was filtered off, washed with diethyl ether, dried in vacuo at 50 °C which afforded 1.26 g (57 %) of the title compound as a solid. M.p.: 245.2-245.6 °C. "H NMR (300 MHz, DMSO-dg) 5 12.32 (s, 1H, NHCO), 7.95 - 7.80 (m, 4H), 4.75 (d, J = 20 Hz, IN), 4.62 (d, J = 20 Hz, 1H), 3.96 - 3.69 (m, 3H), 3.01 (d, J = 18 Hz, 1H), 2.60 (dd, J = 18 Hz, 9 Hz, 1H). Calculated for CigHuNjOsS; C, 53.02 %; H. 3.28 %; N, 6.51 %. Found: C, 53.01 %; H, 3.31 %; N, 6.41 %. EXAMPLE 107 5-(Benzovlamino-methyn-2-(oxalvl-aminoM.7-dthydro-5H-thienof2.3-c]pyran-3-carboxylic acid 2-(tert-Butoxyoxalyl-amino)-5-(1,3-dioxo-1,3-dihydro-isoindol-2-ylmethyl)-4,7-dihydro-5H-thieno[2,3-c]pyran-3-carboxylic acid tert-butyl ester (0.33 g, 0.60 mmol) was dissolved in a solution of ethanol (2 ml) and dichloromethane (3 ml). Hydrazine (28 "1, 0.9 mmol) was added and the reaction stirred under nitrogen at room temperature for 24 h. TLC analysis indicated that starting material was still present. An additional portion of hydrazine (28 |il, 0.9 mmol) was added and the reaction stirred at room temperature for another 16 h, then at 45 °C for 5 h. The mixture was concentrated in vacuo, redissolved in dichloromethane and the insoluble material filtered off. The filtrate was collected and concentrated in vacuo affording cnjde 5-aminomethyl-2-(tert-butoxyoxalyl-amino)-4,7-dihydro-5H-thieno[2,3-c]pyran-3-carboxylic acid fert-butyl ester as a solid, which was can-ied through to the next step without further purification. The above crude 5H-thieno[2,3-c]pyran-3-carboxyiic acid "ert-butyl ester (0.25 g, 0.60 mmol) was suspended in a mixture of dichloromethane and acetonitrile (1:1, 5 ml). Triethylamine (0.25 ml, 1.8 mmol) was added followed by l-hydroxy-benzotriazole hydrate (0.10 g, 0.72 mmol) and 1-(3-dimethyiaminopropyl)-3-ethylcarbodiimide hydrochloride (0.14 g, 0.72 mmol) as solids. The heterogeneous reaction mixture was allowed to stir at room temperature for 2 days, after which the mixture was homogenous. The solvents were evaporated in vacuo, the residue dissolved in dichloromethane washed twice with 1M hydrochloric acid, then with saturated sodium bicarbonate. The organic phase was dried (Na2S04), filtered and concentrated in vacuo affording a solid which was purified by flash chromatography using a mixture of ethyl acetate and hexanes (1:1) as eluent. Pure fractions were collected and evaporated in vacuo affording 50 mg (16 % over two steps) of 5-(benzoylamino-methyl)-2-(te/t-butoxyoxalyl-amino)-4,7-dihydrO"5H-thieno[2.3-c]pyran-3-carboxylic acid tert-butyl ester as a solid. "H NMR (400 MHz, CDCI3) 5 12.46 (s, 1H). 7.81 (d, J = 7 Hz. 2 H). 7.51 -7.42 (m. 3H), 6.72 (bs. 1H), 4.83 (d, J = 17 Hz. 1H). 4.74 (d. J = 17 Hz. 1H), 4.05 - 3.98 (m. 1H), 3.86 - 3.78 (m, 1H), 3.45-3.38 (m. 1H). 2.97 (d, J = 19 Hz, IN), 2.68 (dd, J = 19 Hz, 9 Hz, 1H). 1.61 (s, 9H). 1.58 (s,9H). The above benzoylamino-methyl-thieno[2,3-c]pyran (40 mg, 0.078 mmol) was treated with 20 % trifiuoroacetic acid in dichloromethane (2 ml) for 4 h. The volatiles were evaporated in vacuo and chased twice with dichloromethane. forming a precipitate which was filtered off and dried yielding 30 mg (95 %) of the title compound as a solid. "H NMR (400 MHz. DMSO-de) 5 12.31 (s, 1H). 8.63 (t. J = 4 Hz. 1H), 7.86 (d, J = 7 Hz. 2H), 7.51 - 7.43 (m. 3H). 4.80 (d. J = 17 Hz. 1H). 4.64 (d, J = 17 Hz. 1H), 3.82 (m. 1H). 3.44 (m. 2H). 2.95 (d. J = 18. 1H). 2.52 (dd, J = 18 Hz. 9 Hz. 1H). LC/MS [M-H]: 403.39. HPLC (254.4nm): 2.99 s. 84 %. 5-Benzovloxymethvl-2-(Qxalvl-aminoM7-dihydro-5H-thieno[2.3-clDvran-3-carbQxvlicacid 2-Amino-5-hydroxymethyl-4,7-dihydro-5H-thieno[2,3-c]pyran-3-carboxylic acid fert-butyi ester {0.23 g, 0.87 mmol) benzoic acid (0.10 g, 0.96 mmol) and triethyiamine (0.23 ml, 1.7 mmol) were dissolved in dichloromethane (4 ml) and stirred under nitrogen. 1-(3-Dimethylaminopropyl)-3-ethylcarbodiimide hydrochloride (0.17 g, 0.96 mmol) and 1-hydroxy-benzotriazole hydrate (0.12 g, 0.96 mmol) were added as solids. The reaction mixture was stirred at room temperature for 2 days, after which the solvents were evaporated in vacuo. The crude mixture was dissolved in ethyl acetate and washed with 1N hydrochloric acid, saturated sodium bicarbonate, brine and dried (Na2S04). The solvent was evaporated in vacuo, yielding a yellow solid that was purified by flash chromatography using a mixture of ethyl acetate and hexanes (1:2) as eluent. Pure fractions were collected and evaporated in vacuo affording 0.22 g (70 %) of 2-amino-5-benzoyloxymethyl-4,7-dihydro-5H-thieno[2,3-c]pyran-3-carboxyiic acid tert-butyl ester as a solid. "H NMR (400 MHz, CDCI3) 8 8.06 (d. J = 7 Hz, 2H), 7.55 (t, J = 7 Hz, 1H), 7.42 (t, J = 7 Hz, 2H). 4.64 (s, 2H), 4.44 (d, J = 5 Hz, 2H), 4.03 - 3.97 (m, 1H), 2.88 (d, J = 18 Hz, 1H), 2.64 (dd, J = 17 Hz, 10 Hz, 1H). 1.50 (s, 9H). LC/MS [M+H]: 390.48 To the above carboxylic acid fert-butyl ester (0.18 g, 0.45 mmol) dissolved in dry tetrahy-drofuran (5 ml), was added triethyiamine (0.18 ml, 1.4 mmol) and imidazol-1-yl-oxo-acetic acid tert-butyl ester (0.26 g, 1.4 mmol) under nitrogen. The reaction mixture was stirred at To a solution of 2-amino-5-(1,3-d(QXO-1.3-dihydro-isoindol-2-ylmethyl)-4,7-dihydro-5H-thieno[2,3-c]pyran-3-carboxyiic acid fe/t-butyl ester (0.308 g, 0.74 mmol) in absolute ethanol (5 ml) was added hydrazine (47 (il, 1.48 mmol). The reaction was stirred at 80 °C for 4 h and then at room temperature for another 12 h. The precipitate formed was filtered off and the filtrate concentrated in yaeUQ. To the oily residue was added dichloromethane (15 ml) and the precipitate formed was filtered off. The filtrate was concentrated in vacuo to give 2-amino-5-aminomethyl-4,7-dihydro-5H-thieno[2,3-c]pyran-3-carboxylic acid ferr-butyl ester 0.19 g (90%) as a solid. "H NMR (400 MHz. CDCI3) 5 5.91 (bs, 2H), 4.62 (s, 2H), 3.64 - 3.60 (m, 1H), 2.92 - 2.84 (m. 2H), 2.80-2J5(m, 1H). 2.52 - 2.45 (m, 1H), 1.53 (s,9H). LC'MS [M+H]*: 285 Phthalic dicarboxaldehyde (52 mg, 0.36 mmol) was dissolved in a mixture of anhydrous acetonitrile (2 ml) and acetic acid (44 \x\, 0.72 mmol). The above 2-amino-5-aminomethyl-4J-dihydro-5H-thieno[2,3-c]pyran-3-carboxylic acid tert-butyl ester (0.11 g, 0.36 mmol) was added and the reaction stirred for 20 minutes at room temperature. The volatiles were evaporated in vacuo and the residue dissolved in ethyl acetate (25 ml). The organic mixture was washed with saturated sodium bicarbonate (5 ml), 1 % hydrochloric acid (5 ml), brine (5 ml), dried (NazSOJ, filtered and evaporated in vacuo. The residue was purified by chromatography using a gradient from 15 % ethyl acetate/dichloromethane to 17 % ethyl ace-tate/dichloromethane as eluent affording 45 mg (30 %) of 2-amino-5-(1-oxo-1,3-dihydro-isoindoi-2-ylmethyl)-4,7-dihydro-5H-thieno[2,3-c]pyran-3-Garboxylic acid tert-butyl ester as a solid. "H NMR (400 MHz, CDCI3) 5 7,85 (d, J = 7 Hz, 1H), 7.53 (t, J = 7 Hz, 1H), 7.47 - 7.43 (m. 2H), 4.68 (d, J = 17 Hz, 1H), 4.58-4,51 (m, 3H), 3.99 (dd, J = 14 Hz, 3 Hz, 1H). 3.93-3.89 (m, 1H), 3.66-3.61 (m, 1H), 2.88 (d, J = 17 Hz, 1H), 2.55 (dd, J = 17 Hz, 11 Hz. 1H), 1.52 (s. 9H). To a solution of 2-amino-5-(1-oxo-1,3-dihydro-isoindol-2-ylmethyl)-4,7-dihydro-5H-thieno[2,3-c]pyran-3-carboxyiic acid tert-buXy\ ester (45 mg, 1.1 mmol) in anhydrous dichloromethane (4 ml) was added imidazol-1-yl-oxo-acetic acid fert-butyl ester (73 mg, 3.3 mmol) and thethy-lamine (17 |J.I, 1.1 mmol). The reaction was stirred under nitrogen at room temperature for 5 h. The solvent was evaporated in yasuo and the crude material was dissolved in ethyi ace- tate (20 ml). The organic solution was washed with 0.5 N hydrochloric acid (3 ml), saturated sodium bicarbonate (3 ml), brine (5 ml), dried (Na2S04), filtered and the solvent evaporated in vacuo. The residue was purified by chromatography using dichloromethane (100 %) followed by 17 % ethyl acetate/dichloromethane as eluents affording 54 mg (91 %) of 2-(tert-butoxyoxalyl-amino)-5-(1-oxo-1,3-dihydro-isoindol-2-yimethyl)-4,7-dihydro-5H-thieno[2,3-c]pyran-3-carboxylic acid te/t-butyl ester as a solid. "H NMR (400 MHz, CDCI3) 5 12.50 (s, 1H). 