I actually started crying in clinic. This is such an incredibly impactful study.
For decades, pancreatic cancer has occupied a grim corner of medicine where progress came slowly and hope arrived sparingly — a disease that claimed lives with quiet efficiency while science searched for a foothold. At a major oncology gathering in Chicago, that long stillness was broken when data from a trial of the experimental drug daraxonrasib showed a 60% reduction in death risk for patients with metastatic disease, doubling median survival compared to standard chemotherapy. The moment belongs not only to the scientists who cracked a decades-old molecular puzzle, but to the tens of thousands of patients each year for whom the calendar of survival has always been measured in months.
- Pancreatic cancer has long resisted treatment because KRAS — the mutation driving 90% of cases — was considered nearly impossible to target, leaving patients with metastatic disease facing median survival of just over six months.
- When trial data showing daraxonrasib doubled that survival to 13.2 months appeared on screen in Chicago, the auditorium erupted in a minute-long standing ovation that stopped the presenter mid-sentence.
- The Phase-3 trial of 500 patients was unambiguous: the once-daily pill outperformed chemotherapy on survival, disease progression, and tolerability, with results published simultaneously in the New England Journal of Medicine.
- Oncologists who have spent careers delivering grim prognoses described the moment as a 'grand slam' and a 'game changer,' with one physician of sixteen years admitting she wept in clinic upon seeing the findings.
- The FDA is expected to fast-track review, an expanded access program is already open to eligible patients, and researchers are now testing the drug in earlier cancer stages and in lung, colon, and ovarian cancers driven by the same RAS mutations.
- Daraxonrasib is not arriving alone — a separate trial of elraglusib led by a Malaysian physician also doubled one-year survival rates in combination therapy, signaling that after decades of stagnation, a genuine turning point may be underway.
The auditorium at the American Society of Clinical Oncology's annual meeting in Chicago was not prepared for what appeared on the screen. A 60% reduction in death risk for patients with metastatic pancreatic cancer — one of medicine's most resistant diseases. The room erupted in applause, cheers, and whistles that lasted nearly a minute, forcing presenter Dr. Brian Wolpin to pause with a quiet laugh. "That time was not built into my talk," he said.
The drug behind the ovation was daraxonrasib, an experimental once-daily pill developed by California-based Revolution Medicines. Its significance lay in what it had finally managed to do: switch off the KRAS protein, a mutation present in more than 90% of pancreatic cancer cases that scientists had spent decades trying — and largely failing — to target effectively.
The Phase-3 trial, RASolute 302, enrolled 500 patients whose metastatic disease had progressed despite prior treatment. Half received daraxonrasib; half received standard chemotherapy. The results, published simultaneously in the New England Journal of Medicine, were unambiguous. Patients on the new drug survived a median of 13.2 months, compared with 6.6 months on chemotherapy. The drug also delayed disease progression and caused fewer treatment discontinuations due to side effects.
The oncology community responded with rare unanimity. The chief medical officer of ASCO called it "a grand slam." A gastrointestinal oncology director declared that "RAS targeting has arrived." Dr. Rachna Shroff, who has treated pancreatic cancer for sixteen years, said she began crying in clinic. That emotion was grounded in hard reality: the disease kills roughly 50,000 Americans each year, and metastatic patients have historically faced survival measured in months.
Daraxonrasib has already received FDA fast-track designation, and an expanded access program is open to eligible patients ahead of formal approval. Researchers are now studying the drug in earlier treatment stages and testing it against other RAS-driven cancers, including lung, colon, and ovarian. A separate trial of elraglusib, led by Malaysian physician Devalingam Mahalingam, also doubled one-year survival rates when combined with chemotherapy for advanced pancreatic cancer — a larger confirmatory study is underway. The standing ovation in Chicago carried the weight of decades: not just for one drug, but for the possibility that a disease long considered nearly untreatable may finally be meeting its match.
The auditorium at the American Society of Clinical Oncology's annual meeting in Chicago fell silent when the data appeared on the screen. A 60% reduction in death risk. The room erupted—applause, cheers, whistles that lasted nearly a minute. Dr. Brian M. Wolpin, who was presenting the results, had to pause his talk. "That time was not built into my talk," he said with a laugh once the noise subsided.
