Data from experimental animal models revealed an essential role for factor XII (FXII) in thrombotic occlusive diseases. In contrast to other blood coagulation factors, deficiency in the protease is not associated with abnormal bleeding from injury sites (hemostasis) in patients or in animals. Cumulatively, these findings suggest that FXII could be targeted as a new method of anticoagulation that is devoid of bleeding risks. An FXIIa-neutralizing antibody, 3F7, has been developed that inhibited thrombosis in an extracorporeal membrane oxygenation (ECMO) system as efficiently as heparin. However, in sharp contrast to heparin, 3F7 treatment was not associated with an increase in therapy-associated hemorrhage. In this review, we summarize current knowledge of FXII physiology and pharmacology.
