Portola Pharmaceuticals, Inc. (NASDAQ: PTLA) today announced that it will present preclinical data on its investigational Factor Xa inhibitor antidote andexanet alfa (PRT4445*) in a moderated poster session at the upcoming 2013 European Society of Cardiology (ESC) Congress, which is taking place in Amsterdam from August 31-September 4.
“These data from a preclinical animal model are noteworthy because they demonstrate that the reversal of Factor Xa anticoagulant activity by andexanet alfa has the potential to reduce blood loss in anticoagulated patients experiencing an active bleed, an important point of differentiation with this compound,” said John T. Curnutte, M.D., Ph. D., executive vice president of research and development for Portola. “We have already established in a Phase 2 clinical study that andexanet alfa can reverse the anticoagulant activity of the Factor Xa inhibitor
(apixaban), and, as part of an accelerated development plan, we expect to initiate a pivotal study in 2014 to further assess the effects of andexanet alfa on bleeding.”
Details of the moderated poster presentation follow:
PRT064445 (Andexanet Alfa) Reverses Rivaroxaban Induced Anticoagulation in a Rabbit Liver Laceration “Treatment” Model
August 31, 2013, 16:22 p.m. CEST
Moderated Posters -- Village 9
Stanley Hollenbach, J.D., vice president, pharmacology, Portola Pharmaceuticals
The andexanet alfa abstract is now publically available at
About Andexanet Alfa
Andexanet alfa (proposed INN) is a novel recombinant, modified Factor Xa molecule designed to reverse the anticoagulant activity in patients treated with a Factor Xa inhibitor who suffer an uncontrolled bleeding episode or need to undergo emergency surgery. Andexanet alfa is similar to native Factor Xa, but has been modified to restrict its biological activity to the reversal of the anticoagulant effects of Factor Xa inhibitors. Andexanet alfa acts as a Factor Xa decoy that binds and sequestors direct Factor Xa inhibitors in the blood. Once bound to andexanet alfa, the Factor Xa inhibitors are unable to bind to and inhibit native Factor Xa. The native Factor Xa is then available to participate in the coagulation process and restore hemostasis.