Washington, D.C. 20549
Pursuant to Section 13 OR 15(d) of The Securities Exchange Act of 1934
Date of Report (date of earliest event reported): September 27, 2023
Elicio Therapeutics, Inc.
(Exact name of registrant as specified in its charter)
(State or other jurisdiction of incorporation or organization)
(Commission File Number)
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451 D Street, 5th Floor
Boston, Massachusetts 02210
(Address of principal executive offices, including zip code )
(857) 209-0050
Registrant's telephone number, including area code
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Common Stock, $0.01 par value per shareELTXThe Nasdaq Global Select Market
Indicate by check mark whether the registrant is an emerging growth company as defined in Rule 405 of the Securities Act of 1933 (§230.405 of this chapter) or Rule 12b-2 of the Securities Exchange Act of 1934 (§240.12b-2 of this chapter).
Emerging growth company
If an emerging growth company, indicate by check mark if the registrant has elected not to use the extended transition period for complying with any new or revised financial accounting standards provided pursuant to Section 13(a) of the Exchange Act. o

Item 8.01 Other Events.

On September 27, 2023, Elicio Therapeutics, Inc. (the “Company”) issued a press release announcing updated preliminary data including promising relapse-free survival data from the ongoing Phase 1 (AMPLIFY-201) study of its lead asset, ELI-002. A copy of the press release is attached as Exhibit 99.1 to this Current Report and is incorporated herein by reference. Attached as Exhibit 99.2 and incorporated herein by reference is an updated version of the Company’s corporate presentation, which was uploaded to the Company’s website on September 27, 2023.

Item 9.01. Financial Statements and Exhibits.

(d) Exhibits.

104Cover Page Interactive Data File (embedded within the Inline XBRL document)
Pursuant to the requirements of the Securities Exchange Act of 1934, as amended, the Registrant has duly caused this report to be signed on its behalf by the undersigned hereunto duly authorized.
Elicio Therapeutics, Inc.
Date: September 27, 2023
Robert Connelly
President and Chief Executive Officer
(Principal Executive Officer)


Elicio Therapeutics Presents Updated Preliminary Data Including Promising Relapse-Free Survival Data from the Phase 1 Study of ELI-002 at AACR Special Conference: Pancreatic Cancer

ELI-002 2P is an investigational therapeutic cancer vaccine targeting solid tumors driven by G12D and G12R mutations in KRAS
As of the April 25, 2023 data cut-off date, among the 22 evaluable patients, preliminary data from the trial suggest that those with greater than median T cell response had not reached median Relapse-Free Survival compared to median RFS of 3.91 months for patients with less than median T cell response
Updated data demonstrated 86% reduction in risk of progression or death in patients with large T cell responses induced by ELI-002 2P in the phase 1 study
Elicio plans to initiate a randomized phase 2 study early in 2024 for ELI-002 7P

BOSTON, September 27, 2023 -- Elicio Therapeutics, Inc. (Nasdaq: ELTX, “Elicio Therapeutics” or “Elicio”), a clinical-stage biotechnology company developing a pipeline of novel immunotherapies for the treatment of cancer, today announced promising preliminary relapse-free survival (RFS) data from the ongoing Phase 1 (AMPLIFY-201) study of its lead asset, ELI-002. This study evaluated ELI-002 2P, a 2-peptide formulation designed to treat cancers driven by G12D and G12R mutations in KRAS, as a monotherapy in patients with mutant KRAS-driven solid tumors. The data will be presented September 29th from 4:40pm – 6:40pm ET at the AACR Special Conference on Pancreatic Cancer in Boston, Massachusetts, taking place from September 27-30, 2023.
“Patients with mutant KRAS cancers, particularly pancreatic and colorectal cancers, have a poor prognosis with limited treatment options when tumor DNA or protein biomarkers are detected after standard surgery and chemotherapy. We are encouraged by the early data showing ELI-002 induced T cells can positively impact clinical endpoints including the risk of relapse and death in this study,” said Eileen M. O’Reilly, M.D., Winthrop Rockefeller Endowed Chair of Medical Oncology; Co-Director, Medical Initiatives, David M. Rubenstein Center for Pancreatic Cancer Research; Section Head, Hepatopancreaticobilary & Neuroendocrine Cancers, Memorial Sloan Kettering Cancer Center (MSK).
Christopher Haqq, M.D., Ph.D., Elicio’s Executive Vice President, Head of Research and Development, and Chief Medical Officer, added, “These data provide further support for ELI-002’s mechanism of action and the potential benefit of a lymph node-targeted cancer vaccine. With the data presented here and the data previously reported at ASCO 2023, we have shown ELI-002’s induction of a potent mKRAS-specific T cell response, including both CD4 and CD8 populations, correlated with tumor biomarker responses, which the data suggest may lead to improved clinical outcomes. We are encouraged by these early observations and look forward to continuing to follow and report additional clinical and biomarker data on the AMPLIFY-201 study. Additionally, the AMPLIFY-7P study's independent data monitoring committee supported initiation of a randomized phase 2 trial studying ELI-002 7P as a monotherapy in adjuvant PDAC patients.”

