Targeting the Lymph Nodes to AMPlify Immunotherapy January 2024

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, known as the PSLRA. Statements in this presentation that are not purely historical are forward-looking statements. Such forward-looking statements include, among other things, statements regarding our planned clinical programs, including planned clinical trials and the potential of our product candidates, the unmet need and potential addressable market for our product candidates, the potential clinical utility, potential benefits and market acceptance of our product candidates, the potential advantages of our product candidates over those of existing therapeutics and/or those of our competitors, the expected receipt of clinical data, the timing of initiation of our planned clinical trials, and the advancement of and funding for our developmental programs generally. Actual results could differ from those projected in any forward-looking statements due to numerous factors. Such factors include, among others, our ability to raise the additional funding we will need to continue to pursue our business and product development plans; our expected use of proceeds; the inherent uncertainties associated with developing new products or technologies and operating as a development stage company, including in collaboration with other parties; our ability to develop, complete clinical trials for, obtain approvals for and commercialize any of our product candidates, including our ability to recruit and enroll patients in our studies; our ability to address the requests of the U.S. Food and Drug Administration or other regulatory agencies; our dependence on intellectual property; competition in the industry in which we operate; delays or disruptions due to COVID-19 or geo-political issues, including the conflicts in Ukraine and the Middle East; and market conditions. These forward-looking statements are made as of the date of this presentation, and we assume no obligation to update the forward-looking statements, or to update the reasons why actual results could differ from those projected in the forward-looking statements, except as required by law. You should consult all of the information set forth herein and should also refer to the risk factor disclosure set forth in the reports and other documents we file with the Securities and Exchange Commission (SEC) available at www.sec.gov, including without limitation the Company's Current Report on Form 8-K filed on June 2, 2023, the Company’s Quarterly Reports on Form 10-Q for the quarters ended June 30, 2023 and September 30, 2023, and the Company's other filings from time to time with the SEC. 2

Company HighlightsClinical-stage biotech pioneering novel lymph node targeted cancer immunotherapies 3 Novel Approach to Immunotherapy Amphiphile or “AMP” platform traffics payloads to lymph nodes to generate robust immune responses ELI-002: A Unique Lymph Node Targeted Vaccine Designed to target 7 KRAS mutations that drive ~25% of solid tumors Initial focus is PDAC where ELI-002 could address 88% of incident tumors Phase 1a Clinical Data 84% of patients showed T cell responses with an average 58x increase in T cell numbers 84% of patients showed a decline in tumor biomarker, 24% having complete clearance Patients achieving large T cell response have an 86% decrease in risk of progression or death Anticipated Near Term Catalysts Ongoing: Two Phase 1 trials with additional data available through 2024-2025 Initiation of Phase 2 PDAC monotherapy 1Q 2024

PipelineInnovative pipeline of cancer immunotherapies addressing critical unmet needs 4 CRC: colorectal carcinoma | PDAC: Pancreatic pancreatic ductal adenocarcinoma mKRAS: mutant Kirsten rat sarcoma | mBRAF: mutant homolog B of the Rapidly Accelerated Fibrosarcoma | mTP53: mutant tumor protein p53 Candidate Target Indications Preclinical Phase 1 Phase 2 Phase 3 ELI-002 mKRAS PDAC, CRC ELI-007 mBRAF GI Tumors ELI-008 mTP53 GI Tumors PDAC PDAC Planned Ongoing

Elicio: Amplifying Immunotherapy

The AMP PlatformHarnessing the untapped potential of the lymph nodes for immunotherapy 6 Most immune cells are located in lymph nodes, yet these critical sites are not engaged by conventional immunotherapies AMP promotes targeted delivery of payloads to the lymph nodes via “albumin hitchhiking” AMP harnesses the unique biology of the lymph nodes to enhance the magnitude, potency, and durability of immune responses Blood Lymph Small Molecules Large Molecules (e.g. Albumin) Blood Vessel Lymph Vessel Lymph Nodes Blood Circulation Tissue Injection Site Targeting Immunity in the Lymph Nodes

