Heparin acts by potentiating the activity of antithrombin III, which inhibits both thrombin (Factor IIa) and Factor Xa, key enzymes in the coagulation cascade. This dual inhibition effectively prevents the conversion of fibrinogen to fibrin, thus stopping clot formation. Unlike warfarin, which affects vitamin K-dependent clotting factors indirectly, heparin exerts a rapid anticoagulant effect. This mechanism makes heparin essential in clinical settings requiring immediate anticoagulation, such as during surgery or acute thrombotic events.

Reference: Goodman & Gilman's The Pharmacological Basis of Therapeutics, Brunton L., 13th Edition.