Presentation Summary:
Title: T cell responses and clinical outcomes in pancreatic and colorectal cancer patients with Minimal Residual Disease in AMPLIFY-201, a phase 1 trial of a first-in-class amphiphile lymph node targeted mutant KRAS vaccine
Session: Poster Session C
Presenter: Eileen O’Reilly, M.D., Winthrop Rockefeller Endowed Chair of Medical Oncology; Co-Director, Medical Initiatives, David M. Rubenstein Center for Pancreatic Cancer Research; Section Head, Hepatopancreaticobilary & Neuroendocrine Cancers, Memorial Sloan Kettering Cancer Center (MSK)

Study Design
AMPLIFY-201 is a multicenter Phase 1 trial assessing the safety, immunogenicity and antitumor activity of ELI-002 in patients with mutant KRAS-driven tumors who are at high risk for relapse due to detection of MRD following standard surgery and chemotherapy.
The analysis involved patients with resected PDAC (n=20) or CRC (n=5) tumors harboring KRAS G12D or G12R who had MRD defined as elevated ctDNA and/or serum tumor biomarker (CA19-9/CEA).
Patients received up to six priming doses and four booster doses separated by a 3-month rest period of subcutaneous ELI-002 2P vaccine monotherapy comprised of Amph-peptides (700 mcg each G12D/G12R), admixed with Amph-CpG-7909 at 0.1, 0.5, 2.5, 5.0 and 10.0 mg per cohort dose level.
Primary endpoints included safety and the recommended Phase 2 dose (RP2D) of Amph-CPG-7909, and the secondary endpoint included biomarker reduction/clearance.
Exploratory endpoints included RFS using immune Response Evaluation Criteria in Solid Tumors (iRECIST) and immunogenicity assessed by direct ex vivo Fluorospot and intracellular cytokine staining of peripheral blood mononuclear cells.

Preliminary Study Findings
Direct ex vivo polyfunctional mKRAS-specific T cell responses to ELI-002 2P were observed in 20/23 (87%; 50% induced both CD4+ and CD8+ T cells, median 13-fold and mean 56-fold increase from baseline), with T cell response in 9/9 (100%) patients treated at the highest two dose levels including the 10 mg RP2D.
The median RFS in evaluable pts (n=22) was 16.3 months, and the median OS has not been reached.
Tumor biomarker response was observed in 17/22 (77%), with clearance in 6/22 (27%).
Clinical efficacy correlated with T cell response:
Median tumor biomarker reduction/clearance was -86.9% vs -1.0% in above vs below median T cell responders, respectively (p < 0.0017).
At 7.6 months median follow-up, the median RFS was not reached compared to 3.9 months in above versus below median T cell responders (HR 0.14; 95% CI 0.03-0.61; p = 0.013).
The association of RFS with T cell response was not confounded by other baseline prognostic variables (including tumor stage, recovery from prior cytotoxic therapy as assessed by absolute neutrophil count or immune system subsets such as %CD4+ or %CD8+ of CD3+ lymphocytes).
No safety concerns were identified, and there were no dose limiting toxicities and no ≥ Grade 3 treatment related adverse events.

