A humanized anti-factor XI (FXI) antibody, with potential anti-thrombotic activity. Upon administration, xisomab 3G3 targets and binds to the apple 2 domain of FXI, thereby preventing the binding of FXI to factor XIIa (FXIIa). This blocks factor XIIa-mediated FXI activation without inhibiting FXI activation by thrombin or the procoagulant function of FXIa. The abrogation of FXI activation prolongs the activated partial thromboplastin time (aPTT), and reduces platelet and fibrin accumulation. This results in the inhibition of contact activation-initiated blood coagulation and prevents thrombus formation. FXI contributes to thrombotic disease while playing a limited role in normal hemostasis. Activation of FXI is essential for thrombus growth and stabilization.