Key facts
| International nonproprietary name (INN) | Daraxonrasib |
|---|---|
| Development code | RMC-6236 |
| Brand name | RASONQUE® (United States) |
| Developer | Revolution Medicines, Inc. (Redwood City, California, USA; Nasdaq: RVMD) |
| Drug class | RAS(ON) multi-selective inhibitor; non-covalent tri-complex inhibitor |
| Target | KRAS, NRAS and HRAS in the GTP-bound active (ON) state, including G12X, G13X and Q61X mutants as well as wild-type RAS |
| Administration | Oral, once daily; recommended dose 300 mg until disease progression or unacceptable toxicity |
| First approved indication | Adults with metastatic pancreatic adenocarcinoma who have received at least one prior systemic therapy or who are not candidates for multi-agent systemic therapy |
| FDA approval date | August 26, 2026 |
| Expedited pathways | Breakthrough Therapy Designation (BTD), Orphan Drug Designation, Commissioner's National Priority Voucher (CNPV) pilot, Real-Time Oncology Review (RTOR) pilot; approved approximately 6.5 months ahead of the FDA goal date |
Why daraxonrasib matters
The RAS gene family (KRAS, NRAS, HRAS) is the most frequently mutated oncogene family in human cancer; roughly 30% of solid tumors carry a RAS mutation. In pancreatic ductal adenocarcinoma (PDAC), more than 90% of patients carry a KRAS mutation, predominantly G12D, G12V and G12R. Yet for four decades RAS was regarded as "undruggable" — until the first KRAS G12C inhibitor was approved in 2021. G12C, however, accounts for only 1–2% of KRAS mutations in pancreatic cancer.
Daraxonrasib breaks through on three fronts:
- Broad coverage: it does not depend on a specific mutant residue and is active against KRAS G12D/G12V/G12R/G12C, G13 and Q61 mutants as well as wild-type RAS, covering the vast majority of RAS-mutant pancreatic cancers and a substantial share of RAS-mutant lung and colorectal cancers.
- Direct targeting of the active state: earlier G12C inhibitors could only lock RAS in its inactive (OFF) state. Daraxonrasib directly inhibits RAS in its signalling (ON) state, which in principle is harder to bypass through upstream reactivation.
- Phase 3 survival benefit: RASolute 302 is the first Phase 3 trial in pancreatic cancer to show that a RAS-targeted drug significantly prolongs overall survival — median OS rose from 6.7 to 13.2 months, a 60% reduction in the risk of death.
About the developer
Revolution Medicines is a clinical-stage biopharmaceutical company focused on RAS-addicted cancers. Its RAS(ON) inhibitor pipeline includes the multi-selective daraxonrasib (RMC-6236), the KRAS G12C-selective elironrasib (RMC-6291) and the KRAS G12D-selective zoldonrasib (RMC-9805). The company's core approach is a "tri-complex" chemistry platform that turns the historically undruggable active state of RAS into a tractable therapeutic target.