89 out of 90 patients is a promising stat when it comes to a new pancreatic cancer vaccine.
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| Pancreatic Cancer Vaccine |
That is how often an experimental pancreatic cancer vaccine got the immune system to fight back. The vaccine is called ELI-002 7P, and in a phase 2 clinical trial, nearly every patient who could be assessed developed a stronger T-cell response against the mutated protein driving their cancer. It is one of the most striking immune-response numbers pancreatic cancer research has produced — and it comes with an honest caveat that matters just as much as the headline.
The results come from the randomized phase 2 AMPLIFY-7P trial, published in Nature Medicine on October 23, 2026. The trial enrolled 144 people with stage I-III pancreatic cancer who had already been through surgery and standard treatment and had no sign of recurrence for six months afterward. They were split two-to-one: 96 received the vaccine, and 48 were simply observed, which is the standard approach after surgery and chemotherapy.
What ELI-002 7P Actually Does
To understand why this vaccine is different, you have to understand KRAS. KRAS is a gene that, when mutated, acts like a stuck accelerator pedal, telling cells to keep growing when they should stop. KRAS mutations show up in the vast majority of pancreatic cancers, which is a big reason the disease is so hard to treat: the same mutation driving the tumor also helps it resist therapy.
ELI-002 7P is a cancer vaccine designed to teach the immune system's T cells to recognize seven of the most common KRAS mutations — G12D, G12R, G12V, G12A, G12C, G12S, and G13D. Together, those seven mutations cover about 90 percent of pancreatic ductal adenocarcinomas, the most common form of the disease. The vaccine uses an "amphiphile" design that targets the lymph nodes, where immune responses are organized, so the T cells learn their target efficiently.
Crucially, the vaccine is off-the-shelf. Many cancer vaccines in development are custom-built for each patient from their own tumor, a process that takes weeks and costs a fortune. ELI-002 7P is a fixed formula aimed at mutations shared by most patients, so nobody has to wait for a personalized dose to be manufactured. If it works, it could be given far more widely and far more quickly.
The Trial Numbers, Plainly Stated
Among the 90 vaccine recipients whose immune responses could be measured, 89 developed T-cell responses specifically against mutant KRAS. That is 98.9 percent — the "89 out of 90" figure. Even more striking, 74 of those 90 patients, or 82.2 percent, saw their T-cell response grow to more than 9.17 times its starting level.
That size of response turned out to matter. Patients whose T-cell response crossed that 9.17-fold threshold stayed cancer-free far longer: their median disease-free survival had not even been reached yet at the time of analysis, compared with 6.08 months for patients whose responses stayed below it. In exploratory analyses, stronger immune responses were associated with a 53 percent reduced risk of recurrence. The vaccine also showed signs of "antigen spreading" in 86.7 percent of a smaller group tested — meaning the immune system began recognizing additional tumor targets beyond the ones in the vaccine, a pattern researchers associate with deeper, longer-lasting responses. Median follow-up in the trial was 19.4 months, and a prespecified look at the dosing period showed disease-free survival at six months of 75.7 percent with the vaccine versus 61.7 percent with observation.
The Honest Caveat: The Trial Missed Its Main Goal
Here is the part that keeps this story honest. The AMPLIFY-7P trial did not meet its primary endpoint. Median disease-free survival across all patients was 23.8 months with the vaccine versus 21.2 months with observation alone — a difference that was not statistically significant. In other words, when you compare the two groups as a whole, the trial did not prove that the vaccine delays recurrence.
That sounds contradictory, and it is worth explaining why researchers are not discouraged. The immune-response findings came from analyses that look within the vaccine group, not from the head-to-head comparison the trial was designed around. Those analyses were partly exploratory, meaning they were not the trial's pre-planned main test, and they can overstate an effect. The vaccine arm also happened to include more patients with higher-risk surgical margins — 19 percent had tumor present at or within 1 millimeter of the surgical margin, compared with 10 percent in the observation arm — which may have tilted the overall comparison. A post-hoc multivariate analysis that adjusted for these imbalances did favor the vaccine, with an adjusted hazard ratio of 0.47, and in the subgroup of patients whose tumors were completely removed with clean margins, median disease-free survival was 23.8 months with the vaccine versus 12.8 months with observation. Overall survival data is not yet mature enough to judge, so the long-term picture is still incomplete.
On safety, the vaccine looked manageable: severe side effects occurred in 10.4 percent of vaccine recipients versus 14.6 percent of the observation group, and serious adverse events were actually less common with the vaccine, 6.3 percent versus 8.3 percent.
Why Researchers Are Still Excited About This Pancreatic Cancer Vaccine Treatment
If the trial missed its main goal, why is anyone calling this promising? Because pancreatic cancer has humbled nearly every immunotherapy approach tried against it. The disease is notoriously "cold" to the immune system — tumors hide, suppress immune cells, and return after surgery in most patients. Getting 89 out of 90 patients to mount a measurable, targeted immune response, and seeing the strongest responses track with much longer cancer-free time, is a biological signal researchers have been chasing for years.
That signal is already shaping what comes next. The vaccine's maker, Elicio Therapeutics, has refined its phase 3 strategy around the patients most likely to benefit — those whose tumors were completely removed with clean surgical margins — along with additional vaccine dosing. A confirmatory phase 3 trial is now being designed around that population. Separately, researchers at the University of Miami's Sylvester Comprehensive Cancer Center received a $1 million V Foundation grant to study combining the KRAS-targeted vaccine with a RAS inhibitor drug called daraxonrasib, with or without the immunotherapy nivolumab, to see whether the combination can strengthen responses further. An