ELI-002 CompositionLymph node targeted therapeutic vaccine comprised of AMP-peptides and AMP-CpG 7 G12X G13X D R V C S A D ELI-002 Albumin Binding Lipid for Lymph Node Targeting CpG DNA: TLR-9 Agonist X X Albumin Binding Lipid for Lymph Node Targeting mKRAS Peptide PEG Linker • 2 or 7 AMP-peptides • CD8 and CD4 epitopes • Potent TLR-9 immune activator AMP-mKRAS Peptide Antigen AMP-CpG Adjuvant NH NH O O

Mechanism of ActionAMP immunotherapy generates an anti-tumor immune response via the lymph nodes 8 Tumor Eradication 5 Subcutaneous injection 1 Lymph Node Lymph node targeting 3 Antigen Presenting Cell Delivery to immune cells 4 Albumin-bound Amphiphiles Albumin-bound Amphiphiles Endogenous Albumin Amphiphiles Tissue Injection Site Albumin binding 2 Tumor T Cell

The mKRAS OpportunityELI-002 targets the 7 most common KRAS mutations driving 25% of solid tumors 9 Incidence for the 7 Major Markets (MM): US, France, Germany, Italy, Spain, UK, and Japan Sources for tumor incidence obtained from GLOBOCAN (2020). PDAC: 90% of pancreatic cancers (O’Reilly, 2021), NSCLC 84.3% of lung cancers (SEER, 2021), BTC: 15% of liver cancers + gallbladderSources for KRAS mutation data: Waters & Der, 2018; Ji Luo, 2021, Meng 2021; Hofmann 2022, AACR Project GENIE Registry; Froesch et al, 2022, Gordon et al, 2023 ELI-002 addressable Incidence: ~128k Other KRAS mutations 88% Pancreatic Ductal Adenocarcinoma ~88% Colorectal Cancer ~88% Non-Small Cell Lung Cancer Other mKRAS Opportunities 36% Other KRAS mutations 25% 17% 3-11% No KRAS mutation ELI-002 addressable Incidence: ~192k No KRAS mutation ELI-002 addressable Incidence: ~128k No KRAS mutation ~88% Biliary Tract Cancer Total incidence: ~40k Ovarian CancerTotal incidence: ~62k Other KRAS mutations

ELI-002’s Differentiated Approach to mKRASEarly mKRAS-targeting efforts in the clinic, while promising, leave significant white space 10 7 key mutations Reduced risk of resistance mechanisms Potent activation of immune mechanisms Expansion/activationof T cell response Promotion of anti-tumor T cell function Validates immune-targeting, and affects multiple mutations BUT Poor lymph node targeting and weaker T-cell activation May affect more than one mutation BUT Unlikely to affect all mutations, still subject to bypass resistance mechanisms FDA approvals for LUMAKRAS® & KRAZATI® validate target BUT Only affects one mutation (G12C), subject to multiple resistance mechanisms Lymph Node Targeted Vaccine vs Mutant KRAS Vaccines TargetingMutant KRAS Small Molecules Indirectly Inhibiting Mutant KRAS Small Molecules Directly Inhibiting Mutant KRAS

ELI-002: Clinical Development Program

ELI-002 At-a-GlancemKRAS immunotherapy eliciting strong T cell activity leveraging the AMP platform’s lymph node targeting design 12 2 Peptide (2P) & 7 Peptide (7P) Formulations 2P used in Phase 1 AMPLIFY-201 for clinical proof-of-concept while 7P CMC finalized Program now switches to full 7P formulation, to maximize efficacy and opportunity AMPLIFY Clinical Program Underway Phase 1 AMPLIFY-201 fully enrolled with positive tumor and mechanism of action (T cell) biomarker responses correlating with clinical outcome reported Phase 1/2 AMPLIFY-7P enrollment underway, randomized Phase 2 in PDAC expected to start in 2024 Distinct Clinical & Operational Advantages Vs comparable vaccines including targeting driver mutations and “off-the-shelf”

