For nearly forty years, cancer researchers have struggled with a persistent problem. They knew that a mutation in a gene called KRAS was driving some of the deadliest tumors, including pancreatic, lung, and colorectal cancers. But every attempt to build a drug that could block it came up short. The KRAS protein had no obvious place for a drug molecule to latch onto. Scientists started calling it “undruggable.”
Now, a drug called daraxonrasib may have made headway. When the results from a phase 3 clinical trial were presented at the 2026 American Society of Clinical Oncology annual meeting in late May, the audience stood up to applaud. The drug represents a meaningful step forward in pancreatic cancer treatment.
About the study
The phase 3 trial enrolled 500 patients with metastatic pancreatic cancer whose disease had stopped responding to first-line chemotherapy. This is one of the hardest patient populations to treat. Standard second-line options have historically offered a median survival of just 4.8 to 5.9 months. Patients were randomly assigned to receive either daraxonrasib, an oral pill taken once daily, or standard chemotherapy chosen by their doctor.
Daraxonrasib works differently from earlier attempts to target KRAS. Instead of trying to block the protein directly, it uses what researchers call a “molecular glue” mechanism. The drug essentially glues a helper protein onto the mutant KRAS, locking it in an “off” position so it can no longer send the growth signals that fuel the cancer.
Daraxonrasib nearly doubled survival time
Patients on daraxonrasib lived an average of 13.2 months, compared to 6.7 months for those on standard chemotherapy. That represents a 60% reduction in the risk of death. Such improvement is rarely seen in clinical trials for this disease.
Tumors shrank in 33% of daraxonrasib patients, versus 12% on chemotherapy. Only 1.2% of patients on daraxonrasib stopped treatment due to side effects, compared to 11.2% on chemotherapy. Earlier-stage testing of daraxonrasib showed similar results, with tumors shrinking in 35% of a smaller group of patients and a median survival of 13.1 months.
Why this goes beyond pancreatic cancer
KRAS mutations are among the most common cancer-driving mutations in humans. The mutation that daraxonrasib targets accounts for roughly 40% of pancreatic cancers, approximately 25% of lung cancers, and 40% of colorectal cancers.
The inability to target KRAS for decades meant that patients with these mutations had no drug designed specifically for their tumor’s genetic driver. The molecular glue approach that finally worked in pancreatic cancer is the same mechanism researchers are now testing in lung, colorectal, and other KRAS-driven cancers.
What this means for patients
Daraxonrasib is not yet commercially available, but phase 3 data like this is typically what leads researchers to submit a drug for FDA approval. Patients should ask about genetic testing for their tumor to see if it carries the KRAS mutation. They should also ask their oncologist about clinical trials or expanded access programs. Phase 3 data presented at major oncology conferences like ASCO often precedes an FDA submission within months.
For patients with KRAS-mutated lung or colorectal cancer, the implications are forward-looking. Daraxonrasib is being studied in those tumor types as well. Understanding genetic risk and asking about mutation testing is a reasonable first step.
The takeaway
For 40 years, KRAS was the mutation researchers knew was driving some of the deadliest cancers, but they could not do anything about it. This molecular glue mechanism finally cracked a problem that frustrated oncologists for decades. The phase 3 results show nearly double the survival time, a fraction of the side effects, and a mechanism that applies across multiple cancer types. This is the kind of trial result that moves science forward.
