On May 31st in Chicago, a researcher named Dr. Brian Wolpin walked to a podium in front of 44,000 oncologists and presented data. When he finished, the room — filled with scientists who spend their careers in the cold language of statistics and peer review — stood up and applauded.

This does not happen at cancer conferences. It happened at ASCO 2026.

What Wolpin presented was the result of a phase 3 clinical trial for a drug called daraxonrasib. And what it showed was something that researchers had been trying to achieve for over four decades — a treatment that could meaningfully extend the lives of patients with advanced pancreatic cancer by targeting the gene responsible for driving the disease in 90% of cases.

The gene is called KRAS. For 40 years, it was known as undruggable.

The Cancer That Has Resisted Everything

Pancreatic cancer kills roughly 53,000 Americans every year. It is the third leading cause of cancer death in the United States. It grows silently — causing no clear symptoms until it has already spread — and by the time most patients are diagnosed, surgery is no longer possible.

The five-year survival rate for pancreatic cancer has remained stubbornly around 12% for decades. While survival rates for most other cancers have doubled through modern treatment advances, pancreatic cancer has been, in the words of one researcher at ASCO, one of those really stubborn cancers which has lagged behind.

The reason comes down to biology. The KRAS gene — mutated in over 90% of pancreatic cancer cases — sends signals that cause uncontrolled cell growth. Scientists identified it as a target decades ago. The problem was structural. The protein produced by the mutated gene had a surface so smooth that nothing could bind to it. Every drug designed to block it slipped off. The research community eventually gave up and called it undruggable.

Revolution Medicines did not give up.

What Daraxonrasib Actually Does

Daraxonrasib is what researchers call a RAS multiselective inhibitor. Rather than targeting one specific KRAS mutation, it targets the entire RAS family of mutations — which means it works regardless of which specific variant a patient carries. This is clinically significant because it removes the need for extensive genetic screening before treatment can begin. A doctor doesn’t need to identify the exact subtype. The drug works across the board.

In the RASolute 302 trial, 500 patients with previously treated metastatic pancreatic cancer were split between daraxonrasib and standard chemotherapy. The results showed that daraxonrasib nearly doubled average survival time compared to chemotherapy.

Patients usually feel the difference quite quickly, according to Dr. O’Reilly at Memorial Sloan Kettering. Their pain is better. Memorial Sloan Kettering Cancer Center

ASCO Chief Medical Officer Julie Gralow called the finding a grand slam. Rachna Shroff of the University of Arizona Cancer Center called it a game changer. Tech Times

Vincent Picozzi at Virginia Mason Medical Center went further. He called it the most seminal thing that has occurred in pancreatic cancer since the advent of chemotherapy.

Where Things Stand Right Now

The drug is not yet widely available. But the regulatory process is moving faster than usual because the results are so clear.

The FDA has already granted daraxonrasib Breakthrough Therapy and Orphan Drug designations, and the drug is now permitted via the FDA’s expanded access treatment protocol — making it available to pancreatic cancer patients who have already gone through chemotherapy, with full approval potentially coming later in 2026. UCHealth

Beyond pancreatic cancer, daraxonrasib is being studied for other solid tumor cancers where KRAS mutations are a driver — including lung and colorectal cancer. Preliminary results from those trials are also showing promise.

Meanwhile, a separate line of research presented at the same ASCO conference showed that mRNA vaccines — the same technology used in COVID vaccines — are showing early results in preventing pancreatic cancer recurrence after surgery. A phase 2 trial for one of these vaccines is expected to open later in 2026.

Why This Moment Matters

The standing ovation in Chicago was not sentimentality. It was the accumulated release of four decades of scientific frustration meeting a result that most researchers had stopped fully believing would come.

Pancreatic cancer is the disease that oncologists have historically dreaded telling patients they have — not because treatment was painful, but because the honest prognosis offered so little. A median survival measured in months. A disease that resisted everything the field had learned to do with other cancers.

What daraxonrasib represents is not a cure. It is a proof of concept that the undruggable can be drugged — and that the gene driving the most lethal common cancer on earth is finally yielding to the tools being built to target it.

For the 53,000 Americans diagnosed with pancreatic cancer each year, that is not a small thing. For the researchers who spent careers on a problem the field had quietly abandoned, the standing ovation was the least they deserved.

The next chapter of pancreatic cancer treatment has started. It started in Chicago, on May 31st, when a room full of scientists forgot to be reserved.