Warfarin has been the cornerstone of oral anticoagulant therapy for about 50 years. Its effectiveness has already been proven in the prevention of venous thromboembolism in the prevention of systemic embolism in patients with cardiac valve prostheses or atrial fibrillation and the prevention of acute myocardial infarction (MI) in high-risk men. Warfarin mainly inhibits the vitamin K epoxide reductase enzyme, which prevents the cyclic interconversion of this vitamin. This way, by blocking the cyclic interconversion of vitamin K prevents carboxylation of glutamate residues in terminal regions in K-dependent proteins. Warfarin is the most commonly used oral anticoagulant in clinical practice and is composed of two isomers, R-warfarin, and S-warfarin (5 times more potent than R-isomer), which are metabolized in the liver by different routes.