7.84 (d, J = 8 Hz, 1H), 7.53 (t, J = 7 Hz, 1H). 7.47 - 7.43 (m. 2H), 4.81 - 4.65 (m, 3H), 4.53 (d, J = 17 Hz, 1H), 4.01 (dd, J = 14 Hz, 3 Hz, 1H), 3.96 - 3.89 (m, 1H), 3.69 - 3.62 (m, 1H), 2.97 (d, J = 17 Hz, 1H). 2.63 (dd, J = 17 Hz, 11 Hz, 1H), 1.59 (S.9H), 1.56 (s,9H). APCI'MS [M+H]*: 529.5 The above 2-(tert-butoxyoxalyl-amino)-5-(1-oxo-1,3-dihydro-isoindol-2-ylmethyl)-4,7-dihydro-5H-thieno[2,3"C]pyran-3-carboxylic acid fert-butyl ester (52 mg, 0.098 mmol) was treated with a solution of 50 % trifluoroacetic acid/dichloromethane (3 ml) for 4.5 h at room temperature. The volatiles were evaporated in vacuo and the residue chased three times with dichloromethane (10 ml). The solid formed was filtered off and washed with dichloromethane affording 28 mg (70 %) of the tille compound as a solid. 'H NMR (400 MHz, DMSO-dg) 5 12.32 (s, 1H), 7.69 (d, J = 8 Hz, 1H), 7.61 - 7.59 (m, 2H), 7.51 -7.45(m. 1H), 4.81 (d, J = 15 Hz, 1H), 4.65 (d, J = 15 Hz, 1H), 4.60 (s, 2H), 3.95 - 3.92 (m, 1H). 3.75 (d, J = 5 Hz, 2H), 2.94 (d, J = 16 Hz, 1H), 2.56 (dd, J = 16 Hz, 10 Hz, 1H). APCI'MS [M+nr 417.3 HPLC (254.4nm): 3.079 s (100%) 2-(QyalyUanriino)-6-oxo-4.5.6.7-tetrahvclro-ben2o[b]thiophene-3-carboxylicacid 2-(Ethoxyoxalyi-arnino)-6-oxo-4.5,6,7-tetrahydro-benzo(b]thiophene-3-carboxylic acid (3.0 g, 0.013 mol) was dissolved in a mixture of water (40 ml), ethanol (20 mi) and tetrahydrofuran (20 ml) at room temperature. To the resulting mixture was added 1 N sodium hydroxide (20.24 ml, 20.24 mmol). The resulting reaction mixture was stirred at room temperature for 72 h, pH was adjusted to 3 by addition of concentrated hydrochloric acid. The precipitate was filtered off and washed with water (2x15 ml), diethyl ether (2x15 ml) and dried in vacuo at 50 °C affording 1.96 g (73 %) of the titig compound as a solid. M.p.: > 230 °C Calculated for C."HgNOeS; C. 46.64 %; H, 3.30 %; N. 4.94 %. Found: C, 46.97 %; H, 3.30 %; N, 5.80 %. By a similar procedure as described in Example 81 the following compounds have been prepared. 4-Carboxvmethvl-2-(oxalyl-aminoV4.5.6.7-tetrahvdro-benzQ-[b]thienophene-3-carboxvlic acid: 2-Carbmethoxymethylcyctohexanone was prepared in the same way as described in J. Am. Chem. Soc. 81, 3955-3959 (1959) for 2-carbethoxy-methylcyclohexanone. M.p.: > 250 °C Calculated for CISH"SNIOTSI, 0.75 H2O; C, 45.81 %; H. 4.29 %; N, 4.11 %. Found: C, 45.79 %; H, 4.02 %; N. 4,08 %. By a similar procedure as described in Example 107 the following compounds have been prepared. 2-rOxalvl-amino)-5-(((4-oxo-chromene-4H-3-carbonynamino)methyl')-4.7-dihydro-5H-thifinn[2 3-c]pvran-3-carboxvlic acid: "H NMR (400 MHz, DMSO-dg) 5 12.32 (s, 1H), 9.47 (t, J = 4 Hz, 1H), 9.08 (s, 1H). 8.19 (dd, J = 8 Hz, 2 Hz, IN), 7.90 (dt, J = 8 Hz, 2 Hz, 1H), 7.78 (d, J = 8 Hz, IN), 7.60 (t, J = 8 Hz, 1H), 4.88 (d, J = 15 Hz, 1H), 4.70 (d, J = 15 Hz, 1H). 3.83 - 3.79 (m, 1H), 3.72 - 3.66 (m, 1H), 3.55 - 3.48 (m, 1H), 2.95 (d. J = 15 Hz, 1H), 2.60 (dd, J = 15 Hz, 8 Hz. 1H). LC/MS[M-H]-: 471.4 HPLC (254.4 nm): 3.105 s, 94%. ?-(QxaM-aminoV5-f(f4-oxo-chromene-4H-2-carbonvnamino)methvn-4.7-dihvdro-5H-thienn[2 3-clPvran-3-carboxvlic acid: 'H NMR (400 MHz, DMSO-dg) 5 12.32 (s, 1H), 9.33 (t, J = 4 Hz. 1H), 8.05 (d, J = 8 Hz, 1H), 7.89 (t, J = 8 Hz, 1H), 7.76 (d, J = 8 Hz, 1H). 7.53 (t, J = 8 Hz, 1H), 6.84 (s, 1H), 4.83 (d, J = 15 Hz, 1H), 4.66 (d, J = 15 Hz, 1H), 3.89 - 3.84 (m, 1H), 3.56 - 3.45 (m, 2H), 2.98 (d, J = 18 Hz, 1H), 2.63 - 2.52 (m, 1H, partially obscured by DMSO). LC/MS[M-H]-: 471.4 HPLC (254.4 nm): 2.886 s, 95 %. 5-<'C3-Furan-3-vl-acrvlovlamino)-methvn-2-(oxalvl-amlnoV4.7-dihvdrQ-5H-thienQf2.3-c]pvran-3-carboxvlic acid: "H NMR (400 MHz, DMSO-de) 5 12.32 (s, 1H). 8.20 (t, J = 5 Hz, 1H), 7.99 (s, 1H), 7.71 (s, 1H), 7.33 (d. J = 15 Hz. 1H), 6.68 (s, 1H), 6.42 (d, J = 15 Hz, 1H), 4.81 (d, J = 15 Hz, 1H), 4.65 (d, J = 15 Hz, 1H). 3.74 - 3.67 (m, 1H). 3.44 - 3.34 (m. 2H), 2.91 (d. J = 17 Hz, 1H), 2.53 (dd, 1H, partially obscured by DMSO). LC/MS [M-H]-: 419.4 HPLC (254.4 nm): 2.822 s, 91% 5-((3-Furan-2-yl-acrylovlamino)-methvl)-2-(oxalvl-amino)-4.7-dihydro-5H-thieno[2.3-c]pyran- 3-carbQXvlic acid: "H NMR (400 MHz, DMSO-de) 5 12.32 (s, 1H). 8.37 (t, 1H), 7.77 (s, 1H), 7.23 (d, J = 15 Hz, IN), 6.76 (d, J = 3 Hz, 1H), 6.57 (dd, J = 3 Hz, 2 Hz, 1H), 6.50 (d, J = 15 Hz, 1H), 4.81 (d, J = 15 Hz, 1H), 4.65 (d, J = 15 Hz, 1H), 3.74 - 3.67 (m. 1H), 3.48 - 3.32 (m, 2H), 2.91 (d, J = 17 Hz, 1H), 2.53 (dd, 1H, partially obscured by DMSO). [M-H]: 419.3 HPLC (254.4 nm): 2.815 s, 86% 2-"Oxalvl-aminoV5-<'CC3-oxo-lndane-1-carbonvhamino"nnethvn-4.7-dihvdro-5H-thienor2.3-c]pyran-3-carboxylic acid: 'H NMR (400 MHz, DMSO-dg) 5 12.33 (s, 1H), 8.81 (bs, 1H), 7.74 - 7.62 (m, 3H), 7.47 (t, J = 7 Hz. 1H), 4.83 (d, J = 15 Hz, 1H), 4.67 (d, J = 15 Hz, 1H), 4.29 (t, J = 5 Hz, 1H), 3.41 -3.25 (m, 3H), 2.91 (d, J = 15 Hz, 1H), 2.77 (d, J = 5 Hz, 2H), 2.58 - 2.51 (m, 1H, partially obscured by DMSO). LC/MS [M-H]-: 457.5 HPLC (254.4 nm): 2.634 s, 97 %. By a similar procedure as described in Example 106 the following compound was prepared. 5-(2 4-Dioxo-thiazQlidin-3-vlmethvn-2-(oxalvl-aminoM.7-dihvdro-5H-thienQ[2.3-c]pvran-3-carboxvlic acid: "H NMR (400 MHz, CD3OD and DMSO-dg) 6 4.88 (m, 2H), 3.97 - 3.89 (m, 3H), 3.72 - 3.69 (m. 2H), 3.08 (m, 1H), 3.02 (m, 1H). MS (ESI (-)): 399. HPLC (254.4nm): 2.67. s, 100%. By a simitar procedure as described in Example 81 the following compounds have been prepared. 2-fOxaM-aminoV5-(2'-spiro[1'.3'1dioxolaneW6.7-dihvdro-4H-benzorb1thiQphen-3-carboxylic acid: M.p.: 232 - 234 °C Calculated for C13H13NO7S, 1 x H2O; C, 45.22 %; H, 4.38 %; N, 4.06 %. Found: C, 45.24 %; H, 4.39 %; N, 3.98 %. By a similar procedure as described in Example 107 the following compounds have been prepared. 5-((3.5-Dimethoxy-ben2QvlaminoWmethylV2-fQxalyl-aminoM7-dihvdro-5H-thieno[2.3-c]pvran-3-carboxviic acid: "H NMR (400 MHz, DMSO-de) 5 12.31 (s, 1H), 8.63 (t. J = 5 Hz. 1H), 7.02 (s, 2H), 6.62 (s, 1H), 4.80 (d, J = 15 Hz, 1H), 4.64 (d. J = 15 Hz, 1H). 3.82 - 3.79 (m, 1H). 3.77 (s, 6H), 3.47 -3.45 (m, 2H), 2.94 (d, J = 17 Hz, 1H), 2.53 (dd, J = 17 Hz, 11 Hz, 1H). LC/MS [M-H]-. 463.4 HPLC (254.4 nm): 3.161 s, 93% 5-(5.6'Dichloro-1,3-dioxo-1.3-dihydroHsoindol*2-ylmethyl)-2-("Qxalvl-aminoM.7-dihvdro-5H-thienof2.3-c]pyran-3-carboxylic acid: To a solution of 2-hydroxymethyl-tetrahydro-pyran-4-one (625 mg, 4.81 mmol) in a mixture of pyridine (778 |il, 9.62 mmol) and chloroform (6.0 ml) at 0 °C under nitrogen was slowly added 4-nitrobenzenesuifonyl chloride (1.60 g, 7.22 mmol). The mixture was allowed to By a similar procedure as described in Example 107 the following compounds have been prepared. 5-((3.5-Dimethoxv-benzoylaminoVmethvn-2-(Qxalyl-aminoM.7-dihvdrQ-5H-thieno[2.3-c]pvran-3-carbQxyiic acid: "H NMR (400 MHz, DMSO-ds) 5 12.31 (s, 1H), 8.63 (t. J = 5 Hz, 1H), 7.02 (s, 2H). 6.62 (s, 1H), 4.80 (d, J = 15 Hz, 1H), 4.64 (d, J = 15 Hz, 1H), 3.82 - 3.79 (m, 1H). 3.77 (s, 6H), 3.47 -3-45 (m, 2H), 2.94 (d, J = 17 Hz, 1H), 2.53 (dd, J = 17 Hz, 11 Hz, 1H). LC/MS [M-H]-; 463.4 HPLC (254.4 nm): 3.161 s, 93% 5-(5.6-Dichloro-1.3-dioxo-1.3-dihydroHsoindol-2-vlmethvn-2-(oxalyl-aminoM,7-dihydro-5H-thieno[2.3-c]pvran-3'Carboxylic acid: To a solution of 2-hydroxymethyl-tetrahydro-pyran-4-one (625 mg, 4.81 mmol) in a mixture of pyridine (778 (il, 9.62 mmol) and chloroform (6.0 ml) at 0 °C under nitrogen was slowly added 4-nitrobenzenesulfonyl chloride (1.60 g. 7.22 mmol). The mixture was allowed to warm to room temperature and stirred for 3 h. Chloroform (30 ml) was added and the solution washed with 2.0 N hydrochloric acid (3x10 ml), 5 % NaHCOa (3x10 ml) and water (3 x 10 ml). The organic phase was dried (Na2S04), filtered and the solvent evaporated in yactie. The solid residue was purified by column chromatography on silica gel using a gradient of dichloromethane:hexane:ethyl acetate (1:1:0 to 8:0:2) as eluent. Pure fractions were collected and the volatiles were evaporated in vacya affording 0.98 g (65 %) of 4-nitro-benzenesulfonic acid 4-oxo-tetrahydro-pyran-2-ylmethyl ester as a solid. "H NMR (400 MHz, CDCI3) 5 2.37 (d, 2H, J = 7.8 Hz), 2.57 (m, 1H), 3.63 (m, 1H), 3.89 (m. 1H), 4.20-4.26 (m, 3H), 8.14 (dd, 2H. J = 0.6 Hz, J = 9 Hz), 8.42 (dd, 2H, J = 0.6 Hz, J = 9 Hz). MS m/z: 315.3 (M+). 