Verseon will be starting a first-in-human phase I trial in Australia for its lead-PROAC (PRecision Oral AntiCoagulant) VE-1902, which has successfully completed regulatory toxicology studies and was well-tolerated in 28-day repeat dosing.

Verseon’s PROACs are a novel class of anticoagulants that show efficacy comparable to the NOACs (novel oral anticoagulants) but much-reduced bleeding in preclinical studies. Because of this unique profile, PROACs could have a major impact on the cardiovascular disease market by becoming the first oral anticoagulants suitable for long-term anticoagulant-antiplatelet combination therapy. Such treatment is particularly relevant for tens of millions of patients worldwide with acute coronary syndrome or non-valvular atrial fibrillation comorbid with coronary artery disease.

Professor Keith Fox, Duke of Edinburgh Professor of Cardiology at the University of Edinburgh, commented, “If Verseon’s promising preclinical results translate to benefits in the clinic, these new precision anticoagulants could improve the standard of care for the millions of patients who need prolonged anti-clotting therapy to reduce major adverse cardiac complications.”

“An oral anticoagulant that can be safely co-administered with antiplatelets has been an elusive goal for the global health community for many years due to the high bleeding risk of the NOACs. We believe that our PROACs could be a real lifesaver for a very large, global patient population,” said Eniko Fodor, COO and CFO at Verseon. “We have chosen Australia for our phase I trial because of its excellent clinical trial infrastructure and research incentives. This should allow us to conduct high-quality trials in a cost-effective manner.”

At the recent BIO International Convention, Dr. Anirban Datta, Verseon’s Director of Discovery Biology, presented new ex vivo results for Verseon’s first PROAC clinical trial candidate, VE-1902. In healthy human volunteer blood, VE-1902 inhibits thrombin generation but without the prolonged delay in peak thrombin production observed with NOACs. At efficacious concentrations, VE-1902 is also a 500-fold weaker inhibitor of platelet activation than NOACs.