Coagulation factor V (activated form: Coagulation factor Va) (FV (activated form: FVa))

Coagulation factor V is a large plasma glycoprotein that serves as a critical **cofactor in the prothrombinase complex**, where, once activated (factor Va), it binds to **factor Xa** and greatly accelerates the conversion of prothrombin to thrombin[1][4][3]. Factor V is synthesized in the liver and circulates as an inactive single-chain protein; it becomes activated by proteolytic cleavage (removal of the B domain) via thrombin or factor Xa. The active form, factor Va, is essential for normal blood clotting, and its deficiency leads to bleeding disorders, while certain mutations (especially Factor V Leiden) confer resistance to inactivation and significantly increase thrombosis risk[3][1][2]. Factor V also interacts with protein S and participates in anticoagulant pathways in its precursor form[2]. No currently approved drugs directly target factor Va; its pathological roles are targeted indirectly by anticoagulant drugs. **Note:** "Activated Factor V" refers specifically to the form after proteolytic activation, usually called "Factor Va" in biomedical literature, but the canonical molecule name is "Coagulation factor V"; "Factor Va" refers to the activated, cofactor form present in the prothrombinase complex[1][3][7].

Other names

ProaccelerinLabile factorFV (for inactive form)Factor Va (for active form)

Drugs that act upstream: inhibit the generation of factor Va or the activity of the prothrombinase complex (e.g., via factor Xa inhibitors). Protein-based therapies: Replacement with plasma or recombinant factor V for deficiency.