About ELI-002
ELI-002 is a structurally novel investigational AMP therapeutic immunotherapy targeting mutant KRAS-driven cancers. KRAS mutations are among the most prevalent human cancers. The seven KRAS driver mutations targeted by the ELI-002 7P formulation are present in 25% of all solid tumors. In particular, 93% of pancreatic ductal adenocarcinoma and 52% of colorectal cancers, those most prevalent in the AMPLIFY-201 study, are positive for KRAS mutations. In addition, 27% of non-small cell lung cancers are positive for KRAS mutations. ELI-002 is comprised of AMP-modified mutant KRAS peptide antigens and ELI-004, an AMP-modified immune-stimulatory oligonucleotide CpG adjuvant. The AMP mKRAS peptides and AMP CpG are targeted to the lymph node where they can potentially enhance the action of key immune cells.
ELI-002 2P is currently being studied in a Phase 1 trial (AMPLIFY-201) in patients with high relapse risk mKRAS-driven solid tumors, following surgery and chemotherapy (NCT04853017). ELI-002 7P, is currently being studied in AMPLIFY-7P, a Phase 1/2 trial in patients with high relapse risk mKRAS-driven solid tumors (NCT05726864). The ELI-002 7P formulation is designed to provide immune response coverage against seven of the most common KRAS mutations, thereby increasing the potential patient population for ELI-002 and potentially reducing the chance of bypass resistance mechanisms.

About the Amphiphile Platform
Our proprietary Amphiphile, or AMP, platform delivers investigational immunotherapeutics directly to the “brain center” of the immune system – the lymph nodes. We believe this site-specific delivery of disease-specific antigens, adjuvants and other immunomodulators may efficiently educate, activate and amplify critical immune cells, potentially resulting in induction and persistence of potent adaptive immunity required to treat many diseases. In preclinical models, we have observed lymph node-specific engagement driving therapeutic immune responses of increased magnitude, function and durability. We believe our AMP lymph node-targeted approach will produce superior clinical benefits compared to immunotherapies that do not engage the lymph nodes based upon preclinical studies.
Our AMP platform, originally developed at the Massachusetts Institute of Technology has broad potential in the cancer space to advance a number of development initiatives through internal activities, in-licensing arrangements or development collaborations and partnerships.
The Amphiphile platform has been shown to deliver immunotherapeutics directly to the lymph nodes by latching on to the protein albumin, found in the bloodstream, as it travels to
lymphatic tissue. In preclinical models, we have observed lymph node-specific engagement driving immune responses of increased magnitude, function and durability.

About Elicio Therapeutics
Elicio Therapeutics is a clinical-stage biotechnology company developing a pipeline of novel immunotherapies for the treatment of cancer. By combining expertise in immunology and immunotherapy, Elicio is engineering investigational Amphiphile (AMP) immunotherapies intended to precisely target and fully engage the lymph nodes, the site in our bodies where the immune response is orchestrated. Elicio is engineering lymph node-targeted AMPlifiers, immunomodulators, adjuvants and vaccines for an array of aggressive cancers.

Cautionary Note on Forward-Looking Statements
Certain statements contained in this communication regarding matters that are not historical facts, are forward-looking statements within the meaning of Section 21E of the Securities Exchange Act of 1934, as amended, and the Private Securities Litigation Reform Act of 1995, known as the PSLRA. These include statements regarding Elicio’s planned clinical programs, including planned clinical trials, the potential of Elicio’s product candidates, the expected participation and presentation at upcoming conferences, and other statements regarding management’s intentions, plans, beliefs, expectations or forecasts for the future, and, therefore, you are cautioned not to place undue reliance on them. No forward-looking statement can be guaranteed, and actual results may differ materially from those projected. Elicio undertakes no obligation to publicly update any forward-looking statement, whether as a result of new information, future events or otherwise, except to the extent required by law. We use words such as “anticipates,” “believes,” “plans,” “expects,” “projects,” “future,” “intends,” “may,” “will,” “should,” “could,” “estimates,” “predicts,” “potential,” “continue,” “guidance,” and similar expressions to identify these forward-looking statements that are intended to be covered by the safe-harbor provisions of the PSLRA. Such forward-looking statements are based on our expectations and involve risks and uncertainties; consequently, actual results may differ materially from those expressed or implied in the statements due to a number of factors, including, but not limited to, Elicio’s plans to develop and commercialize its product candidates, including ELI-002; the timing of the availability of data from Elicio’s clinical trials; Elicio’s plans to initiate a randomized phase 2 trial studying ELI-002 7P as a monotherapy in adjuvant PDAC patients early in 2024; Elicio’s plans to research, develop and commercialize its current and future product candidates; Elicio’s ability to enter into new collaborations, in-licensing arrangements or partnerships, and to fulfill its obligations under any such agreements; the clinical utility, potential benefits and market acceptance of Elicio’s product candidates; Elicio’s commercialization, marketing and manufacturing capabilities and strategy; Elicio’s ability to identify additional products or product candidates with significant commercial potential; and developments and projections relating to Elicio’s competitors and our industry.

