05/31/2026 | Press release | Distributed by Public on 05/31/2026 06:06
A new medication could double survival time in patients with advanced pancreatic cancer, according to Phase III clinical trial results presented at the American Society of Clinical Oncology (ASCO) 2026 annual meeting and simultaneously published in The New England Journal of Medicine.
Andrew Hendifar, MD, professor of Medicine and medical director of the Cancer Clinical Trials Office and the Gastrointestinal Oncology Disease Research Group at Cedars-Sinai, was a principal investigator on the trial and a co-author of the study, which was sponsored by Revolution Medicines, makers of the new drug. He sat down with the Cedars-Sinai Newsroom to talk about the study results.
The medication, called daraxonrasib, is the first drug that targets cancer-causing mutations in pancreas cells.
The drug targets a mutation in the KRAS gene, part of the RAS genetic family. KRAS mutations are present in 92% of pancreatic cancers. KRAS genes normally act as an "on-off" switch for cell growth. Mutated KRAS genes are stuck in the "on" position and send out a signal that causes cells to divide and grow uncontrollably, allowing cancer to form.
Daraxonrasib blocks the KRAS signal by fitting into a keyhole-type spot on the gene. That spot has a complex shape and is difficult to reach within the cell. The drug gets around this problem by using a "passenger protein" as a Trojan horse. When the cell allows this protein in, daraxonrasib tags along.
There are no targeted treatments approved for pancreas cancer, and we haven't had any significant progress for a long time. We've only come up with different chemotherapy combinations, and those are only moderately effective. This new treatment is staggeringly better than chemotherapy. Usually, when we think of an improvement in pancreatic cancer survival, we think of 25% improvement. This medication actually doubled survival in patients with advanced disease. We have patients who participated in the trial who are still alive, which is unheard of because the five-year survival rate for pancreatic cancer patients is only 13%-14%. If the drug is approved by the FDA, it will most likely become the new standard of care for advanced pancreatic cancer and could replace chemotherapy as a first-line treatment.
We are now testing the drug in patients with earlier-stage pancreatic cancer, prescribing it while their tumors are still operable and before their cancer spreads.
RAS mutations are one of the most common cancer-causing genetic mutations, and the drug is now being studied in several cancer types. I think it's going to work especially well in tumors that are primarily RAS driven, including colon cancer and lung cancer. It might also work in other cancer types in combination with drugs targeting other genetic mutations, but further research is needed.
This is a win for the field. Until now we have been focused on immune therapies that might make tumors more vulnerable to the body's immune system, and on finding new chemotherapy combinations that kill cancer cells.
This new treatment has given us a new focus, and I think it will spur a lot of scientific discovery over the next few years. There have only been a handful of KRAS researchers and their relevance to therapy was always questioned. That is about to change.
The most important next step for the field is to better understand the biology of cancer. We know that many pancreatic tumors will eventually become resistant to daraxonrasib, and we need to understand how this happens. We also need to identify additional genetic pathways and treatments that can target them. That's how we will turn pancreas cancer from a deadly, deadly cancer into something we can manage-and one day, even cure.
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