KRAS peptide vaccines

ELI-002 2P and ELI-002 7P (amphiphile mutant-KRAS peptide vaccines), mKRAS peptide vaccine, pooled mutant KRAS long-peptide vaccine, TG01 (earlier RAS peptide vaccine), GI-4000 (earlier yeast-based RAS construct)

Oncology & imaging

Awaiting medical reviewEN ES DE FR PT ZH+ Follow for updates

Note on this profile. These are investigational vaccines given only inside clinical trials under oncology supervision. None is approved or available outside trials, and nothing here describes self-preparation.

Summary

Class: Synthetic long peptides spanning common KRAS driver mutations (G12D, G12R, G12V, G12C, G12A, G12S, G13D). In ELI-002 the peptides are conjugated to a lipid "amphiphile" tail and given with a similarly lipid-conjugated CpG oligonucleotide adjuvant (amph-CpG-7909) so both bind albumin and traffic to draining lymph nodes
Mechanism: Raises T cells against the specific mutated KRAS protein driving the patient's tumour — a true tumour-specific target, since the mutation does not exist in normal tissue
Routes studied: Subcutaneous injection, weekly priming doses then booster series; ELI-002 7P in the adjuvant (post-surgery, post-chemotherapy) pancreatic and colorectal setting
Half-life: Not the operative measure; the lipid–albumin design is about lymph-node delivery over hours to days, and the T-cell response over months
Storage: Refrigerated trial product prepared by pharmacy
Regulatory status: Not approved anywhere; investigational. See region table

Doses are as reported in studies or by the community — never recommendations.

1What it is

KRAS is the most frequently mutated oncogene in human cancer — present in roughly 90% of pancreatic ductal adenocarcinomas, about 40% of colorectal cancers and a substantial share of lung adenocarcinomas — and the mutations cluster at a very small number of positions, overwhelmingly codon 12. That makes mutant KRAS an unusual target: it is genuinely tumour-specific like a neoantigen, but it is shared across many patients like a conventional antigen, so an off-the-shelf vaccine covering seven mutations can in principle address most patients with a KRAS-driven cancer. It is, on paper, the best of both worlds.

ELI-002 is the most advanced attempt. Its distinguishing feature is delivery rather than antigen choice: attaching a lipid tail to both the peptides and the CpG adjuvant makes them bind serum albumin, which is naturally trafficked to lymph nodes, concentrating both antigen and adjuvant where T cells are primed instead of leaving them at the injection site. Earlier KRAS-directed vaccines (TG01, GI-4000) tested the antigen idea without this delivery approach and did not produce convincing clinical results.

2How it's thought to work

Lipid-conjugated peptides and CpG adjuvant bind albumin after injection and accumulate in draining lymph nodes.

CpG-7909 is a TLR9 ; delivered to the same node as the antigen, it drives dendritic-cell maturation and a Th1-polarised response.

Long peptides covering the mutated codon are processed and presented on both class I and class II, so CD8+ and CD4+ responses are generated and the approach is not restricted to a single HLA type.

The resulting T cells recognise a sequence that exists only in tumour cells, so on-target autoimmunity should in principle be impossible — a real advantage over gp100 or HER2 vaccines.

The intended setting is minimal residual disease after surgery and chemotherapy, where tumour burden and immunosuppression are at their lowest.

Peptides spanning the specific KRAS mutation a patient's tumour carries. The mutated sequence is foreign to the immune system in a way the normal protein is not.Schematic — not to scale

3What the research shows

Graded A (negative on primary endpoint)

Resected pancreatic cancer, randomised

AMPLIFY-7P, a randomised phase 2 trial of ELI-002 7P versus observation in patients with resected pancreatic ductal adenocarcinoma after standard adjuvant therapy, did not meet its primary endpoint of disease-free survival in the intention-to-treat population (reported June 2026). A post-hoc analysis restricted to patients with complete (R0) resection reported a hazard ratio of 0.65 (p = 0.048) with median disease-free survival of roughly 23.8 versus 12.8 months, and the imbalance in margin-positive (R1) patients favoured the control arm. Overall survival data were immature. The sponsor has stated an intention to run a registrational phase 3 confined to R0-resected patients with extended dosing †. The honest summary: the randomised trial missed its primary endpoint; the R0 analysis is post hoc and hypothesis-generating, and post-hoc subgroups in cancer-vaccine trials have a poor track record (see profiles 232 and 236).

Graded B (strong)

Immunogenicity

Across AMPLIFY-201 (phase 1) and AMPLIFY-7P, mutant-KRAS-specific T-cell responses were induced in the large majority of evaluable patients — reported above 80% in phase 1 and around 99% of evaluable patients in later phase 2 reporting — across diverse HLA types, with both CD4+ and CD8+ responses and reductions in tumour biomarkers in responders (Pant 2024, Nature Medicine). The magnitude of the T-cell response was associated with longer disease-free survival in post-hoc analysis (reported hazard ratio around 0.22 for high versus low responders). This is the strongest immunogenicity data set of any shared-antigen cancer vaccine, and the field has now learned repeatedly that this does not guarantee clinical benefit. [1]

Pooled mutant KRAS long-peptide vaccine with checkpoint blockade

An academic programme has tested a pooled mutant-KRAS long-peptide vaccine with ipilimumab and nivolumab in resected pancreatic and colorectal cancer, reporting immunogenicity and feasibility in small cohorts. Early-phase only.