4-NitrO'benzenesulfonic acid 4-oxo-tetrahydro-pyran-2-ylmethyl ester (0.5 g, 1.59 mmol), ethylene glycol (986 mg, 15.9 mmol) and p-toluene sulfonic acid (61 mg, 0.32 mmol) were refluxed in benzene (20 ml) for 20 h. The solvent was removed in yaeuQ to afford a solid. The solid was dissolved in dichloromethane (30 ml) and successively washed with a saturated aqueous solution of sodium bicarbonate (2x5 ml) and water (2x5 ml). The organic phase was dried (Na2S04), filtered and the solvent removal in yaeuo afforded 582 mg (100 %) of 4-nitro-benzenesulfonic acid 1.4,8-trioxa-spiro[4.5]dec-7-yimethyl ester as a solid. "H NMR (400 MHz, CDCI3) 5 1.53 -1.73 (m, 4H), 3.54 (m, 1H), 3.8 (m, 2H), 3.96 (m, 4H). 4.15 (m, 2H), 8.12 (dd, 2H, J = 1.5 Hz, J = 9.0 Hz), 8.40 (dd, 4H, J = 1.5 Hz, J = 9.0 Hz). MS m/z: 359.3. 3,4-Dichlorophthalimide (90.2 mg, 0.42 mmol) was dissolved in N,N-dimethylformamide (2.0 ml) at room temperature. Sodium hydride (17 mg. 0.42 mmol) was added under nitrogen. 4-Nitro-benzenesulfonic acid 1,4,8-trioxa-spiro[4.5]dec-7-ylmethyl ester (100 mg. 0.28 mmol) was added and the mixture heated to 140 °C for 3 h. After cooling to room temperature the reaction mixture was added to ice water (5 ml) and the mixture extracted with ethyl acetate (3x15 ml). The combined ethyl acetate extracts were washed with 1.0 N hydrochloric acid (2x5 ml), water (2x5 ml), saturated sodium bicarbonate (2x5 ml) and water (2x5 ml). After drying (Na2S04) followed by filtration, the solvent was removed in vacuo affording 97 mg (94 %) of 5,6-dichloro-2-(1,4.8-trioxa-spiro[4.5]dec-7-ylmethyl)-isoindole-1.3-dione as a solid. 'H NMR (400 MHz, CDCI3) 5 1.60 (m, 2H), 1.78 (m. 2H), 3.54 (m, 1H). 3.64 (m, 1H). 3.88 (m, 2H). 3.95 (m, 4H), 7.95 (d. 2H, J = 3 Hz). MS m/z: 373.7 (M+). 5,6-Dichloro-2-(1,4,8-trioxa-spiro[4.5]dec-7-ylmethyl)-isoindole-1,3-dione (87 mg, 0.234 mmol) was dissolved in tetrahydrofuran (2.5 ml). 1.0 N hydrochloric acid (1.0 mi) was added to the solution and the mixture was heated at 75 °C for 20 h. The heterogeneous mixture was evaporated to dryness in vacuo and the resulting solid was dissolved in di-chioromethane (10 mi) and washed with water (3x2 ml). The organic layer was dried (MgSO"), filtered and the solvent evaporated in vacuo affording 62.1 mg (81 %) of 5,6-dichloro-2-(4-oxo-tetrahydro-pyran-2"yimethyl)-isoindole-1,3-dione as a solid. 'H NMR (400 MHz, CDCI3) 5 2.31 - 2.41 (m, 2H), 2.48 (t, 1H, J = 2.0 Hz), 2.62 (m, 1H), 3,60 (m, 1H). 3.72 (m, 1H), 3.99 (m, 2H), 4.29 (m, 1H), 7.96 (d, 2H, J = 2.7 Hz). MS m/z: 331.1 (M+). 5,6-Dichloro-2-(4-oxo-tetrahydro-pyran-2-ylmethyl)-isoindole-1,3-dione (60 mg, 0.18 mmol) was stirred with /e/t-butyl cyanoacetate (33.5 mg, 0.24 mmol), elemental sulfur (6.44 mg, 0.20 mmol) and morpholine (32.4 |.il, 0,37 mmol) in ethanol for 20 h at 50 °C. The volatiles were evaporated in vacuo and the resulting solid was dissolved in dichloromethane (30 ml) and washed with water (2x10 ml). The organic phase was dried (MgS04), filtered and the solvent evaporated in vacuo. The residue (111 mg) was purified by preparative TLC (Kieselgel 6OF254, 1 mm) using a mixture of hexane and ethyl acetate (1:1) as eluent. Pure compound was obtained after evaporation of the solvent in vacuo affording 28 mg (32 %) of 2-amino-5-(5,6-dichloro-1,3-dJoxo-1,3-dihydroHsoindol-2-ylmethyl)-4J-dihydro-5H-thieno[2,3-c]pyran-3-carboxyiic acid te/t-butyi ester as a solid. "H NMR (400 MHz, CDCI3) 5 1.54 (s, 9H), 2.90 (m, 1H), 3.35 (m, 2H). 2.60 (m, 2H), 2.90 (m. 1H), 4.62 (m, 1H), 7.95 (d, 2H, J = 1.8 Hz). MS m/z: 483.3 (M+), 427 (M-57). A mixture of 2-amino-5-(5,6250°C. Calculated for C13H13NO7S; C, 47.70 %; H, 4.00 %; N, 4.28 %. Found: C. 47.93 %; H, 4.09 %; N, 4.27 %. 6-Hvdroxv-2-(oxalvl-amino'>-4.5.6.7"tetrahvdro-ben20[b]thiophen-3-carboxvlic acid: 2-(Ethoxyoxaiyl-amino)-6-(2'-spiro[r,3']dioxolane)-6,7-dihydro-4H-benzo[b]thiophen-3-carboxylic acid ethyl ester (8.7 g, 22.7 mmoi) was dissolved in a ice bath cooled mixture of 25 % trifluoroacetic acid in dichloromethane (100 mi) and water (0.5 ml) was added. The reaction mixture was stirred at 0 °C for 2 h and at room temperature for 48 h. The volatiles were evaporated in vacuo and the residue dissolved in ethanol (100 ml) and evaporated in vacuo (2 times). The solid residue was washed with diethyl ether (80 ml) and dried in vacuo at 50 X affording 6.68 g (88 %) of 2-(ethoxyoxaiyl-amino)-6-oxo-4,5,6,7-tetrahydro-ben20[b]thiophene-3-carboxylic acid ethyl ester as a solid. To a solution of 2-(ethoxyoxalyl-amino)-6-oxo-4,5.6J-tetrahydro-benzo[b]thiophene-3-carboxylic acid ethyl ester (2.0 g, 5.89 mmot) in a mixture of dichloromethane (40 ml) and ethanol (40 ml) was added sodium borohydride (64 mg, 1.77 mmol). The reaction mixture was stirred at room temperature for 64 h, additional sodium borohydride (22.3 mg, 0.59 mmol) was added and stirring was continued for an additional 18 h. Two more portions of sodium borohydride (23 mg and 15 mg) was added during the next 6 h of stirring. To the reaction mixture was added ice cooled saturated ammonium chloride (50 ml) and the resulting mixture was extracted with ethyl acetate (3 x 50 ml). The combined organic extracts were dried (NazSOJ, filtered and evaporated ID vacuo. The residue was dissolved twice in ethyl acetate (100 ml) and evaporated in vacuo. The solid residue was washed with diethyl ether (80 mi) and dried jn vacuo at 50 °C affording 1.46 g (75 %) of 2-(ethoxyoxalyl-amino)-6" hydroxy-4,5,6,7-tetrahydro-benzo[b]thiophene-3-carboxylic acid ethyl ester as a solid. 1.35 g of this material was subjected to column chromatography (slilca gel) using a mixture of ethyl acetate and heptane (1:1) as eluent. Pure fractions were collected and the solvent evaporated in vacuo affording 0.9 g of pure 2-(ethoxyoxalyl-amino)-6-hydroxy-4,5,6 J-tetrahydro-ben2o[b]thiophene-3-carboxylic acid ethyl ester as a solid. "H NMR (300 MHz, CDCI3) 5 1.42 (m. 6H). 1.86 (m, 2H), 2.02 (m. 1H), 2.71 (dd, 1H), 2.85 (m, 1H), 3.00 (m, 2H). 4.19 (bs, 1H), 4.40 (dq, 4H), 12.45 (bs, 1H. NHCO). To a solution of the above di-ethyl ester (0.3 g, 0.88 mmol) in water (10 ml) was added 1 N sodium hydroxide (3.1 ml, 3.08 mmol). The resulting reaction mixture was stirred at room temperature for 16 h. The aqueous phase was acidified by addition of concentrated hydrochloric acid to pH = 1 and the reaction mixture was evaporated in vacuo to Vz the original volume. The precipitate was filtered off. washed with a small portion of diethyl ether and dried in vacuo at 50 °C for 16 h affording 130 mg (52 %) of the title compound as a solid. M.p.: amorph "H NMR (300 MHz, DMSO-dg) 5 1.63 (m. 1H), 1.86 (m, 1H), 2.5 (m, 1H, partly obscured by DMSO). 2.71 (m, 1H), 2.86 (m. 2H), 3.91 (m, 1H), 4.87 (bs, 1H), 12.35 (bs, 1H, NHCO), The following compound was prepared in a similar way as described in example 107. 5-('2-Methvl-4-oxo-4H-quina2olin-3-vlmethvn-2-(oxalvl-aminoM.7-dihvdro-5H-thieno[2.3-c]pyran-3-carboxvlic acid: 'H NMR (400 MHz, DMSO-dg) 5 12.32 (s, 1H), 8.10 (d. J = 8 Hz, 1H), 7.80 (t, J = 7 Hz, 1H), 7.59 (d, J = 8 Hz, 1H), 7.49 (t, J = 7 Hz, 1H), 4.78 (d, J = 15 Hz, 1H), 4.53 (d, J = 15 Hz, 1H), 4.39 (d, J = 15 Hz, 1H), 4.21 (dd, J = 15 Hz, 9Hz, 1H), 4.00 - 3.94 (m. 1H), 3.05 (d, J = 17 Hz, 1H), 2.74 - 2.65 (m, 1H, partially obscured by neighboring singlet), 2.68 (s, 3H). ''C NMR (100.6 MHz, DMSO-dg) 5 167.7, 162.8, 161.6, 157.6, 156.1, 148.3, 146.9, 136.0, 130.5, 127.9, 127.8, 126.5, 121.4, 115.0, 74.4, 65.9, 49.8, 31.4, 25.0. [M-H]-: 442.1 HPLC (254.4 nm): 2.631 s, 81 %. 