Elicio Therapeutics, Inc. · NASDAQ:ELTX
Elicio Therapeutics — Investor Presentation (January 2026)
50 slides from Elicio Therapeutics's investor presentation, January 2026
Slide 1: Targeting the Lymph Nodes to AMPlify Immunotherapy
Targeting the Lymph Nodes to AMPlify Immunotherapy Nasdaq: ELTX January 2026
Slide 2: Disclaimers
Disclaimers No Representation or Warranty We do not make and hereby expressly disclaim any representation or warranty, express or implied, as to the reasonableness of the assumptions made in the Presentation or the accuracy or completeness or the information contained in or incorporated by reference
Slide 3: Disclaimers: Forward-Looking Statements
Disclaimers Forward-Looking Statements This presentation contains forward-looking statements as that term is defined in Section 27A of the Securities Act of 1933, as amended, Section 21E of the Securities Exchange Act of 1934, as amended, and the Private Securities Litigation Reform Act of 1995, kno
Slide 4: Investment Highlights
Investment Highlights Clinical-stage Biotech Developing Novel Lymph Node-targeted “off the shelf” Cancer Immunotherapies • Our proprietary AMP platform is designed to generate robust, functional, and durable immune responses by Leveraging proprietary targeting lymph nodes- the “brain center” of the
Slide 5: Seasoned Management Team
Seasoned Management Team Robert Connelly Peter DeMuth, PhD Christopher Haqq, MD, PhD Preetam Shah, MBA, PhD Megan Filoon, JD Marc Wolfgang, MS Chief Executive Officer Chief Scientific Officer Executive Vice President, Head Chief Strategy and Financial General Counsel, Secretary Chief Technology Offi
Slide 6: Company Pipeline
Company Pipeline Innovative Pipeline of Cancer Immunotherapies Addressing Critical Unmet Needs Candidate Target Indication Setting Preclinical IND Ready Phase 1 Phase 2 Phase 3 ELI-002 7P mKRAS PDAC Adjuvant ELI-002 7P mKRAS CRC Adjuvant ELI-002 7P mKRAS CRC Metastatic ELI-002 7P Neoadjuvant mKRAS P
Slide 7: The Annual Addressable KRAS-mutant Market – A Significant Opportunity
The Annual Addressable KRAS-mutant Market – A Significant Opportunity ELI-002 7P Targets the 7 Most Common KRAS Mutations Driving 25% of Solid Tumors The Annual Incidence of KRAS mutated cancers in US, EU5 and Japan: Pancreatic Ductal Non-Small Cell Lung Other mKRAS Colorectal Cancer Adenocarcinoma
Slide 8: ELI-002's Differentiated Approach to mKRAS Therapy
ELI-002’s Differentiated Approach to mKRAS Therapy Validated mKRAS Target | Differentiated Vaccine Approach | Clinical Stage Small Molecules Personalized Cancer Vaccines Targeting Lymph Node Targeted Vaccine Targeting Inhibiting Mutant KRAS Private Tumor Neoantigens Mutant KRAS FDA approvals for LUM
Slide 9: ELI-002 7P Potential to Address ~48K PDAC Patients Annually
Annually ELI-002 7P has a Potential to Address ~48K PDAC Patients with its Initial Indication, and an Additional ~88K Patients with Subsequent Indications ~160K Incidence of PDAC patients ~48K ~88K (U.S., EU5, Japan) PDAC Resectable Borderline Locally Advanced / Metastatic ~20% ~10% ~70% 88% KRAS ~$
Slide 10: Beyond PDAC, ELI-002 7P Has Significant Potential in KRAS Mutant Cancers
Beyond PDAC, ELI-002 7P has Significant Potential to Transform the Care of KRAS Mutant Cancers ~10K Incidence1 ~$2.4B TAM Annually ~120K Incidence1 Other KRAS ~$28B TAM Annually NSCLC ~210K Incidence1 ~$50B TAM Annually ~160K Incidence1 CRC ~$38.5B TAM Annually PDAC 1Assumes $240K overall cost of th