AMPLIFY-201 Study OverviewPhase 1 dose-ranging study to assess safety and efficacy of ELI-002 2P as adjuvant treatment in patients who completed standard therapy and have molecular disease 13 20-Months Follow-up Boost(4 doses over 4 weeks) Prime(6 doses over 8 weeks) Local Therapy(e.g., Surgery, Chemo) CLINICAL PROGRAM OVERVIEW: NCT04853017 Basket Trial Enrollment Pancreatic Ductal Adenocarcinoma (PDAC) Colorectal Cancer (CRC) n=20 n=5 mKRAS G12D / R – aligned to 2 peptide formulation No metastatic disease after locoregional treatment No radiographic evidence of disease (NED) High risk of relapse (MRD+ ctDNA/serum biomarkers) Key Criteria 1-2 months 3 months 2 months Safety Maximum Tolerated Dose (MTD) or RP2D ctDNA/serum biomarker change from baseline Immunological Responses Relapse Free Survival (RFS) Endpoints 25 patients enrolled across 5 dose cohorts, 23 evaluable at database cutoff (4/25/2023) Advanced: 68% had stage III or oligometastatic resected stage IV disease Pre-treated: All received prior chemo and surgery, 28% had prior radiation Baseline Characteristics

AMPLIFY-201: Tumor Biomarker ResponsesRobust responses observed across tumor types and KRAS mutations with ELI-002 monotherapy 14 24% of patients (6/25) showed complete clearance of ctDNA Most patients (84%, 21/25) showeddecline from baseline in ctDNA or CEA/CA19-9 levels 44% (11/25) showed a >30% reduction in biomarker levels Waterfall displays best response of ctDNA or serum tumor biomarker * Patient biopsied, exhibited T cell infiltration and continued study treatment S Patient underwent splenectomy Data cutoff 6-Sept-23 P P P P P P C P P P P P P P P C P P P P P C P C C Tumor Type D D D D D D D R R D D D D D D D R D R D D D R D D KRAS Biomarker D G12D R G12R P PDAC C CRC ctDNA CEA / CA19-9 -9 -11 -18 -2 S S S S * -2 -11 -17 Cohort 1: 0.1 mg Cohort 2: 0.5 mg Cohort 3: 2.5 mg Cohort 4: 5.0 mg Cohort 5: 10.0 mg AMPLIFY-201 Waterfall Plot: Biomarker Reduction/Clearance Tumor Biomarker Responses

AMPLIFY-201: 84% patients generated mKRAS specific T Cells 15 84% of patients showed T cell responses 100% in two highest dose cohorts, including at the RP2D (10 mg) 58x average fold-change in T cell numbers from baseline (median 13x; range 2-423x) T cells detectable by standard directex vivo FluoroSpot and flow cytometry, with no expansion required AMP-CpG Dose Level ex vivo T cell response (n, %) Average fold-change 0.1 mg 2/3 (67%) 30 0.5 mg 4/6 (67%) 101 2.5 mg 4/5 (80%) 113 5.0 mg 5/5 (100%) 19 10.0 mg 6/6 (100%) 36 Total 21/25 (84%) 58 Responses shown are best overall responses vs baseline for each patient at any timepoint during the assessment period. Data cutoff 6-Sept-23 Median = 13x AMPLIFY-201 T Cell Fold-Changes by Dose Level mKRAS T Cell Responses Baseline Max Response Direct Ex Vivo T Cell Response Response per Dose Level

Clearance Reduction Non-Responder AMPLIFY-201: T Cell Fold-Change Predicts Tumor Biomarker ResponseAll patients with T cell responses over median showed tumor biomarker response 16 Strength of T cell response to ELI-002 is strongly correlated to tumor biomarker response 100% of the above median T cell group respond to ELI-002; in the below median group 67% (8/12) respond to ELI-002 All (100%) of the observed tumor biomarker clearances (6/6) are in the above median T cell group Statistically significant, p-value per Mann Whitney Test (P < 0.0014) Data cutoff 6-Sept-23 P = 0.0014 ≥ Median < Median mKRAS T Cell Response Tumor Biomarker Response Best Overall Tumor Biomarker Response

