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Updated on 12/06/2026 vitamin K antagonists (VKAs) are indirect oral anticoagulants that inhibit vitamin Kdependent -carboxylation of coagulation factors II, VII, IX, and X, as well as proteins C and S VKAs, particularly warfarin, have been used since the mid-20th century for the prevention and treatment of venous thromboembolism and for prevention of cardioembolic stroke in patients with AF or other high-risk cardioembolic conditions are now preferred for most patients requiring anticoagulation because they have predictable pharmacokinetics, fewer interactions, no routine INR-monitoring requirement, and a lower risk of ICH direct oral anticoagulants (DOACs) Mechanism of action warfarin is an indirect oral anticoagulant drug and belongs to the vitamin K antagonist (VKA) class, also known as coumarin anticoagulants inhibits vitamin K epoxide reductase complex 1(VKORC1) depletion of active reduced vitamin K (KH impaired -glutamyl carboxylation of vitamin Kdependent coagulation 2 ) factors II, VII, IX, and X, as well as the regulatory anticoagulant proteins C and S hypofunctional vitamin Kdependent proteins have reduced ability to bind calcium and phospholipid surfaces, thereby impairing coagulation dietary vitamin K can antagonize warfarin because vitamin K can be reduced to KH through warfarin-insensitive reductase pathways, partially restoring -carboxylation Indications In many indications, warfarin has been largely replaced by direct oral anticoagulants (DOACs), when DOACs are appropriate and available prevention of cardioembolic stroke warfarin remains preferred in patients with mechanical heart valves or moderate-to-severe rheumatic mitral stenosis therapy and prevention of cerebral venous thrombosis warfarin is preferred in patients with antiphospholipid syndrome or another high-risk thrombophilia in which DOACs are not recommended VTE prophylaxis and treatment (venous thrombosis/pulmonary embolism) arterial dissection warfarin is rarely required