A new drug targets one of cancer’s master switches

Jun 12th 2026|3 min read

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Scientists are not usually an excitable bunch. So when many thousands of them gave a standing ovation at a conference in Chicago, it meant something special had happened. The applause was for the results of clinical trials of a drug called daraxonrasib, developed by Revolution Medicines, a company based in California. It is designed to treat pancreatic cancer. The drug almost doubled median survival times from 6.7 months to 13.2 months. This victory over one of the most challenging cancers was an emotional moment for many.

The drug is not a cure. Cancers often develop resistance to targeted drugs such as daraxonrasib. Instead, its promise for patients is that, when used alongside other treatments, it might buy them months more life. Pancreatic cancers are aggressive and usually symptomless. They are mostly diagnosed after they have already spread around the body. Few patients survive longer than a year. Pancreatic cancers are also resistant toinhi immunotherapy, a class of treatment that encourages the body’s immune system to fight tumours, and which has had great success in many other areas of oncology. A mutation in a protein called KRAS, which drives most pancreatic cancers, creates an environment around the tumour that is hostile to immune cells.

Daraxonrasib is expected to speed its way through approval in America. Although it was given in the trial to patients who had already tried chemotherapy, it seems likely to become a first-line treatment for the disease. The drug works by inhibiting KRAS. Other work suggests this also changes the environment around tumours in ways that might make them more susceptible to immunotherapy. If that theory proves correct, it could improve survival times still further.

There is a bigger story. KRAS is a molecular switch in the cell that is heavily involved in cell division. It can be either off or on. A single mutation can leave it jammed on, endlessly signalling to cells that they should multiply—and endless growth is the defining pathology of cancer. Stopping KRAS might help in other sorts of tumour where the same mutation drives the disease. Candidates include some colorectal and lung cancers and, to a lesser degree, endometrial, small bowel and stomach cancers.

What is more, KRAS is just one of a family of “oncogenes”—those often involved in cancers—that are collectively known as RAS mutations. Daraxonrasib could, in theory, work to some degree on other RAS-driven cancers such as multiple myeloma, a type of blood cancer. RAS mutations are found in 20% of all cancers, accounting for about 3.4m cases of cancer around the world every year. They have been a promising target since their discovery in 1982. But the structure of the proteins produced by the genes has few molecular chinks into which drugs might get their hooks. For four decades they were considered “undruggable”—but no longer.

This is just the beginning. More refined versions of daraxonrasib will be developed, as will competitor drugs from other companies. There is even hope these drugs might help an entirely different group of cancer patients: children with neuroblastoma, where a different mutation disables a gene that normally acts as a brake on RAS. Tackling one cancer has, potentially, revealed a master switch that enables new treatments for millions of people. Daraxonrasib deserves its standing ovations. ■