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The coagulation cascade and platelet aggregation system collectively mediate hemostasis, preventing blood loss from damaged vessels. The coagulation cascade comprises a sequence of tightly regulated enzyme activations (mainly proteases called clotting factors), which culminate in the conversion of fibrinogen to fibrin, establishing a stable blood clot. Platelet aggregation is a parallel process in which circulating platelets adhere, activate, and aggregate at the site of vessel injury, initially forming a platelet plug (primary hemostasis). Numerous drugs and biological inhibitors target specific steps within these systems—either the enzymatic cascade (e.g., targeting thrombin, factor Xa) or platelet function (via various surface receptors)—to prevent or treat thrombosis, stroke, and other clotting or bleeding disorders. Dysregulation can lead to life-threatening bleeding or thrombosis.
Inhibition of clotting factor synthesis or activity (e.g., vitamin K antagonists reduce synthesis of factors II, VII, IX, X); Direct inhibition of thrombin or factor Xa (e.g., dabigatran, rivaroxaban); Inhibition of platelet aggregation by blocking receptors (e.g., P2Y12 receptor antagonists, GP IIb/IIIa inhibitors)
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