Slide 11: Amphiphile (AMP) Platform
Targeting the Lymph Nodes to Orchestrate Immunity Amphiphile (AMP) Platform
Slide 12: AMP Platform Enables Lymph Node Delivery with Simple and Versatile Application
Amphiphile (AMP) Platform Enables Lymph Node Delivery with Simple and Versatile Application AMP: A Modular Chemical Conjugation Approach for Delivery of Immune Therapeutics to the Lymph Nodes Small Molecules Peptides Nucleic Payload Acids Proteins 1 Albumin Binding Lipid 2 Polymeric Linker 3 Payload
Slide 13: MOA: Targeting the Lymph Nodes with AMP to Orchestrate Immunity
MOA: Targeting the Lymph Nodes with AMP to Orchestrate Immunity Tissue Injection Site Lymph Node AMP Endogenous Albumin Albumin-bound AMP ➢ APC Activation ➢ T / B Cell Response • Expansion • Persistence • Effector function • Phenotype Albumin-bound AMP Antigen Presenting Cell T Cell B Cell Subcutane
Slide 14: AMP-vaccination Induces Coordinated Immune Activation in Lymph Nodes
AMP-vaccination Induces Coordinated Immune Activation in Lymph Nodes Enhanced Antigen-specific T cell Response Magnitude and Functional Quality Albumin-based Delivery to Lymph Nodes Blood IFNγ+ T Cell Response gp100 Antigen Albumin Soluble AMP (65 kDa) 2% 52% IFN-γ Binding to Tissue Albumin CD8 Enha
Slide 15: AMP Platform Technology
AMP Platform Technology Cancer Immunotherapy - Vaccines Versatile | Simple | Clinical Stage Immunotherapy / Combinations 2014 Liu Nature 2016 Moynihan Nature Medicine CAR-T Cell Adoptive Therapy 2018 Moynihan Cancer Immunology Research Applications 2019 Ma Science TCR-T Cell Adoptive Therapy 2021 Ra
Slide 16: ELI-002 2 Peptide (2P) Formulation
Boosting Endogenous Anti-tumor Immunity Targeting mKRAS ELI-002 2 Peptide (2P) Formulation
Slide 17: ELI-002 2 Peptide (2P) Is a Lymph Node Targeted mKRAS Vaccine
ELI-002 2 Peptide (2P) Is a Lymph Node Targeted mKRAS Vaccine Proprietary AMP-CpG Adjuvant Shown to Enhance Immunogenicity in Early-Stage Trials ELI-002 G12X Peptide 2P D R Composition AMP-mKRAS X X Peptide Antigen ELI-002 2P • 2 AMP-peptides • CD8 and CD4 epitopes Albumin Binding Lipid for Lymph PE
Slide 18: ELI-002 2P Phase 1A Study Overview
ELI-002 2 Peptide Phase 1 Study Overview *Published in Nature Medicine ELI-002 2P Phase 1A Phase 1 adjuvant dose-ranging study to assess safety and efficacy of ELI-002 2P in patients who completed standard therapy and have molecular disease ELI-002 MONOTHERAPY: NCT04853017 Monotherapy (no chemo, CPI
Slide 19: 2P Induces Tumor Biomarker Declines in Majority of Phase 1a Patients
ELI-002 2P Induces Tumor Biomarker Declines in Majority of ELI-002 2P Phase 1A Phase 1a Patients Robust responses observed across tumor types and KRAS mutations with ELI-002 monotherapy Tumor Biomarker Responses ELI-002 2P Waterfall Plot: Biomarker Reduction/Clearance Best Overall Biomarker Response
Slide 20: 2P Elicits Robust Immune Responses in Majority of Phase 1a Patients
ELI-002 2P Elicits Robust Immune Responses in Majority of ELI-002 2P Phase 1A Phase 1a Patients 84% of patients generated mKRAS-specific T cells directly ex vivo; 100% at RP2D ELI-002 2P T Cell Fold-Changes mKRAS T Cell Responses Direct Ex Vivo T Cell Response 4 5 0 0.1 mg • T cells detectable by st
Slide 21: 2P: T cell Response Magnitude Correlates with Tumor Biomarker Response
ELI-002 2P: T cell Response Magnitude Correlates with Tumor ELI-002 2P Phase 1A Biomarker Response All patients with T cell responses over the threshold 9.17x showed tumor biomarker response mKRAS T Cell Response Tumor Biomarker Response Best Overall Tumor Biomarker Response Clearance Reduction Non-
