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Mechanism Lab

The coagulation cascade, as anticoagulants see it

Warfarin starves the factory upstream; DOACs handcuff single factors on the line.

carboxylationwhen blocked too wellVitamin K cycle (VKORC1)Hepatic factor synthesisWarfarinFactor XaApixaban / rivaroxabanThrombin (IIa)DabigatranFibrin clotBleeding

Click any node for its role, or open a question below to light the causal path.

Read this pathway as text

The intrinsic and extrinsic arms of the coagulation cascade converge on factor X. Activated factor Xa, with factor Va, converts prothrombin (factor II) to thrombin (IIa). Thrombin converts fibrinogen to fibrin, the clot's mesh. Factors II, VII, IX and X are synthesized in the liver and require vitamin-K-dependent carboxylation to function; warfarin inhibits vitamin K epoxide reductase (VKORC1), so new factors emerge inactive. An effect that takes days as existing factors decay, monitored by the INR. Apixaban, rivaroxaban and edoxaban inhibit factor Xa directly; dabigatran inhibits thrombin directly, immediate, predictable, unmonitored effects.

Last reviewed 2026-08-15 · Goodman & Gilman's The Pharmacological Basis of Therapeutics, 14th ed.