Unlike heparin, the oral anticoagulants induce hypoco-agulability only in vivo. They are vitamin K antagonists. Vitamin K is required to catalyze the conversion of the precursors of vitamin K-dependent clotting factors II, VII, IX, and X. This involves the posttranslational 7-car-boxylation of glutamic acid residues at the N-terminal end of the proteins. The 7-carboxylation step is linked to a cycle of enzyme reactions involving the active hy-droquinone form of vitamin K (K1H2).The regeneration of K1H1 by an epoxide reductase is blocked by the oral anticoagulants. These drugs thus cause hypocoagulabil-ity by inducing the formation of structurally incomplete clotting factors.
Commercial warfarin is a racemic mixture of S- and R-enantiomers; S-warfarin is more potent than R-war-farin.
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