Scientists crack the "undruggable" cancer: new pill nearly doubles survival for one of the world's deadliest diseases

When researchers presented findings from a major cancer drug trial in Chicago on May 31, the audience of normally reserved doctors and scientists rose to their feet and gave a standing ovation. In a world where medical breakthroughs are often incremental and cautiously worded, the reaction said everything.  What they had just heard was genuinely historic. A new drug called daraxonrasib, developed by Revolution Medicines, has nearly doubled survival time in patients with advanced pancreatic cancer — one of the most lethal diseases known to medicine.  The results, simultaneously published in the prestigious New England Journal of Medicine, are being described by cancer specialists as a potential turning point in the treatment of a disease that has resisted meaningful progress for generations. Old survival (chemo) 6.7 months New survival (daraxonrasib) 13.2 months Reduction in death risk 60% Trial patients 500 Why pancreatic cancer is so feared Pancreatic cancer is the third-leading cause of cancer deaths in the United States, killing nearly 53,000 people every year.  It is devastating not just because of how aggressive it is, but because of how quietly it grows. There are no reliable early screening tests, and the disease causes very few noticeable symptoms in its early stages. By the time a patient notices signs such as jaundice — a yellowing of the skin — or persistent abdominal pain, the cancer has typically already spread to other organs.   The numbers are sobering. Of patients diagnosed with metastatic pancreatic cancer between 2015 and 2021, around 97% died within five years.  The average survival after diagnosis of advanced disease, on standard chemotherapy, was less than seven months. For decades, that figure barely moved despite enormous investment in research. Pancreatic cancer became, in the words of many oncologists, a disease that medicine simply could not crack.  The "undruggable" mutation — and how daraxonrasib cracked it The reason pancreatic cancer has been so difficult to treat comes down to a single genetic mutation called KRAS. This mutation is present in more than 90% of all pancreatic tumours and is what drives the uncontrolled cell growth that makes the disease so deadly. For years, cancer researchers tried and failed to develop drugs that could effectively bind to the KRAS protein and neutralise it.  The protein's shape made it almost impossible to target — earning it the nickname "undruggable" within the oncology community. Daraxonrasib takes a different approach entirely.  Rather than attacking KRAS directly, the drug targets a molecule called cyclophilin A — a protein inside cells responsible for folding other proteins into their correct three-dimensional shapes.  The drug attaches to cyclophilin A, and this complex is then able to bind to the active KRAS protein and switch off its ability to instruct cancer cells to keep dividing. Crucially, unlike earlier generation drug