Enodia Therapeutics Inks Pfizer Deal to Develop Sec61-Targeting Small Molecules
Backed by multiple Sec61 inhibitor families, proteomics and cryo-EM datasets, and machine learning-driven design, Enodia Therapeutics’ platform is the foundation of a new research collaboration and license agreement with Pfizer. The post Enodia Therapeutics Inks Pfizer Deal to Develop Sec61-Targeting Small Molecules appeared first on GEN - Genetic Engineering and Biotechnology News .
Biotechnology company Enodia Therapeutics has formed a research collaboration and licensing agreement with pharmaceutical giant Pfizer to develop small molecule inhibitors of Sec61, utilizing Enodia's proprietary platform. The collaboration involves Enodia performing discovery activities to screen, optimize, and develop Sec61 inhibitor candidates targeting multiple collaboration targets.
Upon completion of the collaboration, Pfizer will handle clinical, manufacturing, regulatory, and commercial aspects, while Enodia will receive an upfront payment and is eligible for subsequent milestone payments and royalties on net sales, with the total potential value exceeding $500 million. Enodia specializes in developing novel small-molecule therapies for targeted protein degradation using its platform, which identifies small molecules capable of selectively modulating Sec61 translocon, a novel approach to inhibiting disease-causing proteins during synthesis before pathological effects manifest.
Enodia's platform builds upon a broad chemical space spanning multiple Sec61 inhibitor families, supported by biological datasets, including proteomics, cryo-EM data, and tailored cell-line libraries. Yves Ribeill, Enodia's CEO, highlighted that Enodia has developed a platform enabling selective Sec61 translocon modulation, a novel approach to target pathological proteins while preserving essential physiological functions.
Enodia recently acquired assets from Kezar Life Sciences' Sec61-based discovery and development program, which enhanced its understanding of Sec61 selectivity mechanisms and further strengthened its focus on Sec61-driven selectivity for targeted protein degradation.
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