Antithrombotic drugs are used for the prevention and treatment of thrombosis. Targeting the various components of thrombosis, these agents include (1) antiplatelet agents; (2) anticoagulants; and (3) fibrinolytic agents. This review focuses on anticoagulants. The older classification of anticoagulants into oral and parenteral agents is giving way to one based on their biochemistry. Even so, most oral anticoagulants, notably warfarin, are vitamin K antagonists (VKAs) and thrombin inhibitors make up most parenteral agents. Thrombin inhibitors may be classified as indirect, such as unfractionated heparin (UFH), low molecular weight heparin (LMWH), and the synthetic heparin derivative fondaparinux and idraparinux, or direct inhibitors of thrombin activity, such as argatroban, lepirudin, and bivalirudin. Among the newer agents, all administered orally, are factor Xa inhibitors rivaroxaban and apixaban and the IIa (thrombin) inhibitor dabigatran. Conventionally used anticoagulants warfarin and UFH have been limited by a narrow therapeutic index, the need for laboratory monitoring, and, in the case of warfarin, numerous drug and dietary interactions. Some of the newer anticoagulants circumvent these disadvantages and may dramatically change the way we manage patients who require anticoagulation. This review summarizes the pharmacology of conventional and newer anticoagulants. Vitamin K Antagonists (VKAs) Oral anticoagulant warfarin inhibits the biosynthesis of vitamin K‐dependent procoagulant factors II, VII, IX, and X, reducing the coagulant potential of the blood. The antithrombotic effect of warfarin depends on the reduction in the functional levels of factor X and prothrombin that have half-lives of 36 and 50 hours, respectively. Because the long half-lives of some of these factors, full antithrombotic effect of VKA is