7-(1.3-Dioxo-1.3-dihvdrQ-isQindQl-2-vtmethvlV2-(Qxalvl-amino"-47-dihvdrQ-5H-thienQ c]pyran-3-carboxylic acid: Phthalimidoacetaldehyde diethyl acetal (100 g, 0.38 mol) and 1 N hydrochloric acid (600 ml) was mixture was stirred at reflux temperature for 5 min. or until a homogeneous solution is obtained. The reaction mixture was cooled and the precipitate was filtered off and dried in vacuo at 50 °C for 16 h which afforded 63.3 g (88 %) of phthalimido-acetaldehyde as a solid. "H NMR (300 MHz, CDCI3) 5 4.58 (s, 2H). 7.76 - 7.78(m, 2H), 7.90 - 7.92 (m, 2H). 9.67 (s, 1H). To a mixture of phthalimidoacetaldehyde (64 g, 0.34 mol) and trans-1-methoxy-3-(trimethyisilyloxy)-1,3-butadiene (81.5 g, 0.38 mol) in benzene (600 ml) stirred for 15 min. under nitrogen was added dropwise a 45 % solution of zinc chloride diethyl ether complex in dichloromethane (55.5 ml, 0.17 mol) at 0 °C. The reaction was allowed warm up to room temperature overnight. To the reaction mixture was added water (500 ml) and the resulting mixture was extracted with ethyl acetate (200 ml). The organic extract was washed successively with 1.0 N hydrochloric acid (2 x 200 ml) and brine (200 mi). The organic phase was dried (Na2S04), filtered and the solvent evaporated in vacuo which afforded a slowly crystallising oil (98 g). To the solid was added a mixture of ethyl acetate and diethyl ether (400 ml, 1:1) and the resulting precipitate was filtered off, washed with a small portion of diethyl ether and dried at 50 °C for 1h affording 59.8 g (69 %) of 2-(4-oxo-3,4-dihydro-2H-pyran-2-ylmethyl)-isoindoie-1,3-dione as a solid. The filtrate was evaporated in vacuo and the residue purified by column chromatography on silica gel (1 L) using a mixture of ethyl acetate and heptane (1:2) as eluent. Pure fractions were collected and the solvent evaporated in vacuo to almost dryness, the solid was filtered off and dried in yacye at 50 °C for 16 h affording an additional 15 g (17 %) of 2-(4-oxo-3,4"dihydro-2H-pyran-2-ylmethyl)-isoindole-1,3-dione as a solid. "H NMR (300 MHz, CDCI3) 5 2.61 (d, 2H), 3.85 (dd, 1H). 4.18 (dd, 1H). 4.76 (m, 1H), 5.43 (d, 1H). 7.28 (d, 1H), 7.69 - 7.77 (m, 2H). 7.84 - 7.88 (m, 2H). 2-(4-Oxo-3,4-dihydro-2H-pyran-2-ylmethyi)-Jsoindole-1,3-dione (13 g, 0.051 mol) was dissolved in ethyl acetate (250 ml) and placed in a Parr bottle. 10 % Pd/C (1.5 g) was carefully added and the mixture was shaken under a pressure of 30 psi of hydrogen for 6.5 h (Parr apparatus). Filtration followed by evaporation of the ethyl acetate in vacuo afforded a crude 11.5 g of 2-(4-oxo-tetrahydro-pyran-2-ylmethyl)-isoindole-1,3-dione pure enough for the next step. Analytical pure compound could be obtained by purification of a small sample (250 mg) by column chromatography on silica gel, utilising hexane/ethyi acetate as a gradient (from 100/0 to 50/50). Pure fractions were collected and the solvent evaporated in yaouQ affording 142 mg (55 %) 2-(4-oxo-tetrahydro-pyran-2-ylmethyl)-isoindole-1,3-dione as a solid. "H NMR (400 MHz, CDCy 5 2.30 - 2.68 (m, 4H). 3.62 (m, 1H), 3.74 (m, 1H), 4.00 (m, 2H), 7.75 (m, 2H), 7.88 (m. 2H). To a mixture of 2"(4-oxo-tetrahydro-pyran-2"ylmethyl)-isoindole-1,3-dione (18.7 g, 0.072 mol), "ert-butyi cyanoacetate (11.2 g, 0.079 mol) and elemental sulfur (2.5 g, 0.079 mol) in ethanoi was added morpholin (20 ml) and the resulting mixture was stirred at 50 '"C for 3 h. The cooled reaction mixture was filtered and the voiatiles were evaporated in vacuo. To the residue was added water (200 ml) and diethyl ether 100 ml. A precipitate was filtered off and dried in yi£UQ at 50 °C affording 9.1 g (30 %) of 2-amino-5-(1,3-dioxo-1,3-dihydro-isoindol-2-ylmethyl)-4,7-dihydro-5H-thieno[2,3-c]pyran-3-carboxylic acid fe/t-butyl ester as a solid. The filtrate was extracted with ethyl acetate (2 x 150 ml) and washed with brine (100 ml), dried (Na2S04), filtered and the solvent evaporated in vacuo. The residue (20 g) was purified by column chromatography on silica gel (1 L) using as mixture of hexane and ethyl acetate (1:2) as eluent. Pure fractions were collected and the solvent evaporated in vacuo. The residue was washed with diethyl ether and the solid was filtered off and dried in vacuo at 50 X affording an additional 2.2 g (7 %) of 2-amino-5-(1,3"dioxo-1,3-dihydro-isoindol-2-ylmethyl)-4,7-dihydrO"5H-thieno[2,3-c]pyran-3-carboxylic acid "ert-butyl ester as a solid. The filtrate was evaporated in vacuo affording almost pure 10.2 g (34 %) of 2-amino-7-(1,3- dioxo-1,3-dihydro-isoindol-2-ylmethyl)-4,7-dihydro-5H-thieno[2,3-c]pyran-3-carboxylicacid terf-butyl ester as an oil. 2-amino-5-(1,3-dioxo-1,3-dihydro-isoindol-2-ylmethyl)-4,7«dihydro-5H-thieno[2,3-c]pyran"3-carboxyiic acid terf-butyl ester "H NMR (300 MHz, CDCI3) 5 1.50 (s, 9H). 2.54 - 2.63 (m, 1H), 2.84 - 2.90 (m, 1H), 3.79 (q, 1H), 3.96 - 4,04 (m. 2H), 4.48 - 4.62 (m. 2H), 5.91 (bs, 2H, NHj), 7.70 (m, 2H), 7.84 (m, 2H). 2-amino-7-(1.3-dioxo-1,3-dihydro-isoindol-2-ylmethyl)-4J-dihydro-5H-thieno[2,3-c]pyran-3-carboxyiic acid ferf-butyl ester "H NMR (300 MHz, CDCI3) 5 1.50 (s, 9H), 2.71 - 2.90 (m, 2H), 3.67 - 3.77 (m. 2H). 4.02 -4.15 (m, 2H), 4.90 (m, 1H), 6.04 (bs, 2H. NH"), 7.70 (m, 2H), 7.84 (m, 2H). A mixture of 2-amino-7-(1,3-dioxo-1.3-dihydro-isoindol-2-ylmethyl)-4,7-dihydro-5H-thieno[2,3-c]pyran-3-carboxylic acid tert-hutyi ester (10.2 g, 0.25 mol), imidazol-1-yl-oxo-acetic acid tert-butyl ester (7.2 g, 0.037 mol) in dry tetrahydrofuran (150 ml) was stirred at room temperature for 4 h. An additional portion of imidazof-l-yl-oxo-acetic acid tert-butyl ester (2.0 g, 0.01 mol) was added and the resulting mixture was stirred for 16 h at room temperature. The precipitate was filtered off and washed with small portions of diethyl ether and dried in yasuo affording 3.5 g (26 %) of 2-(tert-butoxyoxalyl-amino)-7-(1.3-dioxo-1.3-dihydro-isoindol-2-ylmethyl)-4,7-dihydro-5H-thieno[2,3-c]pyran-3-carboxylicacid/e/t-butyl ester as a solid. The filtrate was evaporated in vacuo and to the residue was added water (100 ml) and ethyl acetate (100 ml). The precipitate was filtered off and dried in vacuo at 50 °C affording an additional 0.8 g (6 %) of 2-(fert-butoxyoxaiyl-amino)-7-(1,3-dioxo-1,3-dihydro-isoindol-2-ylmethyl)-4,7-dihydro-5H-thieno[2,3-c]pyran-3-carboxylic acid tert-butyl ester as a solid. "H NMR (300 MHz, CDCI3) 5 1.60 (s, 9H), 1.62 (s, 9H). 2.79 - 2.97 (m. 2H). 3.73 (m, 1H). 3.83 • 3.88 (dd. 1H). 4.07 - 4.16 (m, 2H). 5.09 (m, 1H). 7.71 (m. 2H). 7.85 (m. 2H), 12.55 (bs, 1H, NHCO). The above 2-(te/t-butoxyoxalyl-amino)-7-(1,3-dioxo-1,3-dihydroHsoindol-2-ylmethyl)-4.7-dihydro-5H-thieno[2,3-c]pyran-3-carboxyiic acid fe/t-butyl ester (0.8 g, 1.47 mmol) was added to a solution of 25 % trifluoroacetic acid in dichloromethane (30 ml). The reaction mixture was stirred at room temperature for 6 h, at which time, the solvent was removed in vacuo. The residue was precipitated by addition of diethyl ether, filtered off and dried in vacuo at 50 °C affording 0.5 g (79 %) of the titlfi compoun250°C. Calculated for CigHuNAS, 0.5 x H2O; C, 51.94 %; H, 3.44 %; N, 6.38 %. Found: C, 52.02 %; H, 3.37 %; N. 6.48 %. FXAMPLE131 7-(ArfitvtaminQ-methvlV2-(Qxalvl-aminoM.7-dihydrQ-5H4hienQ[2.3-c]pyran-3"" acid: To a mixture of 2-amino-7-(1,3-dioxo-1,3-dihydro-isoindol-2-ylmethyl)-4J-dihydro-5H-thieno[2,3-c]py"an-3-ca"boxyiic acid fe/t-butyl ester (6.0 g, 0.014 mol) in ethanol (100 ml) was added hydrazine hydrate (1.4 ml, 0.028 mol). The reaction mixture was heated at reflux for 1 h, cooled and the precipitate filtered off. The filtrate was evaporated in vacuo and to the residue was added water (100 ml) and the resulting mixture was extracted with diethyl ether (2 X 100 ml). The combined organic extracts were washed with brine (100 ml), dried (Na2S04), filtered and the solvent evaporated in yacuQ affording 2,9 g (71 %) of 2-amino-7-aminomethyl-4,7-dihydro-5H-thieno[2,3-c]pyran-3-carboxylic acid tert-butyl ester as an oil. "H NMR (300 MHz, CDCI3) 5 1.55 (s, 9H), 2.70 - 2.97 (m, 4H), 3.69 - 3.78 (m, 1H), 4.13 (m, 1H), 4.50 (m, 1H), 6.09 (bs, 2H, thiophen-NHj). To a ice water cooled solution of the above 2-amino-7-aminomethyl-4,7-dihydro-5H-thieno[2,3-c]pyran-3-carboxylic acid fert-butyl ester (1.5 g, 5.27 mmol) and triethylamine (1.5 ml) in dichloromethane (50 ml) was added dropwise acetylchloride (0.46 g. 5.80 mmol). The reaction mixture was allowed to reach room temperature and stirred for an additional 0.5 h. The reaction mixture was washed with water (2 x 25 ml), dried (Na2S04), filtered and the solvent evaporated in vacuQ. The residue was purified by column chromatography on silicagel (1 L) using first ethyl acetate and later on a mixture of ethyl acetate and ethanol (20:1) as eluents. Pure fractions were collected and the solvent evaporated in vacuo affording 0.3 g (17 %) of 7-(acetylamino-methyl)-2-amino-4,7-dihydro-5H-thieno[2,3-c]pyran-3-carboxylic acid tert-butyl ester as a solid. "H NMR (300 MHz, CDCia) 5 1.56 (s, 9H), 1.99 (s, 3H), 2.77 (m. 2H), 3.19 (m. 1H), 3.67 -3.79 (m, 2H), 4.09 - 4.16 (m, 1H), 4.63 (m, 1H), 5.91 (bs, 1H), 6.10 (bs, 2H). To a mixture of the above 7-(acetylamino-methyl)-2-amino-4,7-dihydro-5H-thieno[2,3-c]pyran-3-carboxyiic acid tert-butyi ester (0.3 g, 0.92 mmoi) in dry tetrahydrofuran (40 ml) was added dropwise a mixture of Jmidazoi-1-yl-oxo-acetic acid tert-butyi ester (0.22 g, 1.10 mmol) in dry tetrahydrofuran (5 ml). The mixture was stirred at room temperature for 3 h. The volatiies were evaporated in vacuo and the residue was dissolved in ethyl acetate (100 ml) and washed with water (50 ml) and brine (50 ml). The organic phase was dried (Na2S04), filtered and evaporated in vacuo. The residue (0.4 g) was stirred with a mixture of diisopropyi ether (5 ml) and diethyl ether (5 ml). The precipitate was filtered off and the filtrate evaporated in vacuo affording 0.25 g (60 %) of 7-(acetylamino-methyl)-2-(fert-butoxyoxalyl-amino)-4,7-dihydro-5H-thieno[2,3-c]pyran-3-carboxylic acid fe/t-butyl ester as an oil: "H NMR (300 MHz. CDCI3) 5 1.64 (s. 9H), 1.65 (s. 9H), 2.02 (s, 3H), 2.87 (m. 2H). 3.29 (m, 1H), 3.74(m. 1H). 3.89(ddd, 1H), 4.18(m, 1H), 4.78(m. 1H). 5.93(bs, 1H, NHCOMe), 12.5 (s, 1H. NHCOCOOH). The above 7-(acetylamino-methyl)-2-(tert-butoxyoxalyl-amino)-4,7-dihydro-5H-thieno[2,3-c]pyran-3-carboxylic acid fert-butyl ester (0.2 g, 0.44 mmoi) was added to a solution of 25 % trifluoroacetic acid in dichloromethane (20 ml). The reaction mixture was stirred at room temperature for 4 h, at which time, the solvent was removed in vacuo. The residue was precipitated by addition of diethyl ether, filtered off and dried in vacuo at 50 X affording 0.11 g (73 %) of the title compound as a solid. M.p.:220-222°C. "H NMR (300 MHz, DMSO-dg) 5 1.87 (s, 3H), 2.82 (bs. 2H), 3.19 (m, 1H), 3.51 (m, 1H), 3.67 (m, 1H). 4.07 (m. 1H), 4.69 (m, 1H), 8.14 (t, 1H, NHCOMe), 12.3 (s, 1H, NHCOCOOH). To 2-amino-5-(1,3-clioxo-1,3-dihydro-isoindol-2-ylmethyl)-4,7-dihydro-5H-thieno[2,3-c]pyran-3-carboxylic acid fert-butyl ester (4.5 g, 0.011 mole) dissolved in dichloromethane (30 ml), was added sodium bicarbonate (1.0 g, 0.011 mole) dissolved in water (16 ml). The reaction mixture was cooled to 0 °C and 9-fluorenylmethyl chloroformate (3.0 g. 0.012 mole) was added. After stirring for 5 minutes the reaction mixture was warmed to room temperature and stirred vigorously for 16 h. The organic layer was separated and washed with brine (10 ml). The aqueous phase was extracted with dichloromethane (2 x 20 ml) and the combined organic phases were dried (MgSO"), filtered and evaporated in vacuo to give an orange solid which was purified by flash chromatography using dichloromethane as eluent. Pure fractions were collected and evaporated in vacuo affording 5.6 g (81 %) of 5-(1,3-dioxo-1,3-dihydrc-isoindol-2-ylmethyl)-2-(9H-fiuoren-9-ylmethoxycarbonylamino)-4,7-dihydro-5H-thieno{2.3-c]pyran-3-carboxylic acid tert-butyl ester as a solid. "H NMR (400 MHz, CDCI3) 6 10,60 (bs, 1H). 7.87 - 7.84 (m, 2H), 7.75 (d, J = 8 Hz, 2H). 7.73 - 7.70 (m. 2H), 7.60 (d, J = 8 Hz, 2H). 7.39 (t, J = 8 Hz. 2H). 7.30 (t J = 8 Hz, 2H), 4.74 (d. J = 14 Hz, 1H), 4.62 (d, J = 14 Hz, 1H), 4.48 (d, J = 7 Hz, 2H), 4.27 (t, J = 7 Hz, 1H), 4.05 -4.00 (m, 2H), 3.86 - 3.80 (m. 1H), 2,92 (d, J = 17 Hz, 1H), 2.64 (dd, J = 17, 9 Hz. 1H), 1.52 (s, 9H). LC/MSlM+nr: 637.49 The above F-moc protected thieno(2,3-c]pyran (5.5 g, 8.6 mmole) was added at 0 °C to a solution of 20 % trifluoroacetic acid in dichloromethane (30 ml). The reaction was stirred for 4 h at room temperature. The volatiles were evaporated in vafiUQ and the residue was precipitated with diethyl ether, filtered off and dried, which afforded 4.2 g (85 %) of 5-(1,3-dioxo-1,3-dihydro-isoindol-2-ylmethyl)-2-(9H-fluoren-9-ylmethoxy-carbonyiamino)-4,7-dihydro-5H-thieno[2,3-c]pyran-3"Carboxylic acid as a solid. "H NMR (400 MHz, DMSO-de) 5 10.22 (br s, 1H), 7.88 (d , J = 5 Hz, 2H). 7.88 - 7.82 (m, 4H), 7.66 (d, J = 5 Hz, 2H), 7.40 (t, J = 5 Hz, 2H), 7*32 (t, J = 5 Hz, 2H), 4.68 - 4.48 (m, 4H), 4.34 (t, J = 5 Hz, 1H). 3.90-3.81 (m, 2H), 3.72 - 3.67 (m, 1H), 2.87(m, 1H), 2.51 (m, 1H). To Wang-Resin (3.75 g, 4.5 mmol) was added dichloromethane (50 mi) and the mixture was cooled to 0 °C under nitrogen. Diisopropylethylamine (25 ml) was added followed by methanesulfonyl chloride (2.25 ml, 29 mmol). The reaction was stirred at 0 °C for 0.5 h, then at room temperature for another 0.5 h. The resin was filtered off and washed with dichloromethane (2 x 30 mt), N-methylpyn-olidinone (20 ml) and again with dichloromethane (2 X 30 ml). The Wang-resin methansuifonyl ester was dried in vacuo for 2 h and used directly in the next step. To the above Wang-Resin methansuifonyl ester and 5-(1.3-dioxo-1,3-dihydro-isoindol-2-ylmethyl)-2-(9H-fluoren-9-yimethoxy-carbonylamino)-4,7-dihydro-5H-thieno[2,3-c]pyran-3-carboxylic acid (4.85 g, 8.4 mmol) was added N-methylpyrrolidinone (45 ml). Cesium car- bonate (2.2 g, 6.7 mmol) was added and the reaction stired under nitrogen for 16 h and then at 80 °C for 36 h. The mixture was cooled to room temperature, the resin filtered off, washed with water, methanol, and dichloromethane repeatedly and dried in vacuo for 2 h affording 5-(1,3-dioxo-1,3-dihydro-isoindol-2-ylmethyl)-2-(9H-fluoren-9-ylmethoxy-carbonyiamino)-4.7-dihydro-5H-thieno[2,3-c]pyran-3-cartDOxylic acid Wang-Resin ester. The above Wang-Resin ester (4.85 g) was stin-ed in a solution of 20 % piperidine in tetrahy-drofuran (20 ml) for 45 minutes. The resin was then filtered off, washed with tetrahydrofuran (2 X 20 ml), methanol (2 x 20 ml), and dichloromethane (3 x 20 ml) and dried in vacuo for 3 h affording 2-amino-5-(1,3-dioxo-1,3-dihydro-isoindol-2-yimethyl)-4,7-dihydro-5H-thieno[2,3-c]pyran-3-carboxylic acid Wang-Resin ester. The above Wang-Resin ester (4.85 g) was suspended in a mixture of dichloromethane (50 ml) and triethylamine (3.0 ml), lmidazol-1-yl-oxo-acetic acid tert-butyl ester (4,2 g, 0.021 mol) was added under nitrogen and the reaction stirred at room temperature for 16 h. The resin was filtered off. washed with methanol (30 ml) then dichloromethane (30 ml) and this process was repeated twice. The resin was dried in vacuo for several hours affording 2-(fe/t-butoxyoxalyl-amino)-5-(1,3-dioxo-1,3-dihydro-isoindol-2-ylmethyl)-4,7-dihydro-5H-thieno[2.3-c]pyran-3-carboxylic acid Wang Resin. A small sample of the above Wang-Resin ester was treated with 20 % trifluoroacetic acid in dichloromethane (3 ml) for 1 h. The resin was filtered off and the filtrate concentrated in vacuo. The residue was evaporated twice from dichloromethane yielding 30 mg of a solid, which had "H NMR and MS consistent with the compound synthesized in example 106. The loading of the Wang-Resin was thus determined to be 0.6 mmol/g. The above Wang Resin ester (3.0 g, 1.8 mmol) was suspended in dichloromethane (25 ml). Hydrazine (0.14 ml, 4.5 mmol) was added and the reaction stirred under nitrogen at room temperature for 24 hours. The resin