Thromboembolic Adverse Events After Use of Recombinant Human Coagulation Factor VIIa

Abstract

The US Food and Drug Administration (FDA) licensed recombinant human coagulation factor VIIa (rFVIIa) on March 25, 1999, for treatment of bleeding episodes in patients with hemophilia A or B and inhibitors to factor VIII or factor IX.¹ Recombinant FVIIa is structurally nearly identical to human plasma-derived coagulation factor VIIa and is thought to promote hemostasis by activating coagulation factors IX and X when complexed with tissue factor. Factor Xa, in a complex with factor V, calcium, and phospholipids, converts prothrombin to thrombin. Thrombin induces local hemostasis by converting fibrinogen to fibrin, which polymerizes and forms a thrombus in conjunction with platelets at the site of vascular injury. Thrombin can also be generated on the surface of activated platelets by the action of rFVIIa. Given the physiology of activated factor VII, a potential adverse event (AE) of concern is pathological clot formation.