Slide 22: RFS in Full Cohort vs PDAC Subgroup
ELI-002 2P Phase 1A RFS in Full Cohort vs PDAC Subgroup Median follow up has increased to 19.7 months vs 8.5 months in Pant et al., 2024 Nature Med Median RFS times similar for the full cohort and PDAC subgroup: Data cut-off Sept 24, 2024 Relapse-free Survival: Full Cohort (n=25) Relapse-free Surviv
Slide 23: Final Analysis Shows Strong Correlation between RFS and T Cell Response
Final Analysis Shows Strong Correlation between RFS ELI-002 2P Phase 1A and T Cell Response 88% Reduced Risk of Relapse or Death in Patients with T cell Responses above Threshold 9.17x Relapse-free Survival: DCO September 24, 2024 ELI-002 2P Relapse-free Survival DCO 06-Sept-2023 24-Sept-2024 Median
Slide 24: Final Analysis Shows Strong Correlation between OS and T Cell Response
Final Analysis Shows Strong Correlation between OS ELI-002 2P Phase 1A and T Cell Response 77% Reduced Risk of Death in Patients with T cell Responses above Threshold 9.17x Overall Survival: DCO September 24, 2024 ELI-002 2P Overall Survival DCO 06-Sept-2023 24-Sept-2024 Median OS: not reached ≥ Thr
Slide 25: Final Analysis of ELI-002 2P Phase 1: T cell Response Correlated To Clinical Activity
Final Analysis of ELI-002 2P Phase 1: mKRAS T cell Response Correlated ELI-002 2P Phase 1A To Clinical Activity Risk of Relapse and Death Reduced in 68% of Patients with T cell Responses Above 9.17x Threshold Pant et al. Nature Medicine. Wainberg, et al. Nature 2024 Medicine. 2025 Data Cut-off 6 Sep
Slide 26: ELI-002 7P: Enhancing Endogenous Anti-tumor Immunity
Enhancing Endogenous Anti-tumor Immunity by Using Additional Peptides Targeting mKRAS ELI-002 7P: Phase 1a Trial of ELI-002 7-Peptide Formulation First-in-human Study: mKRAS G12x or G13D-expressing, Adjuvant treatment of MRD+ PDAC and CRC
Slide 27: ELI-002 7 Peptide (7P) Is a Lymph Node Targeted mKRAS Vaccine
ELI-002 7 Peptide (7P) Is a Lymph Node Targeted mKRAS Vaccine Proprietary AMP-CpG Adjuvant Shown to Enhance Immunogenicity in Early-Stage Trials ELI-002 G12X G13X Peptide 7P D R V C S A D Optimization of Composition AMP-Peptide Dose AMP-mKRAS X X Peptide Antigen ELI-002 7P • 7 AMP-peptides • CD8 and
Slide 28: ELI-002 7P Phase 1A Study Overview
ELI-002 7P Phase 1A ELI-002 7P Phase 1A Study Overview Phase 1 peptide dose-ranging study to assess safety and efficacy of ELI-002 7P in patients who completed standard therapy and have minimal residual disease ELI-002 MONOTHERAPY: NCT05726864 Monotherapy (no chemo, CPI combo) Complete Local Therapy
Slide 29: 7P Elicits Immune Responses in all Phase 1a Patients
ELI-002 7P Elicits Immune Responses in all Phase 1a Patients ELI-002 7P Phase 1A 100% of patients with robust T cell response mKRAS T Cell Responses ELI-002 7P T Cell Fold-Changes by Dose Level • 100% of patients showed T cell responses Direct Ex Vivo T Cell Response Dose T Cell Response • 4.9 mg do
Slide 30: ELI-002 7P: T Cell Response Magnitude Correlates with Dose
ELI-002 7P: T Cell Response Magnitude Correlates with Dose ELI-002 7P Phase 1A Phase 2 Dose generates higher immune response than seen with ELI-002 2P ELI-002 2P vs ELI-002 7P 4.9 mg ELI-002 2P ELI-002 7P ELI-002 7P (Nat Med) (All) (4.9 mg) • ELI-002 7P data based on n=12 Patients (1.4 mg, n=5; 4.9
Slide 31: 7P: ELI-002 Stimulates Antigen Spreading