17 Strength of T cell response to ELI-002 is correlated to tumor response and duration of ELI-002 administration Patients with both CD4 and CD8 T cell responses have favorable clinical outcomes mKRAS T Cell Response Clinical Response AMPLIFY-201: Majority of Above Median T Cell Responders Include CD4+ and CD8+ Above median mKRAS-specific T cell response correlates to improved clinical outcome Data cutoff 6-Sept-23

AMPLIFY-201: Above Median T Cell Responders Median RFS Significantly Prolonged86% reduction in the risk of progression or death in above median T cell responders 18 At a median follow up of 8.5 months, median RFS was not reached for above median T cell responders1 compared to 4.01 months among below median T cell responders (HR 0.14, 95% CI 0.03-0.63, P=0.0167) 86% Reduction in Risk of Progression or Death in T cell responders to ELI-002 Median overall survival was not reached for either group ≥ Median T Cell Response (n = 13) < Median T Cell Response (n = 12) P = 0.0167 HR: 0.14 (0.03 – 0.63) Median RFS: not reached Median RFS: 4.01 months 1 Above median T cell responder: T cell response ≥ median increase of 12.75 Database cutoff 6-Sept-23 mKRAS T Cell Response Clinical Response Relapse-free Survival

AMPLIFY-201: Safety & TolerabilityELI-002 was well tolerated at all dose levels, with no DLTs or SAEs 19 No Grade 3/4 TEAEs, no CRS, no DLTs at time of data cutoff (6-Sept-2023) 11/25 (44%) had Grade 1 or 2 AEs 3/25 (12%) had injection site reactions 10 mg dose selected as RP2D for Phase 1/2 AMPLIFY-7P study TEAE: Treatment Emergent Adverse Event | CRS: Cytokine release syndrome | DLT: Dose-limiting toxicity | SAE: Serious adverse event | RP2D: Recommended Phase 2 Dose Cohort 1 (0.1 mg) n = 3 Cohort 2 (0.5 mg) n = 6 Cohort 3 (2.5 mg) n = 5 Cohort 4 (5.0 mg) n = 5 Cohort 5 (10.0 mg) n = 6 Overall n = 25 Adverse Event Terma Patients with Any Related TEAE, n (%) 1 (33.3) 3 (50.0) 2 (40.0) 2 (40.0) 4 (66.7) 12 (48.0) Fatigue 0 2 (33.3) 2 (40.0) 1 (20.0) 1 (16.7) 6 (24.0) Injection site reaction* 1 (33.3) 1 (16.7) 0 2 (40.0) 0 4 (16.0) Myalgia 0 0 0 1 (20.0) 2 (33.3) 3 (12.0) Anemia 1 (33.3) 0 1 (20.0) 0 0 2 (8.0) Headache 1 (33.3) 1 (16.7) 0 0 0 2 (8.0) Hot flush 0 1 (16.7) 0 0 1 (16.7) 2 (8.0) Nasal congestion 0 1 (16.7) 0 1 (20.0) 0 2 (8.0) Nausea 1 (33.3) 0 0 1 (20.0) 0 2 (8.0) TEAE: Treatment Emergent Adverse Events with incidence ≥ 5%; data cutoff 6-Sept-2023 a Preferred terms per the Medical Dictionary for Regulatory Activities, version 25.0 *Injection Site Reaction = Injection Site Erythema, Injection Site Induration, Injection Site Swelling, Contusion, Pruritis ELI-002 Safety / Tolerability