was filtered off and washed multiple times, alternating between methanol and dichloromethane. The filtrate was collected and concentrated to yield 260 mg of a solid. The reaction was determined to be incomplete by analysis of the byproduct, at which time the resin was suspended again in dichloromethane (15 ml) and treated with hydrazine (50 \x\) for an additional 16 h. The resin was filtered off and washed as before, yielding an additional 30 mg of byproduct from the filtrate. At this point the reaction was judged to be complete and the resin was dried iQ vacuo for 3 h, yielding 2.67 g of 5-aminomethyl-2-(tert-butoxyoxalyl-amino)-4,7-dihydro-5H-thieno[2,3-c]pyran-3-carboxylicacid Wang-Resin. The resin gave a positive ninhydrin test for amines. The above Wang Resin ester (2.67 g) was suspended in a mixture of tetrahydrofuran and dichloromethane (1:1, 90 ml) and distributed to the OntoBlock (80 wells, 0.02 mmol perweil). The blocks were drained. Meanwhile, 80 carboxylic acids were weighed into individual vials (0.044 mmol per vial). A solution of 1-(3-Dimethylaminopropyl)-3-ethylcarbodiimide hydrochloride (0.85 g, 4.4 mmol), l-hydroxy-benzotriazoie hydrate (0.6 g. 4.4 mmol), and triethy-lamine (1.1 ml, 8.0 mmol) was prepared in N,N-dimethylformamide (100 ml). This solution was added to each vial (1 ml per vial) and then the contents of each via! were transferred to a well of the OntoBlock (occasionally the vials were sonicated to achieve full solubility). The blocks were then shocked for 2 days. After this time the blocks were drained and washed using methanol and dichloromethane. The blocks were then placed in a vacuum dessicator for 2 h, after which 1 mi of a solution of imidazol-1-yl-oxo-acetic acid fert-butyl ester (0.2 M in dichloromethane) was added to each well. The blocks were then shocked for 16 h. Again the blocks were washed using the above method. After washing, 1 ml of a solution of 20 % trifluoroacetic acid in dichloromethane was added to each well and allowed to sit for 45 minutes. The block was drained and the filtrates collected in a microtiter plate. The wells were treated with an additional 0.5 ml solution of 20 % trifluoroacetic acid in dichloromethane and the filtrate again collected. The volatiles were evaporated in vacuo, yielding 80 compounds as solids in the microtiter plate. The plate was analyzed by Mass Spectrometry in which 66 of the wells showed the expected product as the molecular ion. Xi is point of attachment. The percentage means the area of the peak of the HPLC at 220 nm. R Formula Mw LC/MS C24H2oN20gS 496,50 495(M-H,21%) C20H20N2O9S 464.45 463 (M-H,30%) and washed with water (2 x 50 ml), diethyl ether (2 x 30 ml) and dried in vacuo at 50 °C affording 130 mg (30 %) of the title compound as a solid, M.p.:>250°C Calculated for C"oHsNsOgSiNai, 1 x H2O ; C, 39.22 %; H, 2.30 %; N, 9.15 %. Found: C. 39.32 %; H. 2.35 %; N, 8.89 %. EXAMPLE 134 7-fQxalvl-amino"-thieno[2.3-b]pvrazine-6-carboxylicacid: To a solution of 6-amino-thieno(2,3-b]pyrazine-7-carboxylJc acid methyl ester (62.7 mg, 0.3 mmol) in tetrahydrofuran (0.5 ml) was added imidazol-1-yl-oxo-acetic acid te/t-butyl ester (117.6 mg, 0.6 mmol) and triethylamine (42 "l, 0.3 mmol). The resulting mixture was stirred for 20 h at room temperature. The volatiles were removed in yasuQ and the residue was dissolved in ethyl acetate (5.0 mt), washed with 1 % hydrochloric acid (2x2 ml), water (2x2 ml), dried (MgS04), filtered and the solvent evaporated in vacuo affording 96 mg (95 %) of 6-(/ert-butoxyoxalyl-amino)- thieno[2,3-b]pyrazine-7-carboxylic acid methyl ester as a solid. "H NMR (400 MHz, CDCy 5 1.60 (s, 9H), 3.80 (s, 3H), 8.60 (d, 1H, J = 1.5 Hz), 8.70 250°C. "H NMR (300 MHz. DMSO-dg) 5 3.12 (t, 2H), 4.89 (t. 2H), 12.0 (bs. 1H, NHCO). Claims 1. A compound that fulfills ail of the following 3 criteria: (1) has a structure represented by Formula I: where R, R2 and R4 are any chemical group or combination of chemical groups; (2) acts as a phosphotyrosine recognition unit ligand, preferably an inhibitor or modulator of one or more PTPases or proteins that contain SH2 domains; and (3) has a molecular weight below or equal to 2500 daltons 2. A compound according to claim 1 which has a structure represented by Formula II where R, R1and R4 are any chemical group or combination of chemical groups, and R, preferably is H. 3. A compound that fulfills all of the following 3 criteria: (1) has a structure represented by Formula III: where Ri, R2, R3, R4 and R5 are any chemical group or combination of chemical groups, and R3 and R5 may be covaiently linked to each other; (2) acts as a phosphotyrosine recognition unit ligand, preferably an inhibitor or modulator of one or more PTPases or proteins that contain SH2 domains; and (3) has a molecular weight below or equal to 2500 daltons. 4. A compound according to claim 3 which has a structure represented by Formula IV where Ri. R3, R4 and R5 are any chemical group or combination of chemical groups, and R3 and R5 may be covaiently linked to each other, and R preferably is H. 5, A compound according to claim 4 which has a structure represented by Formula V where Ri, R3, R4 and R5 are any chemical group or combination of chemical groups, and R3 and R5 may be covalently linked to each other, and R is preferably H. 6. A compound according to claim 5 which has a structure represented by Formula Vl where R3, R4 and R5 are any chemical group or combination of chemical groups, and R3 and R5 may be covalently linked to each other, and R is preferably H. 7. A compound according to claim 3, which has a structure represented by Formula Vli where A together with the double bond in formula VII represents any aryl as defined above, and Ri, R2, Rs and R4 are any chemical group or combination of chemical groups. 8. A compound according to claim 7, which has a structure represented by Formula viii where A together with the double bond in formula VIII represents any aryl as defined above, and R, R,, R3 and R4 are any chemical group or combination of chemical groups, and R preferably is H. 9. A compound according to claim 7 which has a structure represented by Formula IX where A together with the double bond in formula IX represents any aryl as defined above, and Ri, Rj, R3 and R4 are any chemical group or combination of chemical groups. 10. A compound according to claim 9 which has a structure represented by Formula X where A together with the double bond in formula X represents any aryl as defined above, and R2, R3 and R4 are any chemical group or combination of chemical groups. 11. A compound according to claim 10 which has a structure represented by Formula XI where A together with the double bond in formula Xi represents any aryl as defined above, and R, R3 and R4 are any chemical group or combination of chemical groups, and R preferably is H. 12. A compound according to claim 3 which has a structure represented by Formula XII where R, is a chemical group capable of being a proton donor and/or a proton acceptor, preferably -COOH, 5-tetrazolyl, -NH2, -CONH2, and R, Rj, R3 and R4 are any chemical group or combination of chemical groups. 13. A compound according to any one of the preceding claims which substantially acts as a classical, competitive inhibitor of one or more PTPases. 14. A compound according to any one of claims 1 to 12 which substantially acts as a mixed-type inhibitor of one or more PTPases. 15. A compound according to any one of claims 1 to 14 which substantially acts as an inhibitor of one or more PTPases involved in regulation of tyrosine kinase signalling pathways. 16. A compound according to any one of claims 1 to 14 which substantially inhibits or modulates receptor-tyrosine kinase signalling pathways via interaction with one or more regulatory PTPases, preferably the signalling pathways of the insulin receptor, the iGF-l receptor and/or other members of the insulin receptor family, the EGF-receptor family, the platelet-derived growth factor receptor family, the nerve growth factor receptor family, the hepatocyte growth factor receptor family, the growth hormone receptor family and/or members of other receptor-type tyrosine kinase families. 