ELI-002 7P: ELI-002 Stimulates Antigen Spreading ELI-002 7P Phase 1A Expansion of T cells specific to personalized tumor antigens not targeted by vaccination Antigen Spreading to Personal Tumor Neoantigens Immunogenic Non-immunogenic 10 • ELI-002 7P vaccination led to expansion of T cell responses t
Slide 32: ELI-002 7P Induces Tumor Biomarker Declines in Majority of Phase 1A Patients
ELI-002 7P Phase 1A ELI-002 7P Induces Tumor Biomarker Declines in Majority of Phase 1A Patients Waterfall reflects superiority of 4.9 mg AMP-Peptide 7P dose level Tumor Biomarker Responses ELI-002 7P Waterfall Plot: Biomarker Reduction / Clearance * 100 Amph-Peptides-7P Dose • 71% (5/7) of patients
Slide 33: 7P: T Cell Response Drives Tumor Biomarker Response
ELI-002 7P: T Cell Response Drives Tumor Biomarker Response ELI-002 7P Phase 1A All patients with T cell responses above median showed tumor biomarker response mKRAS T Cell Response Tumor Biomarker Response Best Overall Tumor Biomarker Response Clearance Reduction Non-Responder • Strength of T cell
Slide 34: ELI-002 7P: DFS Strongly Correlates with T Cell Response
ELI-002 7P Phase 1A ELI-002 7P: DFS Strongly Correlates with T Cell Response Improved DFS associated with above median T cell response ELI-002 7P Disease-free Survival Supervised by Median T cell Fold Change 6 mo 12 mo • Induction of above median mKRAS-specific T cell responses by ELI-002 7P associa
Slide 35: ELI-002 7P: Safety
ELI-002 7P: Safety ELI-002 7P Phase 1A ELI-002 7P was well tolerated at all dose levels with no DLTs observed ELI-002 7P Safety / Tolerability ELI-002 7P Dose 1.4 mg 4.9 mg Overall n=6 n=8 n=14 • No DLT observed, No CRS or T cell Toxicities Adverse Event Term a Patients with Any Related TEAE, • Most
Slide 36: Enrollment Complete for ELI-002 7P Randomized Phase 2 PDAC
ELI-002 7P Phase 2 Enrollment Complete for ELI-002 7P Randomized Phase 2 PDAC Event Driven Interim DFS Analysis Completed: Preliminary Signals of Efficacy, IDMC Confirmed Safety Final Analysis Expected 1H 2026 for 2:1 Randomized, Open Label Study CLINICAL STUDY OVERVIEW: NCT05726864 Monotherapy (no
Slide 37: ELI-002 Summary of Phase 1 Clinical Trials
ELI-002 Summary of Phase 1 Clinical Trials 39 patients treated in two Phase 1A trials: ELI-002 2P and ELI-002 7P • MRD+ PDAC (n=33) and CRC (n=6) patients treated after local surgery and chemotherapy (adjuvant setting) • Phase 1 trials included dose-ranging for both peptide and adjuvant components o
Slide 38: ELI-002 7P Generated Robust T Cell Responses In Ongoing Phase 2
ELI-002 7P Phase 2 ELI-002 7P Generated Robust T Cell Responses In Ongoing Phase 2 Response Consistent with Observations in Phase 1 Trials of ELI-002 that Correlated with Clinical Activity Phase 2: mKRAS-specific T cell Responses to ELI-002 7P were Consistent with Previous Phase 1 Observations • ELI
Slide 39: ELI-002 7P Generated Robust T Cell Responses In Phase 2
ELI-002 2P/7P Phase 1, 2 ELI-002 7P Generated Robust T Cell Responses In Phase 2 Immune Response Consistent with Observations in Phase 1 Trials of ELI-002 that Correlated with Clinical Activity ELI-002 2P ELI-002 7P ELI-002 7P ELI-002 7P (Nature Medicine) (4.9 mg) All (1.4 mg & 4.9 mg) (4.9 mg) Phas
Slide 40: ELI-002 7P Generated Robust T Cell Responses Across Diverse HLA Backgrounds
ELI-002 7P Phase 2 ELI-002 7P Generated Robust T Cell Responses In Phase 2 Robust mKRAS-specific Immune Responses Induced Across Diverse HLA Backgrounds Significance Threshold mKRAS T Cell Response in Diverse Patient HLA Backgrounds FDR cutoff (q = 0.05) FDR: False Discovery Rate, Benjamini–Hochberg
