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Pancreatic-head tumours (red, artificially coloured) have proved highly resistant to treatment, but a new drug nearly doubles the lifespan of people with this type of cancer.Credit: PNMB\/Science Photo Library<\/p>\n
The landmark success of a drug against an \u2018undruggable\u2019 cancer<\/a> is spurring fresh optimism in the quest to treat seemingly untouchable tumour targets.<\/p>\n The experimental drug, daraxonrasib<\/a>, disarms all three members of the RAS family of proteins, which are linked to some of the deadliest cancers. Designing drugs that target the RAS proteins has been notoriously challenging<\/a>. But a large clinical trial has found that daraxonrasib nearly doubled survival \u2014 from 6.7 months to 13.2 months \u2014 in people with a form of advanced pancreatic cancer.<\/p>\n The results were presented to a packed room at the American Society of Clinical Oncology annual meeting in Chicago, Illinois, on 31 May, and published in the New England Journal of Medicine1<\/a>. At the conference, the talk was met with a long standing ovation, says Ecaterina Dumbrava, an oncologist at the University of Texas MD Anderson Cancer Center in Houston. \u201cAfter more than a decade without major advances in treatment for pancreatic cancer, seeing this is really emotional,\u201d she says. <\/p>\n That success is raising hopes that other challenging targets might also soon fall. Nature talked to researchers about progress in targeting RAS and other \u201cundruggable\u201d cancer proteins that can\u2019t be bested with conventional approaches.<\/p>\n RAS: locked into overdrive<\/p>\n RAS proteins are molecular on\u2013off switches that help to control cell growth and division. But some mutations leave RAS proteins stuck in the \u2018on\u2019 position, which drives tumour growth.<\/p>\n Ideally, a cancer drug would switch these proteins off. But drugs typically work by nestling into deep pockets on the surfaces of proteins, and RAS proteins are unhelpfully smooth.<\/p>\n Cheap blood test detects pancreatic cancer before it spreads<\/p>\n <\/a><\/p>\n The first anti-RAS drug was approved in the United States in 2021. It targeted only one mutation in one member of the family, a protein called KRAS<\/a>. That meant that the drug was suitable only for a fraction of people with RAS-driven cancers, and even those tumours quickly became resistant to it.<\/p>\n Daraxonrasib, by contrast, switches off all three members of the RAS family. In a trial of 500 people with advanced pancreatic cancer<\/a>, those who received daraxonrasib lived another 13.2 months, compared with 6.7 months for those treated with chemotherapy. Daraxonrasib was developed by Revolution Medicines in Redwood City, California.<\/p>\n Researchers hope that this will be just the starting point. Combining daraxonrasib with other drugs \u2014 such as a single-mutation KRAS drug \u2014 could produce longer-lasting benefits2<\/a>, says Kevan Shokat, a chemical biologist at the University of California, San Francisco. And future variations on daraxonrasib might be able to reduce its toxicity, he adds. \u201cSometimes the very first molecule just shows that it\u2019s possible,\u201d he says.<\/p>\n MYC: smooth operator<\/p>\n About 70% of all cancers are fuelled by excessive levels of a protein called MYC. But MYC, like RAS proteins, has a smooth surface, making anchoring drugs there difficult.<\/p>\n Furthermore, cancer-driving mutations in the MYC gene are rarely a straightforward, single change to a DNA base \u2014 the kind of mutation that might be easily targeted with a drug. Instead, the gene is sometimes duplicated, or other genetic changes make it more active, resulting in more MYC protein than usual. \u201cMYC is going to be a little more complicated\u201d than targeting KRAS, says Shokat.<\/p>\n One leading approach is an experimental drug called OMO-103, made by Peptomyc in Barcelona, Spain. The drug is a \u2018mini protein\u2019 that interferes with MYC\u2019s ability to interact with another protein, and has shown promise in a small trial with 19 participants3<\/a>.<\/p>\n Better treatments on the way for lung cancer that spreads to the brain<\/p>\n <\/a><\/p>\n Other researchers are screening large libraries of compounds in search of those that might inhibit specific functions of the protein. At Oregon Health and Science University in Portland, cancer researcher Rosalie Sears and her collaborators are using artificial intelligence to hunt for compounds<\/a> that bind to the part of MYC that helps to repair damaged DNA \u2014 a crucial ability in rapidly dividing tumour cells. And Michael Cole, a cancer researcher at the Geisel School of Medicine at Dartmouth College in Hanover, New Hampshire, who has been studying MYC for more than 40 years, is looking for compounds that block MYC\u2019s ability to activate certain other genes.<\/p>\n Cole\u2019s effort got a boost from the first KRAS drug, which was approved around the time that he co-founded a company called cosMYC in Cambridge, Massachusetts, to chase such compounds. Buzz around the KRAS-drug approval helped the firm to raise initial financing, says Ed Feris, cosMYC\u2019s chief executive and co-founder. \u201cEveryone was asking, \u2018what can we do next\u2019?\u201d he says. \u201cAnd people were thinking: MYC.\u201d<\/p>\n p53: restoring the guardian<\/p>\n![\"\"](\"https:\/\/www.newsbeep.com\/uk\/wp-content\/uploads\/2026\/06\/d41586-026-01760-w_52128674.jpg\"\/)
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