ANGN Angion Biomedica Corporation

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UNITED STATES

SECURITIES AND EXCHANGE COMMISSION

WASHINGTON, D.C. 20549

 FORM 8-K

CURRENT REPORT

PURSUANT TO SECTION 13 or 15(d) of the

SECURITIES EXCHANGE ACT OF 1934

Date of Report (Date of earliest event reported): June 27, 2024

 

Elicio Therapeutics, Inc.

(Exact Name of Registrant as Specified in Its Charter) 

Delaware		001-39990		11-3430072
(State or Other Jurisdiction  of Incorporation)		(Commission File Number)		(IRS Employer Identification No.)

 

451 D Street, 5th Floor

Boston Massachusetts,  02210

(Address of principal executive offices and Zip Code)

 

(857 209-0050)

(Registrant’s Telephone Number, Including Area Code)

 

Check the appropriate box below if the Form 8-K filing is intended to simultaneously satisfy the filing obligation of the registrant under any of the following provisions (see General Instruction A.2 below):

 

☐	Written communications pursuant to Rule 425 under the Securities Act (17 CFR 230.425)
☐	Soliciting material pursuant to Rule 14a-12 under the Exchange Act (17 CFR 240.14a-12)
☐	Pre-commencement communications pursuant to Rule 14d-2(b) under the Exchange Act (17 CFR 240.14d-2(b))
☐	Pre-commencement communications pursuant to Rule 13e-4(c) under the Exchange Act (17 CFR 240.13e-4(c))

Securities registered pursuant to Section 12(b) of the Act:  

Title of each class		Trading Symbol(s)		Name of each exchange on which registered
Common Stock, $0.01 par value per share		ELTX		The Nasdaq Global 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. ☐

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Item 7.01. Regulation FD Disclosure.

 

On June 27, 2024, Elicio Therapeutics, Inc. (the “Company”) issued a press release announcing preliminary disease-free survival analysis from its ongoing AMPLIFY-7P Phase 1a study of its investigational therapeutic cancer vaccine candidate, ELI-002 7P, in patients with mutated Kirsten rat sarcoma viral oncogene homolog (“mKRAS”)-driven solid tumors.

 

A copy of the press release is furnished as Exhibit 99.1 to this Current Report on Form 8-K and is incorporated by reference herein. A copy of an updated version of the Company’s corporate presentation, which was uploaded to the Company’s website on June 27, 2024, is furnished as Exhibit 99.2 to this Current Report on Form 8-K and is incorporated by reference herein. The exhibits furnished under Item 7.01 of this Current Report on Form 8-K shall not be deemed to be “filed” for purposes of Section 18 of the Exchange Act, or otherwise subject to the liabilities of that section, nor shall they be deemed incorporated by reference in any filing under the Exchange Act or the Securities Act, regardless of any general incorporation language in such filing.

 

Item 8.01. Other Events.

 

On June 27, 2024, the Company announced preliminary disease-free survival analysis from its ongoing AMPLIFY-7P Phase 1a study of ELI-002 7P. The Company’s AMPLIFY-7P Phase 1/2 trial is assessing the safety and efficacy of the 7-peptide version of ELI-002 as adjuvant monotherapy treatment in patients with solid tumors carrying mKRAS. In April 2023, the Company initiated dosing of the Phase 1a portion of the trial enrolling 14 patients through October 2023, who are continuing to be evaluated for safety and efficacy of two ELI-002 AMP-peptide total dose levels (1.4 mg and 4.9 mg) in combination with the 10.0 mg Phase 2 dose of Amph-CpG-7909. The June 2024 preliminary data, which were based upon a May 24, 2024 data cutoff date (14 patients), showed patients receiving ELI-002 7P at the Phase 2 dose of 4.9 mg AMP-peptide (n=8) were yet to reach the median disease-free survival (“DFS”) endpoint. The median follow-up for the DFS endpoint was 29.1 weeks. Further, median DFS has not been reached in patients receiving the 4.9 mg AMP-peptide dose (n=8) in comparison to 12.6 weeks for patients receiving the 1.4 mg AMP-peptide dose (n=6). Patients achieving a reduction in their tumor biomarker levels had no progression events while a median DFS of 11.0 weeks was seen for patients whose tumor biomarker did not respond to ELI-002 7P. Patients with an above median T cell response to ELI-002 7P have had no progression events as of the data cutoff date.

