Novel IP Receptor Agonist CS585

Drug candidate CS585 is an oral, highly potent and selective prostacyclin (IP) receptor agonist that has demonstrated the potential to significantly improve disease mechanisms relevant to cardiovascular disease. While CS585 has not yet been assigned a specific indication for clinical development, preclinical data indicates that it could potentially be used in indications like Pulmonary Hypertension and thrombosis prevention without increased risk of bleeding.

Preclinical data suggest that CS585 provides a new option of activating the IP receptor to decrease platelet reactivity and could represent the first viable option for targeting the IP-receptor on platelets for inhibition of thrombosis with a reduced risk of bleeding. The preclinical results with CS585, including a head-to-head comparison of CS585 and the FDA-approved IP receptor agonists selexipag and iloprost, indicate a favorable profile for inhibiting platelet activation and clot formation. CS585 was shown to be more selective and have a more sustained efficacy than the currently available IP receptor agonists. CS585 also demonstrated a sustained duration of action in mice in the ability to inhibit platelet activation through several routes of administration including oral.

The growing body of evidence around drug candidate CS585 supports favorable tolerability and efficacy in preclinical studies. Recently, the early results from CS585 were published in the top-tier journal Blood showing that CS585 is a highly potent and selective compound given both orally and intravenously and prevents thrombosis for up to 48 hours as observed in preclinical studies. Following the publication, a commentary article and the Blood Podcast highlighted that the new preclinical findings of CS585 could be a significant milestone to improve anti-thrombotic treatment strategies without bleeding.

A license agreement for drug candidate CS585 with the University of Michigan provides Cereno exclusive rights to further development and commercialization of CS585.