Curie Brief
Turn on cookies to sign in
Signing in saves your progress to your Curie account. We can only do that with cookies on — turn them on to continue.
NewsAfter 40+ years of failed attempts to target RAS, the FDA has approved daraxonrasib (Rasonque) for previously treated metastatic pancreatic cancer. The oral pan-RAS inhibitor nearly doubled median overall survival versus chemotherapy (13.2 vs. 6.7 months) in the phase 3 RASolute 302 trial. Experts are calling it a "grand slam" — and the FDA cleared it 6.5 months ahead of its review deadline.
After decades of failed attempts to drug the RAS protein — the mutation driving over 90% of pancreatic cancers — the FDA has approved daraxonrasib (Rasonque, Revolution Medicines) for adults with metastatic pancreatic ductal adenocarcinoma (PDAC) who have received at least one prior systemic therapy or are not candidates for multiagent chemotherapy. The once-daily oral pill works by binding to cyclophilin A, which then locks RAS in its active "ON" state and blocks downstream tumor-signaling pathways — a mechanism that works across both mutant and wild-type RAS.
The approval was based on the phase 3 RASolute 302 trial (n=500), which showed daraxonrasib nearly doubled median overall survival and progression-free survival versus standard chemotherapy, while tripling the objective response rate and significantly delaying deterioration in pain and quality of life. The FDA granted approval 6.5 months ahead of its user fee deadline. Looking ahead, daraxonrasib has also received FDA Breakthrough Therapy Designation in combination with gemcitabine/nab-paclitaxel for first-line PDAC, and is showing early promise in RAS-mutant non-small cell lung cancer.
By the Numbers
Why it matters: Pancreatic cancer has long been one of oncology's most stubborn challenges, with second-line chemotherapy offering only ~6 months of survival. Daraxonrasib's approval marks the first time a targeted therapy has dramatically moved the needle in this disease — and its pan-RAS mechanism opens the door to combination strategies across multiple RAS-driven tumor types.
