The FDA has approved Bayer HealthCare‘s NDA for Adempas (riociguat) tablets for both the treatment of adults with persistent/recurrent chronic thromboembolic pulmonary hypertension (CTEPH) after surgical treatment or inoperable CTEPH to improve exercise capacity and WHO functional class, and the treatment of adults with pulmonary arterial hypertension (PAH) (WHO Group 1) to improve exercise capacity, improve WHO functional class and delay clinical worsening.

In PAH, efficacy was shown in patients on Adempas monotherapy or in combination with endothelin receptor antagonists (ERAs) or prostanoids (inhaled, oral or subcutaneous). Studies establishing effectiveness included predominately patients with WHO functional class II-III and etiologies of idiopathic or heritable PAH (61%) or PAH associated with connective tissue diseases (25%).

Adempas is the only treatment approved in the U.S. for use in two types of pulmonary hypertension (WHO Group 1 and 4). It is the first and only FDA-approved drug therapy for persistent/recurrent CTEPH after surgical treatment or inoperable CTEPH. It is also the only approved oral therapy in PAH with efficacy shown in monotherapy or in combination with ERAs or prostanoids.

For all female patients, Adempas is available only through a restricted program called the Adempas Risk Evaluation and Mitigation Strategy (REMS) Program.

PAH is a disease characterized by elevated pressure in the pulmonary arteries. CTEPH is a form of pulmonary hypertension in which blood clots and thromboembolic occlusion of the pulmonary vessels leads to increased pressure in the pulmonary arteries. The standard treatment for CTEPH is pulmonary endarterectomy, a potentially curative surgery that clears clots and scar material from the blood vessels of the lung.

Adempas is a stimulator of soluable guanylate cyclase (sGC). Pulmonary hypertension is associated with endothelial dysfunction, impaired synthesis of nitric oxide (NO) and insufficient stimulation of the NO-sGC-cGMP pathway. Adempas sensitizes sGC to endogenous NO by stabilizing the NO-sGC binding. Adempas also directly stimulates sGC via a different binding site independently of NO. Adempas restores the NO-sGC-cGMP pathway and leads to increased generation of cGMP with subsequent vasodilation.