It’s not often that you see a standing ovation at a medical conference. But over the weekend, a ballroom full of cancer specialists got to their feet to applaud a slide showing that Revolution Medicine’s daraxonrasib had doubled the survival time of patients with pancreatic cancer.

The response shows the pent-up desperation for progress in one of the toughest-to-treat cancers. And daraxonrasib represents more than progress. It feels more like a paradigm shift.

“It changes everyone’s perception of what you can do for this disease — how you can help people,” says Brian Wolpin, the Dana-Farber Cancer Institute oncologist who led the trial and presented the results at the cancer conference. “It’s really a sea change in how this disease will be handled.”

It was a moment anticipated since RevMed’s April press release showing that in a late-stage clinical trial, people taking its pill lived, on average, 13.2 months compared to 6.7 months for those given chemotherapy. Pancreatic cancer specialists were thrilled, yet also wanted granular data that could teach the field where to go next.

Now, they have it — well, some of it.

Let’s start with the truly amazing news: Daraxonrasib hit every marker important to doctors and patients. The drug doubled survival time and kept tumors from growing for twice as long compared to conventional chemotherapy.

Even better, people taking the drug had about five more months before their quality of life deteriorated compared to those on chemotherapy. And because daraxonrasib is a pill, patients are spared the burden of going to a facility and being tethered to an IV pump. For a cancer known for its brutal progression, those things — being able to receive care at home, having more quality time — truly matter.

Meanwhile, daraxonrasib’s side effects, which got a lot of attention when former Nebraska Senator Ben Sasse discussed participating in the trial earlier this year, are looking manageable.

Like Sasse, most people in the trial experienced a rash (though just 15% had a severe case), and over half had nausea or painful sores in their mouths and throats. Yet very few dropped out of the study, a testament to the significance of the drug’s efficacy, says Eileen O’Reilly, a pancreatic cancer specialist at Memorial Sloan Kettering Cancer Center who was the lead author of a NEJM paper detailing the results.

“I wouldn’t want to in any way minimize the importance of the rash — it’s a real issue,” says O’Reilly. But “patients speak with their feet,” and in her four years of treating people with RevMed’s drug, most are very reluctant to discontinue it.

One key question remains open, though: Does daraxonrasib work equally well across each of the genetic drivers of this deadly cancer? Some 90% of pancreatic cancers are caused by mutations in a protein called KRAS. Whereas many other treatments in development target the individual mutation underlying someone’s disease, daraxonrasib shuts down the whole family of proteins. Oncologists want to know if that broad activity leads to broad efficacy.

Any nuances have real-world implications for how this drug is used, says Manuel Hidalgo, the director of NYU Grossman School of Medicine’s Gastrointestinal Cancer Center. There’s no question that daraxonrasib, once approved, will instantly become oncologists’ most important new tool for slowing pancreatic cancer. But Hidalgo says the conversations he has with patients could change if some mutations are less responsive to the drug — for example, someone might want to consider a clinical trial of a more targeted therapy before trying daraxonrasib.

Understanding the intricacies of where this groundbreaking treatment works well, and where there is room for improvement, will be crucial for the continued advancement of the field.

Those data are coming, Wolpin told me. And at least in the initial look, there doesn’t seem to be a dramatic difference between the three main genetic drivers, he said.

There’s so much hope for what could come next in pancreatic cancer, that every bit of information should be squeezed out of this trial and made available to oncologists as quickly as possible.

“It resets the entire process,” Hidalgo says. “It resets the way patients are going to be treated, the way the drugs are going to be developed, and I think that five years from now, building upon this is going to be quite amazing.”

This latest dataset is from people whose tumors continued to grow, despite chemotherapy. But RevMed’s drug is expected to be practice-changing, meaning people newly diagnosed with pancreatic cancer are likely to be offered it, too. Oncologists are eager to see whether the benefits expand in that earlier setting.

Other questions being urgently explored: What if it’s used to shrink tumors before a person’s pancreas is removed? Could it help if given after surgery? Are there benefits to combining it with chemo, immunotherapy or experimental treatments that target specific mutations in RAS?

The list of clinical trials to run is long. “I won’t say it’s endless, but it’s almost endless,” O’Reilly says.

That’s a good problem to have. As each of those trials starts to provide answers, they might not elicit applause, but they hopefully will mean steady progress — leading eventually to a cure.

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This column reflects the personal views of the author and does not necessarily reflect the opinion of the editorial board or Bloomberg LP and its owners.

Lisa Jarvis is a Bloomberg Opinion columnist covering biotech, health care and the pharmaceutical industry. Previously, she was executive editor of Chemical & Engineering News.

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