New factors emerge from time to time, and it is not possible for us to predict all such factors, nor can we assess the impact of each such factor on the business or the extent to which any factor, or combination of factors, may cause actual results to differ materially from those contained in any forward-looking statements. These risks are more fully discussed in the
current report on Form 8-K that was filed with the SEC on June 2, 2023 and Elicio’s periodic reports and other documents filed from time to time with the SEC. Forward-looking statements included in this release are based on information available to Elicio as of the date of this release. Elicio does not undertake any obligation to update such forward-looking statements to reflect events or circumstances after the date of this release, except to the extent required by law.

Media Contact
Gloria Gasaatura
LifeSci Communications

Investor Relations Contact
Heather DiVecchia
Elicio Therapeutics

Targeting the Lymph Nodes to AMP-lify Immunotherapy September 2023 1

Disclaimers 2 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 conflict in Ukraine; 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. Prospective investors 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, including without limitation the Company's Current Report on Form 8-K filed on June 2, 2023, and the Company's other filings from time to time with the SEC.

Company Highlights 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 mKRAS 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 PROMISING INITIAL PHASE 1a CLINICAL DATA • 87% of patients showed T cell responses with an average 56x increase in T cell numbers • 77% of patients showed a decline in tumor biomarker including 27% of patients having complete clearance of ctDNA • 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 3 Clinical-stage biotech pioneering novel lymph node targeted cancer immunotherapies KRAS: Kirsten Rat Sarcoma | PDAC: Pancreatic Ductal Adenocarcinoma | RP2D: Recommended Phase 2 Dose

CANDIDATE TARGET INDICATIONS PRECLINICAL PHASE 1 PHASE 2 PHASE 3 ELI-002 * mKRAS PDAC, CRC, NSCLC ELI-007 mBRAF GI tumors ELI-008 mTP53 GI tumors Pipeline 4 Innovative pipeline of cancer immunotherapies addressing critical unmet needs * Ph1/2 combination study with CPI in planning stages CRC: colorectal carcinoma | NSCLC: non-small cell lung carcinoma| CPI: Checkpoint inhibitor | mBRAF: mutant homolog B of the Rapidly Accelerated Fibrosarcoma | mTP53: mutant tumor protein p53 PDAC PlannedOngoing

5 Elicio: Amplifying Immunotherapy

The AMP Platform • 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 6 Harnessing the untapped potential of the lymph nodes for immunotherapy Blood Lymph Small Molecules Large Molecules (e.g. Albumin) Blood Vessel Lymph Vessel Lymph Nodes Blood Circulation Tissue Injection Site

Mechanism of Action 7 AMP immunotherapy generates an anti-tumor immune response via the lymph nodes Tumor Eradication 5Subcutaneous injection 1 Lymph Node Lymph node targeting 3 Antigen Presenting Cell Delivery to immune cells 4 Albumin-bound Amphiphiles T CellAlbumin-bound Amphiphiles Endogenous AlbuminAmphiphiles Tissue Injection Site Albumin binding 2 Tumor

10 15 20 25 30 35 0 20 40 60 80 100 Days Tu m or S ize (m m 2 ) 0 20 40 60 80 100 % T um or S pe ci fic a m on g CD 8+ T C el ls CD8+ T Cell Response AMP Anti-Tumor Activity 8 Several studies demonstrate amplifying T cells in lymph nodes enhances cancer immunotherapy CR: 8/10 CR: 2/10 CR: 0/10 Tumor Size Survival In mice, AMP leads to greatly increased T cell response Leading to greater and more durable tumor reduction With tumor eradication in 80% of AMP-treated animals Source: Elicio data on file. Study used HPV-driven tumors and HPV E7 protein antigen to validate anti-cancer immunotherapeutic potential of AMP platform Antigen + AMP-CpGAntigen + Soluble CpGMock 0 20 40 60 0 20 40 60 80 100 Days % S ur vi va l Mock SOL AMP

