{{Drugbox | Verifiedfields = changed | Watchedfields = changed | verifiedrevid = 470633864 | IUPAC_name = ethyl 2-[[(1R)-1-cyclohexyl-2-[(2S)-2-[[4-(N-hydroxycarbamimidoyl)phenyl]methylcarbamoyl]azetidin-1-yl]-2-oxo-ethyl]amino]acetate | image = Ximelagatran.svg | width = 230 | tradename = Exanta | pregnancy_category = Uncategorized | legal_status = Withdrawn from market | routes_of_administration = Oral (tablets) | bioavailability = 20% | metabolism = to melagatran | elimination_half-life = 3–5 hours | excretion = Renal (80%) | IUPHAR_ligand = 6381 | CAS_number_Ref = | CAS_number = 192939-46-1 | ATC_prefix = B01 | ATC_suffix = AE05 | ChEMBL_Ref = | ChEMBL = 522038 | PubChem = 9574101 | DrugBank_Ref = | DrugBank = DB04898 | ChemSpiderID_Ref = | ChemSpiderID = 7848559 | UNII_Ref = | UNII = 49HFB70472 | KEGG_Ref = | KEGG = D01981 | C=24 | H=35 | N=5 | O=5 | molecular_weight_comment = (429 g/mol after conversion) | smiles = O=C(NCc1ccc(C(=N\O)\N)cc1)[C@H]3N(C(=O)[C@H](NCC(=O)OCC)C2CCCCC2)CC3 | StdInChI_Ref = | StdInChI = 1S/C24H35N5O5/c1-2-34-20(30)15-26-21(17-6-4-3-5-7-17)24(32)29-13-12-19(29)23(31)27-14-16-8-10-18(11-9-16)22(25)28-33/h8-11,17,19,21,26,33H,2-7,12-15H2,1H3,(H2,25,28)(H,27,31)/t19-,21+/m0/s1 | StdInChIKey_Ref = | StdInChIKey = ZXIBCJHYVWYIKI-PZJWPPBQSA-N }}Ximelagatran (Exanta or Exarta''', H 376/95) is an anticoagulant that has been investigated extensively as a replacement for warfarin that would overcome the problematic dietary, drug interaction, and monitoring issues associated with warfarin therapy. In 2006, its manufacturer AstraZeneca announced that it would withdraw pending applications for marketing approval after reports of hepatotoxicity (liver damage) during trials, and discontinue its distribution in countries where the drug had been approved (Germany, Portugal, Sweden, Finland, Norway, Iceland, Austria, Denmark, France, Switzerland, Argentina and Brazil). Method of action Ximelagatran, a direct thrombin inhibitor, was the first member of this class that can be taken orally. It acts solely by inhibiting the actions of thrombin. It is taken orally twice daily, and rapidly absorbed by the small intestine. Ximelagatran is a prodrug, being converted in vivo'' to the active agent melagatran. This conversion takes place in the liver and many other tissues through hydrolysis and dehydroxylation (replacing the ethyl and hydroxyl groups with hydrogen). Uses Ximelagatran was expected to replace warfarin and sometimes aspirin and heparin in many therapeutic settings, including deep venous thrombosis, prevention of secondary venous thromboembolism and complications of atrial fibrillation such as stroke. The efficacy of ximelagatran for these indications had been well documented, except for non valvular atrial fibrillation. An advantage, according to early reports by its manufacturer, was that it could be taken orally without any monitoring of its anticoagulant properties. This would have set it apart from warfarin and heparin, which require