Life sciences · Journal article
Nature Medicine · October 23, 2026
No summary has been generated for this record yet. What follows is drawn from its source metadata only.
Journal article.
No findings were extractable from the material analysed.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
The source did not state who this applies to in practice.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
This record has not been graded across any dimension yet. Treat the label above as provisional and read the source.
What is missing. This record has no bottom line, key findings, reported figures, evidence dimensions. That is a gap in the analysis, not a judgement about the study.
Camupepimut (ELI-002 7P) drives mutated KRAS (mKRAS)-specific T cell responses that correlated with disease-free survival (DFS) and overall survival (OS) in patients with mKRAS pancreatic adenocarcinoma (PDAC) in the phase 1 AMPLIFY-201 trial. In the phase 2 AMPLIFY-7P trial, patients with stage I-III KRAS-mutated PDAC without recurrence within 6 months of standard therapy were randomized 2:1 to camupepimut (n = 96) or standard-of-care/observation (n = 48). Stratification balanced nodal status. The primary DFS endpoint was not met (median 23.8 versus 21.2 months; HR 0.85, P = 0.5329). However, prespecified and exploratory analyses were informative. A numerical DFS advantage at 6 months of 14.0% (75.7% versus 61.7%; HR 0.55, P = 0.0557) corresponded to camupepimut dosing. Post hoc multivariate Cox regression analysis of DFS indicated an improved outcome for camupepimut (adjusted HR 0.47, P = 0.0086), a worse outcome for stage III disease (adjusted HR 2.29, P = 0.0127), an elevated baseline CA19-9 (adjusted HR 3.16, P < 0.0001) and baseline circulating tumor DNA (ctDNA) positivity (adjusted HR 5.99, P < 0.0001). Prespecified subgroup analyses addressing prognostic and predictive factors suggested DFS benefit for camupepimut (ctDNA negative: HR 0.51, P = 0.0280; no prior radiation: HR 0.59, P = 0.0221). Exploratory analysis demonstrated that ex vivo mKRAS-specific T cell responses were robust (98.9%, 89/90) and associated with antigen spreading (86.7%, 13/15). In camupepimut-treated patients, mKRAS-specific T cell response >9.17-fold over baseline (82.2%, 74/90) correlated with improved DFS (HR 0.22, P < 0.0001), with the median DFS not reached versus 6.08 months for above and below 9.17-fold, respectively. Camupepimut safety was similar to observation, with grade ≥3 adverse events in 10.4% (10/96) versus 14.6% (7/48), and few serious AEs (6.3%, 6/96 versus 8.3%, 4/48; reflecting progression/surgical complication). These efficacy and immunogenicity signals will inform a refined strategy for a confirmatory phase 3 trial. ClinicalTrials.gov identifier: NCT05726864. As presented at the ESMO Congress 2026, in a randomized phase 2 trial evaluating an off-the-shelf lymph node-targeting peptide vaccine in patients with mutated KRAS pancreatic cancer within 6 months of standard curative intent therapy, the primary endpoint of disease-free survival was not met, but prespecified subgroup analyses showed significant disease-free survival benefit in the vaccine arm for patients with circulating tumor DNA-negative disease and in those without prior radiation treatment.