Slide 41: ELI-002 7P Robust Antigen Spreading Responses
ELI-002 2P/7P Phase 1, 2 ELI-002 7P Generated Robust T Cell Responses In Phase 2 Robust Antigen Spreading Responses Induced Targeting Personalized Tumor Antigens ELI-002 2P ELI-002 7P ELI-002 7P (Nature Medicine) All (1.4 mg & 4.9 mg) (4.9 mg) Phase 1 (n=25) Phase 1 (n=12) Phase 2 (n=90) Patients MR
Slide 42: Key Milestones Achieved and Future Growth Catalysts
Key Milestones Achieved and Future Growth Catalysts ELI-002 Clinical Development Future Growth Catalysts ✓ Preliminary Phase 1 T Cell and biomarker response (ASCO) ❑ Initiate ELI-002 7P + CPI investigator-sponsored clinical combination study in neo-adjuvant PDAC and potential other ELI-002 7P combin
Slide 43: Investment Highlights
Investment Highlights Clinical-stage Biotech Developing Novel Lymph Node-targeted “off the shelf” Cancer Immunotherapies • Our proprietary AMP platform is designed to generate robust, functional, and durable immune responses by Leveraging proprietary targeting lymph nodes- the “brain center” of the
Slide 44: Appendix: Other Pipeline Assets
Appendix: Other Pipeline Assets
Slide 45: ELI-007 (BRAF) and ELI-008 (p53)
ELI-007 (BRAF) and ELI-008 (p53) Designing an AMP-Vaccine Targeting Mutant BRAF and p53 ELI-007 ELI-008 Mutant % Patients Mutant % Patients AMP-BRAF AMP-p53 1 V600E ~90% 1 R248W 3.53% Peptide Antigen Peptide Antigen 2 V600K ~5% 2 R248Q 4.37% 3 R175H 5.60% • 2 AMP-peptides • Up to 12 AMP-peptides 4 R
Slide 46: ELI-007: Why Target mutant BRAF with Vaccine Immunotherapy?
ELI-007: Why Target mutant BRAF with Vaccine Immunotherapy? Mutant BRAF is a Common Cancer Driver Mutant BRAF is a Promising Tumor Antigen • Prevalent among numerous tumor types • Truncal: mutations occur early, expressed uniformly in tumor cells • Overall poor clinical prognosis • Limited therapeut
Slide 47: ELI-007 Is a Lymph Node Targeted mBRAF Vaccine Immunotherapy
ELI-007 Is a Lymph Node Targeted mBRAF Vaccine Immunotherapy AMP-modification enhances BRAF V600E-specific T cell responses Experimental Schema: Mutant Peptide T Cell Response: BRAF V600 Spleen Day 35 BRAF V600E 29-mer BRAF V600K 29-mer Stim: V600E or V600K Peptide Pool Mock T Cells: V600E T Cells:
Slide 48: ELI-008: Why Target mutant p53 with Vaccine Immunotherapy?
ELI-008: Why Target mutant p53 with Vaccine Immunotherapy? Mutant p53 Drives ~30% of Human Cancers Mutant p53 is a Promising Tumor Antigen • Prevalent among numerous tumor types • Truncal: mutations occur early, expressed uniformly in tumor cells • Limited therapeutic options • Driver: mp53 signalin
Slide 49: ELI-008 Is a Lymph Node Targeted mp53 Vaccine Immunotherapy
ELI-008 Is a Lymph Node Targeted mp53 Vaccine Immunotherapy AMP-modification enhances p53 hot-spot mutant-specific T cell responses Experimental Schema: Mutant Peptide T Cell Response: p53 Spleen Day 35 p53 R248Q 30-mer p53 R20175H 30-mer Stim: p53 R248Q, R175H, or R273H OLPs p53 R273H 30-mer Mock T
Slide 50: ELI-004: AMP-CpG Combination with Radiation to Induce Tumor-specific Immunity In Situ
ELI-004: AMP-CpG Combination with Radiation to Induce Tumor-specific Immunity In Situ Tumor Lymph Node Tumor AMP- CpG Tumor Antigen + AMP-CpG Uptake Tumor Cell Killing Releases Additional Tumor Antigen Release Antigen Presenting Cell T Cells Antigen into Lymph Nodes Local Therapy Radiation + Tumor C
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