Sanofi ended the Phase 1 first-in-human study of SAR448272, an oral STAT6 degrader, and terminated the program outright. Nurix Therapeutics disclosed the decision on November 3, roughly two months after the molecule entered the clinic.
Neither company gave a reason, and no efficacy or safety data was released.
The hit lands on Nurix’s milestone ledger. Under the 2019 collaboration, the Brisbane, California company stood to collect development, regulatory and commercial payments plus royalties on SAR448272. All of it is gone.
The molecule was meant to prove the platform. Nurix used its DEL-AI discovery engine to design compounds that recruit E3 ligases and mark target proteins for destruction. Sanofi exercised a 2025 license extension covering two transcription-factor programs for autoimmune and inflammatory disease, one of them STAT6. That protein sits on the signaling path driving type 2 inflammation, the biology behind asthma, atopic dermatitis and eosinophilic conditions.
Nurix’s guidance holds. Cash and securities totaled $1.1B at the end of August, enough runway into the second half of 2029, and the forecast never leaned on SAR448272.
Three programs carry the story now. Bexobrutideg, a BTK degrader partnered with Roche, is in Phase 3 for chronic lymphocytic leukemia. The wholly owned CBL-B inhibitor NX-1607 runs Phase 1b cohorts in lung, colon, prostate cancer and melanoma. GS-6791/NX-0479, an IRAK4 degrader for rheumatoid arthritis, is in Phase 1 with Gilead. The second licensed transcription-factor program from Sanofi survives, with Nurix holding a US co-development option after proof of concept.
The pattern is familiar in degrader deals. Large partners sign broad collaborations, take a couple of assets into humans, then prune hard. Sanofi’s exit removes one candidate from a crowded autoimmune pipeline and signals how fast big pharma judges a platform’s first clinical output.
