BY THE OPTIMIST DAILY EDITORIAL TEAM
In a 500-patient trial at American Society of Clinical Oncology’s (ASCO) annual meeting in Chicago, a daily pill called daraxonrasib doubled average survival time in patients with advanced pancreatic cancer. Those on the drug lived for an average of 13.2 months. Those on standard chemotherapy lived for 6.6 to 6.7 months. Side effects were fewer, too.
Oncologists at the conference called it a grand slam. It’s also what four decades of failing to crack one specific gene looks like when it finally works.
Why KRAS proved so hard to target
Pancreatic cancer kills more people than almost any other cancer. More than half of patients are only identified after the disease has spread, and treatments have barely changed in decades. The five-year survival rate for advanced cases is around three percent.
One gene is behind most of it. Over 90 percent of patients with pancreatic ductal adenocarcinoma, the most common form, carry a mutation in KRAS — one that keeps sending growth signals to cells that should stop dividing. Block it, and you could stop the cancer. Researchers have been trying since the 1980s.
The problem: KRAS has no obvious pocket where drug molecules can latch on. For decades, the field wrote it off as undruggable.
How daraxonrasib switches off the signal
Daraxonrasib is a Ras(On) multi-selective inhibitor. It works by gluing molecules together to grip and shut down the KRAS protein, cutting off the growth signal entirely. It does this regardless of which KRAS variant a patient carries, and even when no variant is present. Earlier drugs in this space only worked against specific mutations. This one doesn’t have that restriction.
“The idea of targeting Kras has always been the holy grail in most malignancies, but specifically in pancreas cancer, because it is nearly ubiquitous and it is an early driver of pancreas cancer growth,” said Dr. Rachna Shroff, chief of oncology at the University of Arizona Cancer Center. “The Ras revolution is here, and this study is proof of principle that targeting Kras in pancreatic cancer is feasible and effective.”
Trial results: 13.2 months versus 6.6
The trial was led by researchers at the Dana-Farber Cancer Institute in Boston. All 500 participants had pancreatic cancer that had spread. Those on daraxonrasib lived for an average of 13.2 months; those on chemotherapy, 6.6 to 6.7 months.
Shroff, who had no involvement in the study, said she wept reading 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.”
Dr. Julie Gralow, ASCO’s chief medical officer, called the results a gamechanger. Others at the conference called it a home run. “I would actually say it’s a grand slam,” Gralow said.
Paula Hanford, chief executive of UK-based Pancreatic Cancer Action, called it one of the most significant treatment developments she had seen. “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.”
What comes next for patients and other cancers
Half of all people diagnosed with pancreatic cancer die within three months. Having a drug that works doesn’t solve that; getting it to patients does. Anna Jewell, director of services, research and innovation at Pancreatic Cancer UK, put it simply: “More time with those we love most is truly priceless. We must do everything possible to ensure the most promising new treatments are available.”
KRAS mutations show up in roughly a third of all human tumors, not just pancreatic ones. Similar drugs are already in trials for lung and colon cancers. Researchers in Chicago said daraxonrasib’s results give the broader Ras-targeting approach something it hasn’t had before: proof that it works.
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