The mKRAS Opportunity 9 ELI-002 targets the 7 most common KRAS mutations driving 25% of solid tumors ELI-002 addressable Incidence: ~128k Other KRAS mutations 88% Pancreatic Ductal Adenocarcinoma Other KRAS mutations ~88% Colorectal Cancer ~88% Non-Small Cell Lung Cancer ~88% Other mKRAS Opportunities 36% Other KRAS mutations 25% 17% 3-11% Biliary Tract Cancer Total incidence: ~40k Ovarian Cancer Total incidence: ~62k 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 + gallbladder Sources 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 No KRAS mutation ELI-002 addressable Incidence: ~192k No KRAS mutation ELI-002 addressable Incidence: ~128k No KRAS mutation

mKRAS Differentiation 10 Early mKRAS-targeting efforts in the clinic, while promising, leave significant white space 7 key mutations Reduced risk of resistance mechanisms Potent activation of immune mechanisms Expansion/activation of 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 Targeting Mutant KRAS Small Molecules Indirectly Inhibiting Mutant KRAS Small Molecules Directly Inhibiting Mutant KRAS

ELI-002 Composition 11 Lymph node targeted therapeutic vaccine comprised of AMP-peptides and AMP-CpG ELI-002 Albumin Binding Lipid for Lymph Node Targeting CpG DNA: TLR-9 Agonist X X Albumin Binding Lipid for Lymph Node Targeting mKRAS PeptidePEG Linker • 2 or 7 AMP-peptides • CD8 and CD4 epitopes • Potent TLR-9 immune activator AMP-mKRAS Peptide Antigen AMP-CpG Adjuvant G12X G13X D R V C S A D NH NH O O

Preclinical Validation of ELI-002 12 ELI-002 enhances in vivo measures of immune responses across a range of KRAS mutations Robust activity against 7 most common KRAS mutations Spleen T Cell Response Stimulation G12D G12V G12S G12A G12C G12R G13D Vehicle Adjuvant Only ELI-002 -20 0 20 40 60 80 % S pe ci fic K ill in g In V iv o Spleen T Cell Target Killing: G12D Mock SOL AMP Increased T cell activation | Enhanced cytokine production | Enhanced T cell proliferation | Improved cytotoxic function

13 ELI-002: Lymph node targeted mKRAS immunotherapy

ELI-002 At-a-Glance 14 mKRAS immunotherapy eliciting strong T cell activity leveraging the AMP platform’s lymph node targeting design 2 PEPTIDE (2P) AND 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 AND OPERATIONAL ADVANTAGES • Vs comparable vaccines including targeting driver mutations and “off-the-shelf” 2P contains: G12D, G12R, 7P contains: G12D, G12R, G12V, G12C, G12S, G12A, G13D

AMPLIFY-201 Study Overview Elicio Non-Confidential 15 Phase 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 20-Months Follow-up Boost (4 doses over 4 weeks) Prime (6 doses over 8 weeks) Local Therapy (e.g., Surgery, Chemo) C L I N I C A L P R O G R A M O V E R V I E W : N C T 0 4 8 5 3 0 1 7 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-month 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

P P P P P P P C P P P P P C P P C P C P C PTumor Type D D D D D D D D R D D D D D R R D D D R D DmKRAS Biomarker -100 -75 -50 -25 0 25 50 75 100 28 0 90 38 22 -2 8 -3 0 -4 1 -4 4 -4 7 -7 4 -1 00 -1 00 -1 00 -1 00 -1 00 -1 00 Be st O ve ra ll Bi om ar ke r R es po ns e (% o f Ba se lin e) -9 -1 1-20 -1 8 -2 AMPLIFY-201 Biomarker Responses 16 Robust responses observed across tumor types and KRAS mutations with ELI-002 monotherapy • 27% of patients (6/22) showed complete clearance of ctDNA • Most patients (77%, 17/22) showed decline from baseline in ctDNA or CEA/CA19-9 levels • 45% (10/22) showed a >40% reduction in biomarker levels • Waterfall displays best response of ctDNA or serum tumor biomarker AMPLIFY-201 Waterfall Plot: Biomarker Reduction/Clearance One patient was not evaluable for biomarker response at database cutoff * Patients biopsied, both exhibited T cell infiltration and continued study treatment Data cutoff 25-Apr-23 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 D G12D R G12RP PDAC C CRC ctDNA CEA/CA19-9 **

