 Inhibitors of FIX activity, such as active site-inactivated factor IXa FIXai or monoclonal antibodies against FIX e.g., the antibody BC2, have exhibited potent anticoagulant and antithrombotic activity in multiple animal models, including various animal models of arterial thrombosis and stroke Benedict et al., 1991; Choudhri et al., 1999; Feuerstein et al., 1999; Spanier et al., 1998a; Spanier et al., 1997; Spanier et al., 1998b; Toomey et al., 2000. In general, these studies have shown that FIXa inhibitors have a higher ratio of antithrombotic activity to bleeding risk than unfractionated heparin in animals. However, in these studies, at doses marginally higher than the effective dose, animals treated with these agents have exhibited bleeding profiles no different than heparin. Such an experience in well-controlled animal studies suggests that, in the clinical setting, the ability to control the activity of a FIXa inhibitor would enhance its safety and facilitate its medical use. In addition, FIXai has been shown to be safe and effective as a heparin replacement in multiple animal surgical models requiring anticoagulant therapy, including rabbit models of synthetic patch vascular repair, as well as canine and non-human primate models of CABG with cardiopulmonary bypass Spanier et al., 1998a; Spanier et al., 1997; Spanier et al., 1998b. FIXai has also been used successfully for several critically ill patients requiring cardiopulmonary bypass and in the setting of other extracorporeal circuits such as extracorporeal membrane oxygenation Spanier et al., 1998a by physicians at the Columbia College of Physicians and Surgeons, on a compassionate care basis. Thus, FIXa is a validated target for anticoagulant therapy in coronary revascularization procedures both CABG and PCI, and for the treatment and prevention of thrombosis in patients suffering from acute coronary syndromes. 