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Coagulation factor V (FV) is a critical 330 kDa glycoprotein that functions as a non-enzymatic cofactor in the blood coagulation cascade [Wikipedia, 2024; NIH, 2025]. Synthesized primarily in the liver and stored in platelet alpha-granules, it circulates in plasma as an inactive procofactor [StatPearls, 2022]. Upon vascular injury, FV is activated by thrombin or factor Xa to form factor Va (FVa), which then assembles with factor Xa, calcium ions, and a phospholipid surface to form the prothrombinase complex [NIH, 2025; AHA Journals, 2025]. This complex is responsible for the rapid conversion of prothrombin to thrombin, a central step in clot formation [MDPI, 2023]. Factor V also plays an anticoagulant role by acting as a cofactor for activated protein C (APC) in the inactivation of factor VIIIa [AHA Journals, 2025]. Mutations in the F5 gene can lead to either bleeding disorders like parahemophilia or thrombotic conditions, most notably Factor V Leiden, which causes resistance to APC-mediated inactivation [NIH, 2026; ResearchGate, 2025]. Therapeutic interventions include replacement therapy with fresh frozen plasma or factor V concentrates for deficiency, while research into monoclonal antibodies like D9 explores FV as a target for novel anticoagulants [NIH, 2025; ResearchGate, 2025].
Acts as a non-enzymatic cofactor for factor Xa in the prothrombinase complex to convert prothrombin to thrombin; also acts as an anticoagulant cofactor for activated protein C (APC) to inactivate factor VIIIa [NIH, 2025; AHA Journals, 2025].
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