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Warfarin

Catalog No. DB00682 Name DrugBank
CAS Number 81-81-2 Website http://www.ualberta.ca/
M. F. C19H16O4 Telephone (780) 492-3111
M. W. 308.32794 Fax (780) 492-1071
Purity Email david.wishart@ualberta.ca
Storage Chembase ID: 564

SYNONYMS

IUPAC name
2-hydroxy-3-(3-oxo-1-phenylbutyl)-4H-chromen-4-one
IUPAC Traditional name
rodex
Brand Name
Warficide
Marevan
Athrombin-K
Place-Pax
Mar-Frin
Warfarin Plus
Zoocoumarin
Athrombine-K
Coumaphene
Coumefene
Jantoven
Kumatox
Kypfarin
Maveran
Panwarfin
Sofarin
Vampirinip III
Warf 42
Warfarat
Warfarin Q
Warfarine
Warfilone
Coumadin Tabs
Athrombin
Brumolin
Co-Rax
Coumaphen
Coumarins
D-Con
Dethmor
Dethnel
Dicusat E
Kumadu
Latka 42
Prothromadin
RAX
Rosex
Sorexa Plus
Temus W
Tox-Hid
Coumadin
Coumafen
Coumafene
Frass-Ratron
Kumader
Solfarin
Tintorane
Vampirinip II
Synonyms
Warfarin sodium

DATABASE IDS

CAS Number 81-81-2

PROPERTIES

Hydrophobicity(logP) 3
Solubility 17 mg/L

DETAILS

Description (English)
Item Information
Drug Groups approved
Description An anticoagulant that acts by inhibiting the synthesis of vitamin K-dependent coagulation factors. Warfarin is indicated for the prophylaxis and/or treatment of venous thrombosis and its extension, pulmonary embolism, and atrial fibrillation with embolization. It is also used as an adjunct in the prophylaxis of systemic embolism after myocardial infarction. Warfarin is also used as a rodenticide. [PubChem]
Indication For the treatment of retinal vascular occlusion, pulmonary embolism, cardiomyopathy, atrial fibrillation and flutter, cerebral embolism, transient cerebral ischaemia, arterial embolism and thrombosis.
Pharmacology Warfarin, a coumarin anticoagulant, is a racemic mixture of two active isomers. It is used in the prevention and treatment of thromboembolic disease including venous thrombosis, thromboembolism, and pulmonary embolism as well as for the prevention of ischemic stroke in patients with atrial fibrillation (AF).
Toxicity LD50=374 (orally in mice)
Affected Organisms
Humans and other mammals
Biotransformation Metabolized stereo- and regio-selectively by hepatic microsomal enzymes. S-warfarin is predominantly metabolized by cytochrome P450 (CYP) 2C9 to yield the 6- and 7-hydroxylated metabolites. R-warfarin is metabolized by CYP1A1, 1A2, and 3A4 to yield 6-, 8-, and 10-hydroxylated metabolites. Hydroxylated metabolites may be further conjugated prior to excretion into bile and urine. UGT1A1 appears to be responsible for producing the 6-O-glucuronide of warfarin, with a possibly contribution from UGT1A10. Five UGT1As may be involved in the formation of 7-O-glucuronide warfarin. S-warfarin has higher potency than R-warfarin and genetic polymorphisms in CYP2C9 may dramatically decrease clearance of and increase toxicity of the medication.
Absorption Rapidly absorbed following oral administration with considerable interindividual variations. Also absorbed percutaneously.
Half Life R-warfarin t1/2=37-89 hours; S-warfarin t1/2=21-43 hours.
Protein Binding 99% bound primarily to albumin
Elimination The elimination of warfarin is almost entirely by metabolism. Very little warfarin is excreted unchanged in urine. The metabolites are principally excreted into the urine; and to a lesser extent into the bile.
Distribution * 0.14 L/kg
Clearance * 0.065 +/- 0.025 mL/min/kg [CYP2C9 Genotype *1/*1]
* 0.041 +/- 0.021 [CYP2C9 Genotype *1/*2 or *1/*3]
* 0.020 +/- 0.011 [CYP2C9 Genotype *2/*2, *2/*3, or *3/*3]
References
Ansell J, Hirsh J, Poller L, Bussey H, Jacobson A, Hylek E: The pharmacology and management of the vitamin K antagonists: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest. 2004 Sep;126(3 Suppl):204S-233S. [Pubmed]
Whitlon DS, Sadowski JA, Suttie JW: Mechanism of coumarin action: significance of vitamin K epoxide reductase inhibition. Biochemistry. 1978 Apr 18;17(8):1371-7. [Pubmed]
Li T, Chang CY, Jin DY, Lin PJ, Khvorova A, Stafford DW: Identification of the gene for vitamin K epoxide reductase. Nature. 2004 Feb 5;427(6974):541-4. [Pubmed]
Rost S, Fregin A, Ivaskevicius V, Conzelmann E, Hortnagel K, Pelz HJ, Lappegard K, Seifried E, Scharrer I, Tuddenham EG, Muller CR, Strom TM, Oldenburg J: Mutations in VKORC1 cause warfarin resistance and multiple coagulation factor deficiency type 2. Nature. 2004 Feb 5;427(6974):537-41. [Pubmed]
Hirsh J, Fuster V, Ansell J, Halperin JL: American Heart Association/American College of Cardiology Foundation guide to warfarin therapy. J Am Coll Cardiol. 2003 May 7;41(9):1633-52. [Pubmed]
External Links
Wikipedia
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REFERENCES

  • Ansell J, Hirsh J, Poller L, Bussey H, Jacobson A, Hylek E: The pharmacology and management of the vitamin K antagonists: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest. 2004 Sep;126(3 Suppl):204S-233S. Pubmed
  • Whitlon DS, Sadowski JA, Suttie JW: Mechanism of coumarin action: significance of vitamin K epoxide reductase inhibition. Biochemistry. 1978 Apr 18;17(8):1371-7. Pubmed
  • Li T, Chang CY, Jin DY, Lin PJ, Khvorova A, Stafford DW: Identification of the gene for vitamin K epoxide reductase. Nature. 2004 Feb 5;427(6974):541-4. Pubmed
  • Rost S, Fregin A, Ivaskevicius V, Conzelmann E, Hortnagel K, Pelz HJ, Lappegard K, Seifried E, Scharrer I, Tuddenham EG, Muller CR, Strom TM, Oldenburg J: Mutations in VKORC1 cause warfarin resistance and multiple coagulation factor deficiency type 2. Nature. 2004 Feb 5;427(6974):537-41. Pubmed
  • Hirsh J, Fuster V, Ansell J, Halperin JL: American Heart Association/American College of Cardiology Foundation guide to warfarin therapy. J Am Coll Cardiol. 2003 May 7;41(9):1633-52. Pubmed