The drug being celebrated was daraxonrasib, an experimental pill developed by California-based Revolution Medicines. What made the moment so extraordinary was what it represented: a genuine breakthrough against one of medicine's most intractable enemies. For decades, scientists had struggled to develop treatments that could effectively target KRAS, a gene mutation present in more than 90% of pancreatic cancer cases. The protein it produces had seemed almost impossible to switch off. Now, suddenly, it appeared they had done it.
The Phase-3 trial, called RASolute 302, enrolled 500 patients with metastatic pancreatic cancer whose disease had continued to progress despite previous treatment. Half received a daily dose of daraxonrasib; the other half received standard chemotherapy. The results, published simultaneously in the New England Journal of Medicine, were stark. Patients taking the new drug survived a median of 13.2 months, compared with 6.6 months for those on chemotherapy. The drug also delayed disease progression longer and caused fewer patients to stop treatment because of side effects.
The reaction from the oncology community was immediate and visceral. Dr. Julie Gralow, the chief medical officer of the American Society of Clinical Oncology, told reporters the findings were "much more than a home run"—she called it "a grand slam." Dr. Mark Lewis, a gastrointestinal oncology director, wrote on social media that it felt as though "RAS targeting has arrived." Dr. Rachna Shroff, chief of hematology and oncology at the University of Arizona Cancer Center, described it as "a game changer." She added something more personal: "Having treated pancreatic cancer for 16 years, I actually started crying in clinic. This is such an incredibly impactful study for our patients."
That emotion was grounded in brutal reality. Pancreatic cancer remains one of the world's deadliest malignancies. In the United States alone, it claims roughly 50,000 lives each year. Patients with metastatic disease—cancer that has spread beyond the pancreas—have historically faced particularly grim odds. For many years, the median survival for these patients measured in months, not years. The doubling of survival time that daraxonrasib achieved, while still measured in months rather than years, represented a fundamental shift in what was possible.
Daraxonrasib works by switching off the active RAS proteins that drive tumor growth. It is taken as a once-daily pill, a form that offers practical advantages over intravenous chemotherapy. The FDA is expected to fast-track its review of the drug, which has already received special designations for promising treatments targeting rare and serious diseases. Regulators have also authorized a program allowing eligible patients with previously treated metastatic pancreatic cancer to access the drug before formal approval is granted.
The research is not stopping here. Scientists are now studying daraxonrasib in earlier stages of pancreatic cancer treatment and testing it against other cancers driven by RAS mutations, including lung, colon, and ovarian cancers. Notably, daraxonrasib is not alone in generating optimism. Earlier this year, Malaysian doctor Devalingam Mahalingam led a clinical trial that found another experimental drug, elraglusib, doubled one-year survival rates when combined with standard chemotherapy for advanced pancreatic cancer. Researchers are pursuing a larger study to confirm those findings. After decades of stagnation, multiple new treatment approaches are finally gaining traction against a disease that has long seemed nearly untreatable. The standing ovation in Chicago was not just for one drug. It was recognition that the long scientific struggle against pancreatic cancer may finally be turning.
Notable Quotes
I would actually say it's a grand slam— Dr. Julie Gralow, ASCO chief medical officer, on the trial results
Having treated pancreatic cancer for 16 years, I actually started crying in clinic. This is such an incredibly impactful study for our patients— Dr. Rachna Shroff, chief of hematology and oncology at University of Arizona Cancer Center
The Hearth Conversation Another angle on the story
Why did doctors actually stand up and applaud? That's unusual for a medical conference.
Because for decades, KRAS has been considered untargetable. Oncologists have watched pancreatic cancer patients die knowing the mutation was driving the disease but unable to stop it. When they saw a 60% reduction in death risk, they saw the end of an era of helplessness.
But 13 months versus 6 months—that's still a death sentence, isn't it?
Yes, but it's a reprieve. It's time for more treatment, time with family, time that didn't exist before. And it's proof the approach works. The next generation of these drugs will likely do better.
Why is this happening now? Why couldn't they do this ten years ago?
The science of protein degradation and targeted inhibition had to mature. You need the right tools, the right understanding of how the protein folds and functions. Sometimes breakthroughs are about patience and accumulation of knowledge.
The doctor who cried—was that real emotion or performance?
That was real. She'd been treating the same disease the same way for 16 years. Watching people die from something you couldn't stop changes you. When you finally can, it breaks something open.
What happens to the patients who don't have the specific KRAS mutations this targets?
That's the next question. The trial focused on certain mutations. There are others. But the principle—that you can target RAS—now that's proven. The field will expand from here.