At a cancer research conference in Chicago, doctors wept. After four decades of trying to target a gene that drives pancreatic cancer, researchers have finally succeeded with a daily pill called daraxonrasib — one that has doubled average survival time for patients with advanced disease.
The stakes could hardly be higher. Pancreatic cancer kills more people than almost any other cancer, with a five-year survival rate of around three percent for advanced cases. More than half of patients are diagnosed only after the disease has already spread. And the treatments available have barely changed in decades. Into this grim landscape comes a result that oncologists at the American Society of Clinical Oncology's annual meeting in Chicago are calling a grand slam.
In a 500-patient trial led by researchers at Dana-Farber Cancer Institute in Boston, patients taking daraxonrasib lived for an average of 13.2 months, compared to 6.6 to 6.7 months for those on standard chemotherapy. They also experienced fewer side effects. Dr. Rachna Shroff, chief of oncology at the University of Arizona Cancer Center, described the moment she read those numbers: "Having treated pancreatic cancer for 16 years, I actually started crying in clinic. This is such an incredibly impactful study for our patients."
The breakthrough centers on a single gene called KRAS. Over 90 percent of patients with pancreatic ductal adenocarcinoma — the most common form of the disease — carry a mutation in this gene, one that keeps sending faulty growth signals telling cells to divide when they should stop. Blocking KRAS has long been the holy grail of cancer research. But the gene has no obvious pocket where drug molecules can attach, leading researchers since the 1980s to consider it undruggable.
Daraxonrasib solved this puzzle with an elegant mechanism. As a Ras(On) multi-selective inhibitor, it works by gluing molecules together to physically grip and shut down the KRAS protein, cutting off the growth signal entirely. Unlike earlier drugs in this class, it works regardless of which KRAS variant a patient carries — or even when no specific variant is present. This universality matters because it removes a major barrier to treatment.
Dr. Julie Gralow, ASCO's chief medical officer, called the results a gamechanger. Paula Hanford, chief executive of Pancreatic Cancer Action in the UK, placed it in historical context: "For far too long, people diagnosed with pancreatic cancer have had incredibly limited treatment options and survival rates that have remained devastatingly low. To see a trial showing the potential to nearly double survival time in advanced pancreatic cancer is hugely encouraging."
The work doesn't end with pancreatic cancer. KRAS mutations appear in roughly a third of all human tumors, including lung and colon cancers. Similar drugs targeting this pathway are already in trials for these diseases. Researchers said daraxonrasib's results give the broader Ras-targeting approach something it has never had: proof that the strategy actually works.
Of course, having an effective drug and getting it to patients are two different challenges. Half of all pancreatic cancer diagnoses result in death within three months. Anna Jewell, director of services, research and innovation at Pancreatic Cancer UK, distilled the next step: "More time with those we love most is truly priceless. We must do everything possible to ensure the most promising new treatments are available."