At the site of a vascular wound, tissue factor is exposed, which acts as a physiological cofactor for Factor VIIa, and the tissue factor/FVIIa complex activates the clotting cascade. Tissue factor/FVIIa activates factor X either directly or indirectly through the activation of factor IX, and the resultant factor Xa activates prothrombin to thrombin. Thrombin converts fibrinogen to fibrin and also activates platelets, resulting in the formation of a fibrin-platelet thrombus. Thrombin can also activate factor XI, and factor XIa in turn activates FIX, thus serving as a tertiary pathway of thrombin generation. Warfarin is a vitamin K antagonist and targets prothrombin, factor VII, factor IX, and factor X (Red), with factor X and prothrombin being the main targets. Heparin, lowmolecular-weight heparin (LMWH), and the synthetic pentasaccharide fondaparinux serve as anticoagulants by activating antithrombin, a plasma serine protease inhibitor that functions as the major physiological regulator of the clotting cascade; antithrombin then inhibits factor Xa and thrombin. Both the direct thrombin inhibitors and the direct factor Xa inhibitors inhibit their respective targets directly without the need of antithrombin.