Actelion to Present Further Data on Selexipag (Uptravi) for PAH During 2015 European Respiratory Society (ERS) Congress

Actelion Pharmaceuticals, a biopharmaceutical company developing pulmonary arterial hypertension (PAH) therapies, recently announced the presentation of further data from its pivotal Phase III GRIPHON study testing investigational PAH treatment selexipag (Uptravi) during the 2015 European Respiratory Society (ERS) Congress, which will take place in Amsterdam, Netherlands.

The presentation is titled “Effect of selexipag on long-term outcomes in key subgroups of patients with pulmonary arterial hypertension (PAH): GRIPHON study results,” and will be orally presented by Professor Olivier Sitbon from the Hospital Le Kremlin Bicêtre in Paris, France on September 30 at 11.15.

The GRIPHON study included 1,156 patients with PAH that were randomly assigned to receive selexipag or placebo. Results showed that selexipag significantly reduced the risk of morbidity/mortality events up to end of treatment by 40%.

The researchers further examined the effect of selexipag versus placebo in prespecified subgroups of background PAH therapy, aetiology, age, and region. The results showed that the majority of the patients receiving an endothelin receptor antagonist (ERA) and/or a phosphodiesterase type 5 inhibitor (PDE5i) at baseline (80%), had idiopathic, heritable, HIV or drug-induced PAH (62%) and were aged <65 years (82%).

Overall, selexipag significantly reduced the risk of M/M events vs PBO and similar treatment effects were seen irrespective of background therapy, aetiology, age and region.

During the Congress, further details will be presented regarding macitentan (Opsumit^®) as well, in a poster titled “Pharmacokinetics and safety of concomitant macitentan and hormonal contraceptives.” Dr. Noémie Hurst will present this post on September 28 from 10.45 am.

Selexipag selectively targets the prostacyclin receptor (also called IP-receptor). The IP receptor is one of 5 types of prostanoid receptor. Prostacyclin activates the IP receptor inducing vasodilation and inhibiting proliferation of vascular smooth muscle cells. Unlike prostacyclin analogs, the therapy is selective for the IP receptor over other prostanoid receptors.