17. A compound according to any one of claims 1 to 14 which substantially inhibits or modulates non-receptor tyrosine kinase signalling through modulation of one or more regulatory PTPases, preferably modulation of members of the Src kinase family or other intracellular kinases. 18. A compound according to any one of claims 1 to 14 which substantially inhibits or modulates the activity of one or more PTPases that negatively regulate signal transduction pathways, 19. A compound according to any one of claims 1 to 14 which inhibits or modulates the activity of one or more PTPases that positively regulate signal transduction pathways, preferably CD45. 20. A compound according to any one of claims 1 to 14 which inhibits or modulates the activity of one or more PTPases that positively regulate signal transduction pathways in immune cells. 21. A compound according to any one of claims 1 to 14 which inhibits or modulates the activity of one or more PTPases that negatively regulate signal transduction pathway. 22. A compound according to any one of claims 1 to 14 which inhibits one or more PTPases via binding to the active site of said PTPase(s) or to other sites that negatively influences the binding of substrate to said PTPase(s), an allosteric modulator. 23. A compound according to any one of claims 1 to 14 which modulates the activity of one or more PTPases via interaction with structures positioned outside of the active sites of the enzymes, preferably SH2 domains. 24. A compound according to any one of claims 1 to 14 which modulates the signal transduction pathways via binding of the compounds of the invention to SH2 domains or PTB domains of non-PTPase signalling molecules. 25. A compound according to any of the preceding claims characterized by being a selective PTPase inhibitor or a compound that is a selective phosphotyrosine recognition unit ligand. 26. A compound according to any of claims 1 to 24 characterized by being a non-selective PTPase inhibitor. 27. A compound according to claim 26 characterized by being an inhibitor or modulator of at least 4 PTPases or 4 PTPase families. 28. A compound according to claim 25 characterized by being selective for a PTPase not described herein. 29. A compound according to claim 25 characterized by being selective for a PTPase listed in Table 1. 30. A compound according to claim 25 characterized by being selective for the PTPa family. 31. A compound according to claim 25 characterized by being selective for PTPa. 32. A compound according to claim 25 characterized by being selective for PTPe. 33. A compound according to claim 25 characterized by being selective for CD45. 34. A compound according to claim 25 characterized by being selective for PTPp family. 35. A compound according to claim 25 characterized by being selective for PTPp. 36. A compound according to claim 25 characterized by being selective for PTP-DEP1. 37. A compound according to claim 25 characterized by being selective for PTP-LAR family. 38. A compound according to claim 25 characterized by being selective for PTP-LAR. 39. A compound according to claim 25 characterized by being selective for PTPa. 40. A compound according to claim 25 characterized by being selective for PTP5. 41. A compound according to claim 25 characterized by being selective for PTPji family. 42. A compound according to claim 25 characterized by being selective for PTP)i. 43. A compound according to claim 25 characterized by being selective for PTPK. 44. A compound according to claim 25 characterized by being selective for PTP1B family. 45. A compound according to claim 25 characterized by being selective for PTP1B. 46. A compound according to claim 25 characterized by being selective for TC-PTP. 47. A compound according to claim 25 characterized by being selective for SHP-PTP family. 48. A compound according to claim 25 characterized by being selective for SHP-1. 49. A compound according to claim 25 characterized by being selective for SHP-2. 50. A compound according to claim 25 characterized by being selective for PTPi; family. 51. A compound according to claim 25 characterized by being selective for PTP*:;. 52. A compound according to claim 25 characterized by being selective for PTPy. 53. A compound according to claim 25 characterized by being selective for PTP-PEST family. 54. A compound according to claim 25 characterized by being selective for PTPH1 family. 55. A compound according to claim 25 characterized by being selective for PTPH1. 56. A compound according to claim 25 characterized by being selective for PTPD1. 57. A compound according to claim 25 characterized by being selective for PTPD2. 58. A compound according to claim 25 characterized by being selective for PTPMEG1. 59. A compound according to claim 25 characterized by being selective for IA-2 family. 60. A compound according to claim 25 characterized by being selective for IA-2. 61. A compound according to claim 25 characterized by being selective for IA-2p. 62. A compound according to claim 25 characterized by being selective for PTP\|; family. 63. A compound according to claim 25 characterized by being selective for PTP\|/. 64. A compound according to claim 25 characterized by being selective for PTPp. 65. A compound according to claim 25 characterized by being selective for PTPtf). 66. A compound according to any one of the preceding claims having a molecular w/eight of less than 1000 Daltons, and preferably of more than 100 Daltons. 67. A compound according to any one of the preceding claims having a Kj value of less than 200 p.M against one or more PTPases. 68. A compound according to any one of the preceding claims having a Kj value of less than 2 laM against one or more PTPases. 69. A compound according to any one of the preceding claims having a Kj value of less than 100 nM against one or more PTPases. 70. A compound according to any one of the preceding claims having a IC50 value of less than 200 M against one or more molecules with phosphotyrosine recognition unit(s). 71. A compound according to any one of the preceding claims having a IC50 value of less than 2 M against one or more molecules with phosphotyrosine recognition unit(s). 72. A compound according to any one of the preceding claims having a IC50 value of less than 100 nM against one or more molecules with phosphotyrosine recognition unit(s). 73. A compound according to any one of claims 1 to 66 having a Kj value of < 2 ^M against one or two PTPases or PTPase families and a K, value of > 50 ^M against at least two other PTPases or PTPase families. 74. A compound according to any one of claims 1 to 66 having a Kj value of < 100 nM against one or two PTPases or PTPase families and a Kj value of > 10 ^M against at least two other PTPases or PTPase families. 75. The use of a compound according to any one of the preceding claims for preparing a me dicament for modulating the activity of one or more PTPases or other molecules with phos photyrosine recognition unit(s). 76. The use of a compound according to any one of claims 1 to 74 for preparing a medicament for managing, treating or preventing type I diabetes, type 11 diabetes, impaired glucose tolerance, insulin resistance, obesity, immune dysfunctions including autoimmunity and AIDS, diseases with dysfunctions of the coagulation system, allergic diseases, osteoporosis, proliferative disorders including cancer and psoriasis, diseases with decreased or increased synthesis or effects of growth hormone, diseases with decreased or increased synthesis of homiones or cytokines that regulate the release of/or response to grovirth hormone, diseases of the brain including Alzheimer's disease and schizophrenia, and infectious diseases. 