Background
Daraxonrasib (RMC-6236) is an oral RAS(ON) multiselective inhibitor that targets GTP-bound mutant and wild-type RAS, broadening the reach of RAS-directed therapy beyond single-allele inhibitors.
Phase 1–2 results
In 168 patients with previously treated RAS-mutated PDAC, the 26 patients with RAS G12 mutations receiving 300 mg in second line achieved an ORR of 35%, median duration of response 8.2 months, mPFS 8.5 months, and mOS 13.1 months. Grade ≥3 treatment-related adverse events occurred in 30%.
What comes next
The phase 1–2 study was not randomized against chemotherapy, so it cannot establish comparative superiority. A phase 3 first-line study is evaluating daraxonrasib alone or with gemcitabine/nab-paclitaxel against chemotherapy in untreated metastatic pancreatic cancer.
Serial blood-based analyses in first-line combination work have shown deep reductions in RAS ctDNA. These molecular responses are promising, but ctDNA clearance remains a biomarker rather than evidence of cure.
Molecular structure
The RCSB PDB 9BGC structure captures daraxonrasib (RMC-6236) in a tri-complex with KRAS G12R and CypA, illustrating how the inhibitor occupies a composite pocket at the protein-protein interface.
Daraxonrasib bound in the RAS(ON) tri-complex
X-ray structure of daraxonrasib (A1AHB/RMC-6236) bridging KRAS G12R and CypA, with GNP/Mg marking the active nucleotide-bound state.
- KRAS
- chain A
- CypA
- chain C
- Daraxonrasib
- A1AHB
- GNP/Mg
- RAS(ON)