 

Item 9.01. Financial Statements and Exhibits.

 

(d) Exhibits. The following exhibits are being furnished herewith: 

Exhibit Number		Exhibit Title or Description
99.1		Press Release, dated June 27, 2024
99.2		Corporate presentation dated June 27, 2024
104		Cover Page Interactive Data File (embedded within the Inline XBRL document)

 

SIGNATURE

 

Pursuant to the requirements of the Securities Exchange Act of 1934, the registrant has duly caused this report to be signed on its behalf by the undersigned hereunto duly authorized.

 

		Elicio Therapeutics, Inc.
Date:	June 27, 2024	By:	/s/ Robert Connelly
		Name:	Robert Connelly
		Title:	President and Chief Executive Officer  (Principal Executive Officer)

 

Exhibit 99.1

 

Elicio Therapeutics Announces Preliminary Disease-Free Survival

analysis from the Ongoing AMPLIFY-7P Phase 1a Study of ELI-002 7P

 

ELI-002 7P administered as a monotherapy at the Phase 2 dose shows

preliminary encouraging Disease-Free Survival data in pancreatic ductal adenocarcinoma

 

BOSTON, June 27, 2024 – 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 new preliminary data from the ongoing AMPLIFY-7P Phase 1a study of its off-the-shelf investigational therapeutic cancer vaccine candidate, ELI-002 7P. The preliminary data showed patients receiving ELI-002 7P at the Phase 2 dose of 4.9mg AMP-peptide were yet to reach the median disease-free survival (“DFS”) endpoint as of the May 24, 2024 data cutoff date.

 

The AMPLIFY-7P study is evaluating the 7-peptide formulation, ELI-002 7P, in patients with mKRAS-driven solid tumors following standard locoregional treatment. Data were based on the May 24, 2024 data cutoff date of 14 patients with minimal residual disease who enrolled in the Phase 1 cohort of the AMPLIFY-7P study, with a median follow up for the DFS endpoint of 29.1 weeks:

 

●

The median DFS has not yet been reached (n=14).

●

The median disease-free survival (“mDFS”) has not been reached in patients receiving the 4.9mg AMP-peptide dose (n=8) vs. 12.6 weeks for patients receiving the 1.4mg AMP-peptide dose (n=6).

●

Patients achieving a reduction in their tumor biomarker levels had no progression events vs. mDFS of 11.0 weeks for patients whose tumor biomarker did not respond to ELI-002 7P.

●

Patients with an above median T cell response to ELI-002 have had no progression events.

 

Christopher Haqq, M.D., Ph.D., Elicio’s Executive Vice President, Head of Research and Development, and Chief Medical Officer, added, “We are encouraged to see patients who received the 7-peptide version of ELI-002 at the Phase 2 dose continuing to do well at this early timepoint of the Phase 1 trial. Furthermore, the DFS data from the entire 14-patient cohort correlate strong T cell response after receiving ELI-002 with reductions in their tumor biomarker levels and reduced risk of progression or death. These findings replicate the results in the AMPLIFY-2P trial of similar patients published in Nature Medicine. We look forward to providing additional clinical data updates from the AMPLIFY Phase 1 trials expected later in 2024 and the randomized Phase 2 interim analysis expected in first quarter of 2025.”

 

About ELI-002 
Our lead product candidate, ELI-002, is a structurally novel investigational Amphiphile (“AMP”) cancer vaccine that targets cancers that are driven by mutations in the mKRAS-gene—a prevalent driver of many human cancers. ELI-002 is comprised of two powerful components that are built with our AMP technology consisting of AMP-modified mutant KRAS peptide antigens and an AMP-modified CpG adjuvant that is available as an off-the-shelf subcutaneous administration. 

