The FDA has approved daraxonrasib, the first medicine targeting the RAS family of proteins to reach pancreatic cancer. In a 500-patient trial, median survival was 13.2 months against 6.7 on chemotherapy.
Pancreatic cancer kills more than 50,000 people a year in the United States, and in more than nine out of ten of them the tumour is driven by a mutation in a RAS gene, the switch that tells a cell when to grow. For decades that switch was called undruggable. On 26 August 2026 the US Food and Drug Administration approved daraxonrasib, sold as RASONQUE, the first medicine aimed at RAS to reach the disease. In the trial behind the approval, half the people taking it were still alive at 13.2 months, up from 6.7 months on chemotherapy.
How we know
The approval rests on RASolute 302, an open-label trial, meaning everyone involved knew which treatment was being given. It enrolled 500 patients across North America, Europe and Asia whose pancreatic cancer had spread and had started growing again after one previous course of treatment, and split them evenly between daraxonrasib and the chemotherapy their own doctor would otherwise have chosen. Median overall survival, the point at which half the group had died, was 13.2 months on the drug against 6.7 months on chemotherapy. The hazard ratio was 0.40, meaning that at any moment in the trial people on daraxonrasib were dying at 40 percent of the rate of those on chemotherapy. Progression-free survival, the time before the cancer started growing again, was 7.2 months against 3.6, and tumours shrank measurably in 30 percent of patients on the drug and 11 percent on chemotherapy. Every one of those differences carried a p-value below 0.0001, and progression was judged by a blinded independent review of the scans rather than by the treating doctors, which is the usual guard on an open-label trial.
Why it matters
Mutated RAS jams in the on position and keeps telling the cell to divide, and for years nobody could find a surface on the protein that a drug would stick to. Daraxonrasib gets round the problem sideways: it works as a molecular glue, binding the RAS protein to a second protein called cyclophilin A so the growth signal cannot pass. About 80 percent of people with pancreatic cancer are diagnosed only after it has already spread, so second-line treatment, the course given once the first has stopped working, is where most patients actually stand. This is the first time the mutation at the centre of the disease has been the target rather than the obstacle.
This buys months, not a cure. Median survival on daraxonrasib was 13.2 months, and the five-year relative survival for metastatic pancreatic cancer in the United States is still around 3 percent. The gain was measured only in people whose cancer had already progressed once, so it says nothing yet about first-line treatment, and the label carries warnings for skin and soft tissue toxicity, mouth sores, diarrhoea, gastrointestinal perforation and inflammation of the lungs. The most common side effects were rash, mouth inflammation, nausea and diarrhoea.
What is RAS, and why has it been so hard to target?
RAS is a family of genes, and the proteins they make, that act as switches for cell growth. More than 90 percent of pancreatic cancers carry a mutation in KRAS, a member of that family, which leaves the switch stuck on. The trial's lead investigator says blocking RAS signalling proved extraordinarily challenging, because researchers could not find a surface on the protein that a drug would bind to.
Who can be prescribed daraxonrasib?
The FDA approved it for adults with metastatic pancreatic adenocarcinoma who have had at least one prior systemic therapy, or who are not candidates for multiagent therapy. The recommended dose is 300 mg taken by mouth once a day, continuing until the disease progresses or the side effects become unacceptable.
How strong is the evidence?
RASolute 302 randomised 500 patients one to one between daraxonrasib and standard chemotherapy, and progression was judged by a blinded independent review rather than by the treating doctor. Survival, progression-free survival and response rate all improved with a p-value below 0.0001. The trial was open-label, meaning patients and doctors knew which treatment was being given.
What is not solved yet?
Median survival went from 6.7 months to 13.2, which is months rather than a cure, and five-year survival for metastatic pancreatic cancer in the United States remains around 3 percent. The result covers only second-line treatment, after a first course has failed. The drug also carries warnings for gastrointestinal perforation and lung inflammation among others.
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