Baseline Max response 0 5 10 20 30 40 50 450 Fo ld c ha ng e fr om b as el in e 2 AMPLIFY-201 T Cell Responses 17 Vast majority of patients showed robust T cell response across dose cohorts Direct Ex Vivo Immune Response AMP-CpG Dose Level ex vivo T cell response (n, %) Average fold-change 0.1 mg 2/3 (67%) 30 0.5 mg 5/6 (83%) 82 2.5 mg 4/5 (80%) 113 5.0 mg 5/5 (100%) 19 10.0 mg 4/4 (100%) 26 Total 20/23 (87%) 56 Response per Dose Level • 87% of patients showed T cell responses • 100% in two highest dose cohorts, including at the RP2D (10 mg) • 56x average fold-change in T cell numbers from baseline (median 13x; range 2-423x) • T cells detectable by standard direct ex vivo FluoroSpot and flow cytometry, with no expansion required AMPLIFY-201 T Cell Fold-Changes by Dose Level Responses shown are best overall responses vs baseline for each patient at any timepoint during the assessment period. Data cutoff 25-Apr-23 Median = 13x

≥Median <Median -100 0 100 200 300 T Cell Response (Fold change from baseline) Be st O ve ra ll Bi om ar ke r R es po ns e (% o f Ba se lin e) ✱✱P = 0.0017 AMPLIFY-201 T Cell Fold-Change Predicts Tumor Biomarker Response 18 All patients with T cell responses over median showed tumor biomarker response ≥ edian < Median • 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 50% 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 < 0.0017) Best Overall Biomarker Response Clearance Reduction Non-Responder

0 3 6 9 12 15 18 0 25 50 75 100 Months Re la ps e- fr ee S ur vi va l ( % ) At risk ≥ Median 12 8 4 1 0 0 0 < Median 10 5 1 1 1 1 0 ≥ Median T Cell Response (n = 12) < Median T Cell Response (n = 10) P = 0.0134 HR: 0.1376 (0.03106 – 0.6096) Median RFS: not reached Median RFS: 3.91 months AMPLIFY-201: Median Relapse-Free Survival of Above Median T Cell Responders was Significantly Prolonged 86% reduction in the risk of progression or death in above median T cell responders • At a median follow up of 7.6 months, median RFS was not reached for above median T cell responders1 compared to 3.91 months among below median T cell responders (HR 0.14, 95% CI 0.031-0.61, P=0.0134) • 86% Reduction in Risk of Progression or Death in T cell responders to ELI-002 • Median overall survival was not reached for either group 1 Above median T cell responder: T cell response ≥ median increase of 13x (database cutoff 25-Apr-23) 19

ctDNA CA19-9 / CEA D G12D R G12R P PDAC C CRC Co ho rt T Cells ≥ Median < Median CD4 CD8 x no ICS Biomarker Non-responder Biomarker Reduction Biomarker Clearance Prime Immunization Complete Boost Immunization Complete Subsequent Therapy iCPD RFS Censor Date + Death On Treatment Ongoing Follow-up 0 8 16 24 32 40 48 56 64 72 80 002-001-111-013 002-001-102-003 002-001-109-002 002-001-101-003 002-001-102-026 002-001-102-027 002-001-106-016 002-001-111-014 002-001-102-013 002-001-113-001 002-001-113-004 002-001-111-018 002-001-102-025 002-001-102-024 002-001-102-022 002-001-110-009 002-001-102-023 002-001-111-017 002-001-106-010 002-001-106-009 002-001-102-018 002-001-106-002 Weeks on Study 326496128160 4 2 7 3 14 1 5 10 17 13 9 21 22 8 6 12 15 11 19 20 18 16 Weeks After Surgery x x x C P P C P P P P P P C P C P P P P P P C P P D D R D D R D D R D D D D D D D D R D D D D 1 2 3 2 4 4 4 3 5 5 4 2 1 2 3 3 4 5 3 2 1 2 AMPLIFY-201 Swimmer’s Plot and ELI-002 Induced T Cells 20 Above median mKRAS-specific T cell response correlates to improved clinical outcome • 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 Data cutoff 25-Apr-23