Earlier RAS vaccines

TG01 (a RAS peptide vaccine with GM-CSF) reported immune responses and some survival signal in small resected pancreatic cohorts; GI-4000 (a yeast-based mutant RAS construct) did not show benefit in a randomised adjuvant pancreatic trial. Neither established efficacy.

4Reported side effects and interactions

Literature-reported

reactogenicity is the dominant finding — injection-site reactions, fever, chills, fatigue and flu-like symptoms, consistent with a TLR9 adjuvant, mostly grade 1–2 and in the days after dosing. No dose-limiting toxicity was reported in phase 1 and no treatment-related grade 3 cytokine-release events were described. Because the target sequence does not exist in normal cells, no autoimmune toxicity would be expected and none has been reported.

Community-reported

Community use: essentially none documented.

Theoretical. CpG-class adjuvants carry a theoretical risk of provoking or worsening autoimmune disease, which is why patients with active autoimmune conditions are generally excluded. Vaccine-induced T cells could in principle cause inflammation at sites of occult tumour.

Interactions. checkpoint inhibitors (studied in combination in academic trials); corticosteroids and ongoing cytotoxic chemotherapy blunt responses, which is why vaccination follows completion of adjuvant chemotherapy.

Markers researchers commonly monitor

From trial protocols:

Marker	Why it's watched
Tumour KRAS mutation genotype	the eligibility gate; the vaccine must match the patient's mutation.
Mutant-KRAS-specific T-cell response magnitude and fold change (ELISpot, flow cytometry, cytolytic assays)	the pharmacodynamic readout, and in these trials a post-hoc predictor of disease-free survival. Treat predictive claims from post-hoc analyses cautiously.
Circulating tumour DNA (ctDNA), especially mutant KRAS allele fraction	the most informative minimal-residual-disease marker in this setting and increasingly the primary biological endpoint in adjuvant vaccine trials.
CA 19-9	the standard pancreatic tumour marker; reductions in vaccine responders were reported in phase 1.
Disease-free and overall survival with protocol imaging	the endpoints that will decide the question.
Resection margin status (R0 versus R1)	not a monitoring marker but the variable the entire post-hoc story turns on; any future claim must be read in light of how it was balanced.
CBC, CMP, temperature and injection-site assessment post-dose	reactogenicity and routine safety.

Free for everyone. Safety information is never behind a paywall.

5Formulation and administration context

Supplied as refrigerated vialled amphiphile peptide mixture and amphiphile CpG adjuvant, drawn up and combined by trial pharmacy and given subcutaneously by trained staff — six weekly priming doses followed by a booster series, with longer maintenance dosing planned for the phase 3. No HLA pre-selection is required, which is a practical advantage over profiles 231, 232 and 236; tumour KRAS genotyping is the eligibility test instead. There is no self-prepared, compounded or outpatient version of these products and no dose calculation appropriate to publish.

6Commonly studied alongside

CpG-7909 (TLR9 agonist adjuvant, integral to ELI-002); ipilimumab and nivolumab (academic pooled-peptide programme); adjuvant mFOLFIRINOX or gemcitabine-based chemotherapy as the preceding standard of care. Conceptually related: neoantigen peptide vaccines (profile 238), IMA901 and multi-peptide vaccines (profile 236).

Informational cross-links. Not stack recommendations.

7Regulatory status by region

Region	Status (checked —)
United States	Not FDA-approved; investigational. A registrational phase 3 in R0-resected pancreatic cancer has been announced as an intention, not initiated results †
European Union	Not authorised
United Kingdom	Not licensed
Australia	Not approved
South Africa	Not registered with SAHPRA
Sport	Not listed by WADA; no performance application

8Open questions

Will the R0-restricted post-hoc effect hold up in a prospective randomised phase 3, or follow the pattern of profiles 232 and 236?
Can ctDNA clearance serve as a validated surrogate endpoint for adjuvant cancer vaccines, which would make these trials far faster?
Does lymph-node-targeted delivery of antigen and adjuvant represent a genuine step change, or an incremental improvement in immunogenicity that still does not reach clinical benefit?

9References

1Pant S et al. (2024). Lymph-node-targeted, mKRAS-specific amphiphile vaccine in pancreatic and colorectal cancer: the phase 1 AMPLIFY-201 trial. Nature Medicine. PubMed · DOI
2Elicio Therapeutics (2026). Results from the phase 2 AMPLIFY-7P study of ELI-002 7P in adjuvant pancreatic cancer — sponsor announcement, June 2026 [verify; peer-reviewed publication pending]. PubMed
3Zhang Y, Jaffee EM et al. (2024). Pooled mutant KRAS long peptide vaccine with ipilimumab and nivolumab in resected pancreatic and colorectal cancer — early-phase report. Journal of Clinical Oncology abstract or primary report [verify]. PubMed
4Palmer DH et al. (2020). TG01/GM-CSF and adjuvant gemcitabine in patients with resected RAS-mutant adenocarcinoma of the pancreas (CT TG01-01). Cancer Immunology, Immunotherapy. PubMed · DOI
5Moore MJ et al. (2015). GI-4000 plus gemcitabine versus gemcitabine alone in patients with resected pancreas cancer with activating RAS mutations — randomised trial. Journal of Clinical Oncology abstract [verify]. PubMed
6ClinicalTrials.gov. NCT05726864 — AMPLIFY-7P. PubMed

References are being resolved to PubMed/DOI identifiers; links search PubMed for the citation until then.

† Being confirmed by our reviewers against current sources.

10Community

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Self-reported side effects Phase 2

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11Page history

31 Oct 2026Profile published — awaiting medical review

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