 

ELI-002 2P (2 peptide formulation) is currently being studied in an ongoing Phase 1 (AMPLIFY-201) trial in patients with high relapse risk mKRAS-driven solid tumors, following surgery and chemotherapy (NCT04853017). ELI-002 7P (7 peptide formulation) is currently being studied in a Phase 1/2 (AMPLIFY-7P) trial in patients with mKRAS-driven pancreatic cancer (NCT05726864). The ELI-002 7P formulation is designed to provide immune response coverage against seven of the most common KRAS mutations present in 25% of all solid tumors, thereby increasing the potential patient population for ELI-002.

 

About Elicio Therapeutics 
Elicio Therapeutics, Inc. (Nasdaq: ELTX) is a clinical-stage biotechnology company advancing a pipeline of novel lymph node-targeted immunotherapies for the treatment of some of the most aggressive cancers. By combining expertise in immunology and immunotherapy, Elicio is harnessing the natural power of the immune system with the AMP technology, which allows for therapeutic payloads to be delivered directly to the lymph nodes, with the goal of enhancing the immune system’s cancer-fighting capabilities. By targeting cancer immunotherapies to the core of the immune response, AMP aims to optimize the lymph nodes’ natural ability to educate, activate and amplify cancer-specific T cells, which are essential for recognizing and eliminating tumor cells. Engineered to synchronize immunity in these highly potent sites, AMP is built to enhance the magnitude, potency, quality and durability of the immune response to drive antitumor activity. The Company’s R&D pipeline includes off-the-shelf therapeutic cancer vaccines ELI-002, (targeting mKRAS-driven cancers) as well as ELI-007 and ELI-008 (targeting BRAF-driven cancers and p53 hotspot mutations, respectively). For more information, please visit www.elicio.com. 

 

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, 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 initiation of Elicio’s planned clinical trials; the timing of the availability of data from Elicio’s clinical trials, including additional clinical data updates from the AMPLIFY Phase 1 trials anticipated later in 2024 and the randomized Phase 2 interim analysis anticipated in the first quarter of 2025; and Elicio’s plans to research, develop and commercialize its current and future product candidates.

 

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 our Annual Report on Form 10-K filed with the SEC on March 29, 2024, as amended on April 29, 2024, under the heading “Risk Factors”, and any subsequent 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.

  

Investor Relations Contact
Brian Piekos

Elicio Therapeutics
IR@elicio.com
857-209-0153 

 

 

Exhibit 99.2

 

Targeting the Lymph Nodes to AMPlify Immunotherapy Nasdaq: ELTX June 2024

Disclaimers 2 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 th e P resentation or the accuracy or completeness or the information contained in or incorporated by reference into the Presentation. We will not have any liabili ty for any representations or warranties, express or implied, contained in, or omissions from, the Presentation. The data contained herein is derived from various internal and external sources. We do not assume any obligation to provide the recipient with access to any additional information or to update the information in the Presentation. Industry and Market Data The Presentation contains certain market data and other statistical information such as the size, growth and share of the ind ust ries and the market segments we operate in, which are based on information from independent industry organizations and other third - party sources, industry publications, surveys and forecasts. Such data may include projections based upon a number of assumptions. Neither we nor any third parties that provide information to us guarantee the accuracy, completeness, timeliness or availability of any information. We are not responsible for any errors or omissions (negligent or otherwise), regardless of the cause, or the results obtained from the use of such content. We do not give any express or implied warranties, including, but not limited to, any warranties of merchantability or fitness for a particular purpose or use, and we expressly disclaim any respo nsi bility or liability for direct, indirect, incidental, exemplary, compensatory, punitive, special or consequential damages, costs, expenses, legal fees or losses (including lost income or pro fit s and opportunity costs) in connection with the use of the information herein. The industry may not grow at the rate projected by market data, or at all. Failure of our industries to g row at the projected rate may have a material adverse effect on our business and the market price of our securities. In addition, if any one or more of the assumptions underlying the market dat a a re later found to be incorrect, actual results may differ from the projections based upon these assumptions. You should not place undue reliance on these forward - looking statements.

