In vivo, Ralinepag, at a dosage of 30 mg/kg administered orally, significantly mitigates the monocrotaline (MCT)-induced escalation in pulmonary arterial pressure and the thickening of the pulmonary vessel wall in rats, indicating its potential therapeutic benefit in conditions associated with pulmonary arterial hypertension^[1].

Ralinepag is a potent non-prostanoid prostacyclin receptor agonist, demonstrating exceptional efficacy with EC50 values of 8.5 nM for both human and rat IP receptors, and a slightly higher affinity for the human DP1 receptor with an EC50 of 850 nM. Its receptor binding affinity is significant across various species for the prostaglandin receptor, displaying Kis of 1.2 nM in monkeys, 3 nM in humans, 76 nM in rats, and 256 nM in dogs for the IP receptor using the ligand [³H]-iloprost. Additionally, Ralinepag exhibits binding affinities with Kis of 2.6 μM for human DP1, 9.6 μM for EP1, 610 nM for EP2, 143 nM for EP3v6, and 678 nM for EP4 receptors, employing [³H]-PGE2 as the ligand. Importantly, Ralinepag does not significantly affect cytochrome P450 enzymes, with IC50 values exceeding 50 μM for enzymes including CYPs 1A2, 2D6, 3A4, 2C8, 2C9, and 2C19, nor does it impact hERG channel functional activity in patch clamp assays, with an IC50 surpassing 30 μM. Moreover, Ralinepag efficiently inhibits ADP-induced human platelet aggregation, demonstrating an IC50 of 38 nM^[1].