Membrane-bound factor Xa catalyzes the activation of small amounts of thrombin. The amino terminal portion of prothrombin is released as an activation peptide, which can be cleaved further by activated thrombin. Neither the full-length activation peptide nor its cleavage products have known functions.

Factor Xa (aka Factor X heavy chain), a cleavage product of coagulation factor X (F10), is a vitamin K-dependent glycoprotein able to convert prothrombin to thrombin during the blood clotting process. Factor Xa is a target for direct oral anticoagulant (DOAC) drugs that are direct factor Xa inhibitors (the so-called 'xabans') and used in the treatment and prevention of thromboembolic disorders (Galanis et al. 2014). Rivaroxaban (brand name Xarelto) binds to and inhibits both free factor Xa and factor Xa bound in the prothrombinase complex (Va:Xa) (Roehrig et al. 2005). Rivaroxaban was the first medically approved drug of this class (Abrams & Emerson 2009, Misselwitz et al. 2011). In patients with non-valvular atrial fibrillation, 'xabans' appears to be as effective as warfarin in preventing nonhemorrhagic strokes and embolic events (Patel et al. 2011, Gomez-Outes et al. 2013). The most serious side-effect of rivaroxaban is GI bleeding, and with there being no antidote for rivaroxaban, bleeding events can be difficult to manage (Siegal et al. 2014). Other 'xabans' such as apixaban (Bhanwra & Ahluwalia 2014), edoxaban (Minor et al. 2015), eribaxaban (Bondarenko et al. 2013) and betrixaban (Zhang et al. 2009) share a similar mechanism of action to rivaroxaban (Nutescu et al. 2016). Unlike warfarin, the 'xabans' exhibit a predictable dose response and do not require routine coagulation monitoring.