77. The use of a compound according to any one of claims 1 to 74 for preparing a medicament for managing, treating or preventing type 1 diabetes, type II diabetes, impaired glucose tolerance, insulin resistance, and/or obesity. 78. The use of a compound according to any one of claims 1 to 74 for preparing a medicament for managing, treating or preventing conditions with immune dysfunctions, including autoimmunity such as rheumatoid arthritis, systemic lupus erythematosus. 79. The use of a compound according to any one of claims 1 to 74 for preparing a medicament for use as an immunosuppressant. 80. The use of a compound according to any one of claims 1 to 74 for preparing a medicament for managing or treating conditions with immune dysfunctions including AIDS. 81. The use of a compound according to any one of claims 1 to 74 for preparing a medicament for managing, treating or preventing allergic diseases, including asthma and allergic skin diseases. 82. The use of a compound according to any one of claims 1 to 74 for preparing a medicament for managing, treating or preventing proliferative disorders, including cancer. 83. The use of a compound according to any one of claims 1 to 74 for preparing a medicament for managing, treating or preventing osteoporosis. 84. The use of a compound according to any one of claims 1 to 74 for preparing a medicament for managing, treating or preventing psoriasis. 85. The use of a compound according to any one of claims 1 to 74 for preparing a medicament for managing, treating or preventing diseases with decreased or increased synthesis or effects of growth hormone, diseases with decreased or increased synthesis of hormones or cytokines that regulate the release of/or response to growth hormone. 86. The use of a compound according to any one of claims 1 to 74 for preparing a medicament for managing, treating or preventing diseases with dysfunctions of the coagulation system. 87. The use of a compound according to any one of claims 1 to 74 for preparing a medicament for managing, treating or preventing diseases of the brain including Alzheimer's disease and schizophrenia. 88. The use of a compound according to any one of claims 1 to 74 for preparing a medicament for managing, treating or preventing infectious diseases. 89. A pharmaceutical composition comprising an effective amount of a compound according to any one of claims 1 to 74 together with a pharmaceutically acceptable carrier or diluent. 90. The pharmaceutical composition according to claim 89 comprising between 0.5 mg and 1000 mg of a compound according to any one of the claims 1 to 74 per unit dose. 91. A method of modulating the activity of one or more PTPases or other molecules with phosphotyrosine recognition unit(s) in a subject in need of such management comprising administering to said subject an effective amount of a compound or composition according to any one of claims 1 to 74. 92. A compound according to any one of claims 1 to 74 coupled to a suitable solid-phase matrix. 93. A method for isolating a protein or a glycoprotein with affinity for a compound accord ing to any one of claims 1 to 74 from a biological sample, comprising: • contacting an immobilized compound according to claim 89 with said biological sample in order for said immobilized compound to form a complex by binding said protein or glycoprotein, • removing unbound material from said biological sample and isolating said complex, and • extracting said protein or glycoprotein from said complex. 94. A method for isolating a protein-tyrosine phosphatase with affinity for a compound ac cording to any one of claims 1 to 71 from a biological sample, comprising • contacting an immobilised compound according to claim 89 with said biological sample in order for said immobilised compound to form a complex by binding said protein-tyrosine phosphatase • removing unbound material from said biological sample and isolating said complex • extracting said protein-tyrosine phosphatase. 95. A method for isolating a Src-homology 2 domain containing protein or a phosphotyro- sine binding domain containing protein with affinity for a compound according to any one of the preceding compound claims from a biological sample, comprising • contacting an immobilized compound according to claim 89 with said biological sample in order for said immobilized compound to form a complex by binding said Src-homology 2 domain containing protein or a phosphotyrosine binding domain containing protein • removing unbound material from said biological sample and isolating said complex • extracting said Src-homology 2 domain containing protein or a phosphotyrosine binding domain containing protein from said complex. 96. A compound according to any one of claims 1 to 71 coupled to a fluorescent or radioactive molecule. 97. A method for coupling a fluorescent or radioactive molecule to a compound according to any one of claims 1 to 71 comprising • contacting said compound with said fluorescent or radioactive molecule in a reaction mixture to produce a complex • removing uncomplexed material and isolating said complex from said reaction mixture. 98. A method for detecting protein-tyrosine phosphatase or other molecules with phosphotyrosine recognition unit(s) in a cell or in a subject using a compound according to claim 93 comprising • contacting said cell or an extract thereof or a biological sample from said subject or by injecting said compound into said subject in order for said compound to produce a complex with said protein-tyrosine phosphatase or said molecules with phosphotyrosine recognition unit(s) • detecting said complex, thereby detecting the presence of said protein tyrosine phosphatase or said other molecules with phosphotyrosine recognition unit(s). 99. A method for quantifying the amount of protein-tyrosine phosphatases or other mole cules with phosphotyrosine recognition unit(s) in a ceil or in a subject using a compound according to claim 93 comprising • contacting said cell or an extract thereof or a biological sample from said subject or by injecting said compound into said subject in order for said compound to produce a complex with said protein-tyrosine phosphatase or said molecules with phosphotyrosine recognition unit(s) • measuring the amount of said complex, thereby detecting the presence of said protein tyrosine phosphatase or said molecules with phosphotyrosine recognition unit(s). 100. A method for determining the function of a given protein-tyrosine phosphatase or group of protein-tyrosine phosphatases or said molecules with phosphotyrosine recogni tion unit(s) in a cell or a subject using a compound according to claim 93 comprising • contacting said cell or an extract thereof or a biological sample from said subject or by injecting said compound Into said subject in order for said compound to produce a complex with said protein-tyrosine phosphatase or said molecules with phosphotyrosine recognition unit(s) • measuring the biological effects induced by said complex. 101. A compound which after uptake in cells or mammals has a stnjcture and a function as defined in any one of claims 1 to 71. 102.A compound substantially as hereinbefore described with reference to the accompanying drawings. 103 .The use of the compound substantially as hereinbefore described with reference to the accompanying drawings. 104. A pharmaceutical composition substantially as hereinbefore described with reference to the accompanying drawings. 105. A method of modulating the activity of one or more PTPases or other molecules substantially as hereinbefore described with reference to the accompanying drawings. 106.A method for isolating a protein or a glycoprotein with affinity for a compound substantially as hereinbefore described with reference to the accompanying drawings. 107. A method for determining the function of a given protein-tyrosine phosphatase substantially as hereinbefore described with reference to the accompanying drawings.