AMPLIFY-201 T Cell Tumor Infiltration 21 Preliminary clinical evidence shows dense T cell tumor infiltration following ELI-002 therapy • 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 associated with 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). Hpf: High-powered field

AMPLIFY-201 Safety & Tolerability 22 ELI-002 was well tolerated at all dose levels, with no DLTs or SAEs 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 Term Patients with Any Related TEAE, n (%) 1 (33.3) 3 (50.0) 2 (40.0) 3 (60.0) 2 (33.3) 11 (44.0) Injection site reaction 0 1 (16.7) 1 (20.0) 1 (20.0) 0 3 (12.0) Fatigue 0 1 (16.7) 2 (40.0) 0 1 (16.7) 4 (16.0) Headache 1 (33.3) 1 (16.7) 0 0 1 (16.7) 4 (16.0) Asthma 0 0 0 0 1 (16.7) 1 (4.0) Dyspnea 0 0 0 0 1 (16.7) 1 (4.0) Nausea 1 (33.3) 0 0 1 (20.0) 0 2 (8.0) Diarrhea 0 0 0 0 1 (16.7) 1 (4.0) Anemia 1 (33.3) 0 0 0 0 1 (4.0) Contusion 1 (33.3) 0 0 0 0 1 (4.0) Dry skin 0 1 (16.7) 0 0 0 1 (4.0) Herpes simplex reactivation 0 1 (16.7) 0 0 0 1 (4.0) Hot flush 0 1 (16.7) 0 0 1 (16.7) 2 (8.0) Myalgia 0 0 0 1 (20.0) 0 1 (4.0) Nasal congestion 0 1 (16.7) 0 1 (20.0) 0 2 (8.0) Lymphadenopathy 0 0 0 0 1 (16.7) 1 (4.0) Pruritus 0 0 0 1 (20.0) 0 1 (4.0) • No Grade 3/4 TEAEs, no CRS, no DLTs at time of data cutoff (April 25, 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

AMPLIFY-201 Results Summary 23 ELI-002 monotherapy generates clinically relevant and robust immune response WELL TOLERATED WITH 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 • ctDNA and serum tumor biomarker reductions and 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-SPECIFIC T CELL RESPONSES • T cell response and tumor infiltration observed in AMPLIFY-201 historically associated with survival in PDAC 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) TEAEs: Treatment Emergent Adverse Events | CRS: Cytokine Release Syndrome | DLTs: Dose Limiting Toxicity | AE: Adverse Events | KRAS: Kirsten Rat Sarcoma | PDAC: Pancreatic Ductal Adenocarcinoma

ELI-002 Differentiation* 24 Distinct clinical and operational advantages over comparable cancer vaccines 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 * 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 4 7 Anti-Tumor Immune Responses Clinical Programs In Early Disease Lymph Node Engagement Exclusively Targeting KRAS Mutations “Off-the-Shelf” SLATE-KRAS: Shared neoantigen vaccine vs KRAS GRANITE: Individualized neoantigen vaccine Sh ar ed K RA S N eo an tig en V ac ci ne s Pe rs on al ize d N eo an tig en V ac ci ne s

ELI-002 Anticipated Milestones 25 Milestone Timing AMPLIFY-7P Phase 1a First Patient Enrolled 2023 Apr AMPLIFY-201 Interim Analysis biomarker and safety 2023 Jun AMPLIFY-201 Interim Analysis RFS of T cell responders 2023 Sep AMPLIFY-7P Randomized Phase 2 Initiation (PDAC) 2024 Q1 AMPLIFY-7P Phase 1a data 2024 1H AMPLIFY-201 Clinical outcomes 2024 1H