The development of persistent inhibitory antibodies to factor VIII and factor IX is a serious and costly complication of replacement therapy that can occur in people with hemophilia (Wight. Haemophilia. 2003). The ultimate goal of treatment is to permanently eradicate the inhibitor by ITI, thereby making it possible to routinely provide treatment with replacement therapy (DiMichele. Haemophilia. 1998; Wight. Haemophilia. 2003). Due to its cost, ITI therapy is not generally available worldwide, and it is known to fail in a substantial number of cases. Native prothrombin complex concentrates (PCCs), or their activated forms (aPCCs), have been used for decades as hemostatic bypassing agents in people with high-responding inhibitors (Sjamsoedin. New England Journal of Medicine. 1981; Hedner. Lancet. 1988). More recently, recombinant factor VIIa (rFVIIa) has been added as a treatment option (Lusher. Blood Coagulation & Fibrinolysis. 1998; Turecek. Haemophilia. 2004). The bypassing mechanisms of these agents are different and not fully understood (Negrier. Thrombosis and Haemostasis. 1997). Although successfully used in a variety of challenging clinical situations, aPCC and rFVIIa are not always effective. The different mechanisms of action provide a theoretical foundation for inter- as well as intra-individual variation in the clinical efficacy between the two agents. The FENOC study evaluated two bypassing agents used in the treatment of joint bleeding in congenital hemophilia A complicated by inhibitors. The study was designed to test the equivalence of the two products.