Cough-focused biotech Seyltx has secured the option to license a portfolio of eight GluN2B antagonists from NeurOp, including one candidate that has completed a phase 1 trial.
The drugs are all negative allosteric modulators of GluN2B, a subunit of NMDA that Seyltx said has been identified as a primary target for cough suppression in preclinical studies. The companies touted the agreement as an opportunity to combine “Seyltx's expertise in chronic cough therapeutic development with NeurOp's expertise in NMDA receptor biology.”
Cambridge, Massachusetts-based Seyltx is already working on an NMDA receptor inhibitor of GluN2B in the form of its lead therapy ifenprodil, which was shown to significantly reduce coughing in a phase 2 study back in 2022.
“We are incredibly excited about this option agreement with NeurOp, which significantly strengthens our pipeline for chronic cough therapies,” Seyltx CEO Dietrich Stephan, Ph.D., said in a company release.
The agreement offers “a promising avenue to provide potentially superior treatment options” for patients with chronic cough and idiopathic pulmonary fibrosis by “addressing the condition with a centrally acting non-narcotic solution,” Stephan added.
The current expectation is that today’s deal will be converted into Seyltx’s worldwide license agreement for the eight assets within 12 months. The release didn’t include financial details of a potential licensing agreement.
“This agreement with Seyltx is a testament to the sophistication of our team’s expertise in the NMDA receptor biology and the development of our GluN2B antagonists,” NeurOp’s executive chairman James McNamara, M.D., said in the release.
“Seyltx's deep understanding and focus on chronic cough make them an ideal partner to further develop and bring these important compounds to patients in need,” McNamara added. “We look forward to a very productive partnership.”
The widely used cough suppressant dextromethorphan is an NMDA receptor antagonist. Seyltx and Atlanta-based NeurOp are banking on targeting the GluN2B subunit as a way to “achieve robust cough suppression, while avoiding the adverse event profile observed with non-specific NMDA antagonists.”