AMPLIFY-201: T Cell Tumor InfiltrationPreliminary clinical evidence shows dense T cell tumor infiltration following ELI-002 therapy 20 72 T cells/hpf at time of progression,29x the expected 2-3 T cells / hpf in PDAC 1 T cell tumor infiltration was associated with complete ctDNA clearance in this patient T cell tumor infiltration has been associatedwith increased survival in pancreatic cancer 2 Tumor Biopsy CD3 Immunohistochemistry: T Cell Receptor (brown)Pancreatic tumor, 2.5 mg dose level 1 Ademmer 1988 Clin Exp Immunol 112:21 2 Ino, Y., Yamazaki-Itoh, R., Shimada, K. et al. Immune cell infiltration as an indicator of the immune microenvironment of pancreatic cancer. Br J Cancer 108, 914–923 (2013). https://doi.org/10.1038/bjc.2013.32 Hpf: High-powered field T Cell Tumor Infiltration Tumor Biopsy: CD3 Immunohistochemistry

AMPLIFY-201: Clinical Data SummaryELI-002 monotherapy generates robust immune response that correlates with clinical benefit 21 Well Tolerated No Dose Limiting Toxicity No Grade 3/4 TEAEs, no CRS, No DLTs; 11/25 (44%) had Grade 1 or 2 AEs Promising Preliminary Data Significant reduction in risk of progression or death with large T cell response Tumor biomarker reductions, clearance across different tumor types and KRAS mutations T cell response strongly correlates with tumor biomarker reduction/clearance and relapse free survival benefit Robust mKRAS T Cell Responses T cell response and tumor infiltration observed in AMPLIFY-201 historically associated with survival in PDAC Able to generate KRAS-specific CD4+ and CD8+ response in majority of patients with large T cell response Among evaluable patients 100% of patients maintained elevated KRAS-specific T cell response post-boost 90% of patients developed T cell responses to two or more KRAS antigens RP2D Selected AMPLIFY-7P IDMC has recommended the phase 2 dose of ELI-002 7P Randomized PDAC Phase 2 next portion of study to open (Q1 2024)

ELI-002 Differentiation*Distinct clinical and operational advantages over comparable cancer vaccines 22 ELI-002 SLATE-KRAS - - GRANITE - - - ** - Autogene-cevumeran - - ** - mRNA-4157 - - ** - Enhanced immune responses, no spleen requirement Broadest coverage vs driver mutations, limits resistance Fast, predictable, lower cost, no manufacturing risk *** Immunogenicity against tumor neoantigens Activates immune system while still strong 4 7 Anti-Tumor Immune Responses Clinical ProgramsIn Early Disease Lymph Node Engagement Exclusively Targeting KRAS Mutations “Off-the-Shelf” Shared KRAS Neoantigen Vaccines Personalized Neoantigen Vaccines * Based on publicly available information** Personalized neoantigen vaccines encode for multiple neoantigens which may or may not include KRAS neoantigens, but do not exclusively target KRAS driver mutations *** No risk associated with ‘just-in-time’ manufacturing that impacts availability; Product candidates not evaluated in a head-to-head study; comparisons based on public information KRAS mutations targeted: Elicio 7P: G12D, G12R, G12V, G12C, G12A, G12S, G13D, SLATE: G12C, G12D, G12V, Q61H

Continuing Execution Momentum into 2024 23 AMPLIFY-201 Updated Clinical data (1Q-2024) AMPLIFY-7P PDAC Phase 2 Initiation (1Q-2024) AMPLIFY-7P Phase 1a data (1H-2024) AMPLIFY-201 Clinical Immune (1H-2024) Response follow up 2024 Anticipated Milestones 2023 Accomplishments AMPLIFY-201 Completed Phase 1a enrollment AMPLIFY-7P Initiated Phase 1a study AMPLIFY-201 Presented Preliminary Safety, Immune and Biomarker Response data from Phase 1a study (ASCO) Received second GIRF grant to fund p53/ BRAF program AMPLIFY-201 Presented T Cell response and Relapse Free Survival data (AACR Special Conference Pancreas) Presented positive preclinical data for p53 / BRAF program (SITC) Presented AMPLIFY-201 Immune Response durability data (SITC)

Targeting the Lymph Nodes to AMPlify Immunotherapy January 2024