vHospital
Anticoagulant

Warfarin: Mechanism of Action

Warfarin is an anticoagulant that prevents blood clot formation and is used to treat or prevent deep vein thrombosis, pulmonary embolism, and atrial fibrillation.

MechanismInteractionsEvidenceClinical Studies

Warfarin inhibits VKORC1, depleting vitamin K-dependent coagulation factors with significant inter-individual variability driven by CYP2C9 and VKORC1 polymorphisms.

How It Works

Warfarin is a racemic mixture of R- and S-enantiomers that competitively inhibits vitamin K epoxide reductase complex 1 (VKORC1), preventing regeneration of active vitamin K (vitamin K hydroquinone). Without active vitamin K, γ-carboxylation of coagulation factors II, VII, IX, X and anticoagulant proteins C and S cannot occur. Non-carboxylated factors accumulate while active factors decline over 2–5 days. The S-enantiomer is ~3–5× more potent than R-warfarin and is metabolised by CYP2C9 (loss-of-function variants *2, *3 dramatically increase S-warfarin exposure, requiring lower doses). VKORC1 promoter polymorphisms alter pump sensitivity. FDA recommends pharmacogenetic testing to guide initial dosing.

Receptor / Target Profile

Pharmacokinetics

Onset of Action

INR begins rising at 8–12 hours; peak INR effect at 36–72 hours; full anticoagulant effect 5–7 days

Half-Life (t½)

36–42 hours (R-warfarin ~45 hours; S-warfarin ~29 hours)

Near-complete oral absorption (>95%). Highly protein-bound (>99% albumin). Narrow therapeutic index (INR 2–3 most indications, 2.5–3.5 mechanical mitral valve). CYP2C9 and VKORC1 genetic variants explain ~50% of warfarin dose variability. Crosses placenta — teratogenic in first trimester; may be used with monitoring in second/third trimester for mechanical valve patients.

Conditions Treated with Warfarin

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