Disclaimers 3 Forward - Looking Statements The Presentation contains forward - looking statements as that term is defined in Section 27A of the Securities Act of 1933, as am ended, Section 21E of the Securities Exchange Act of 1934, as amended, and the Private Securities Litigation Reform Act of 1995, known as the PSLRA. Certain statements in the Pre sen tation that are not purely historical are forward - looking statements. Such forward - looking statements include, among other things, statements regarding our planned clinical progr ams, 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 ut ility, 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 ou r c ompetitors, 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 genera lly . No forward - looking statement can be guaranteed, and actual results may differ materially from those projected. We undertake no obligation to publicly update any forward - looking sta tement, whether as a result of new information, future events or otherwise, except to the extent required by law. We use words such as “aim,” “anticipate,” “assume,” “believe,” “co nte mplate,” “continue,” “could,” “due,” “estimate,” “expect,” “goal,” “intend,” “may,” “objective,” “plan,” “predict,” “potential,” “positioned,” “seek,” “should,” “target,” “will,” “woul d,” and other similar expressions that are predictions of or indicate future events and future trends, or the negative of these terms or other comparable terminology to identify these forward - lookin g 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 uncertaintie s; 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, our financial co ndi tion, including our ability to obtain the funding necessary to advance the development of ELI - 002 and any other future product candidates, and our ability to continue as a going concern and o ur cash runway; our plans to develop and commercialize our product candidates, including ELI - 002; the timing of initiation of our planned clinical trials, including the initiation of an ELI - 002 Phase 1B Colorectal Cancer study; our ability to advance ELI - 007 and/or ELI - 008 into Phase 1 trials; the timing of the availability of data from our clinical trials, including data anticipated from our Phase 1A trials of ELI - 002 2P and ELI - 002 7P and the Phase 2 trial of ELI - 002 7P; the timing for completion of enrollment in our Phase 2 trial of ELI - 002 7P; the timing of any planned investigational new drug application or new drug application; our plans to research, develop and commercialize our current and future product candidat es; our ability to successfully collaborate with existing collaborators or enter into new collaborations, and to fulfill our obligations under any such collaboration agreements; the c lin ical utility, potential benefits and market acceptance of our product candidates; our commercialization, marketing and manufacturing capabilities and strategy; our ability to identify add iti onal products or product candidates with significant commercial potential; our ability to advance ELI - 002 outside of pancreatic ductal adenocarcinoma monotherapy and our pipeline pr ograms; developments and projections relating to our competitors and our industry; the impact of government laws and regulations; our ability to protect our intellectual property po sition covering ELI - 002 and other product candidates we may develop, including the extensions of existing patent terms where available; and our estimates regarding future revenue, e xpe nses, capital requirements and need for additional financing. 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 our Annual Report on Form 10 - K filed with the SEC on March 29 , 2024 , as amended on April 29 , 2024 , under the heading “Risk Factors”, and any subsequent 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 us as of the date of the Presentation . We do not undertake any obligation to update such forward - looking statements to reflect events or circumstances after the date of the Presentation, except to the extent required by law .

4 Amphiphile (“AMP”) Technology • AMP delivers payloads to lymph nodes eliciting immune responses with increased magnitude, function, and durability • Designed to harness the lymph nodes’ natural ability to educate, activate and amplify differentiated T cell responses, which are essential for recognizing and eliminating tumor cells • AMP technology offers broad immunotherapy applications; initially focused on cancer vaccine applications ELI - 002 Lymph Node Targeted mKRAS Cancer Vaccine • Off - the - shelf cancer vaccine candidate targeting seven most common KRAS mutations that drive 25% of solid tumors • Adjuvant treatment for patients with high relapse risk mKRAS+ pancreatic (PDAC) and colorectal cancer (CRC) • Advantageous lymph node - targeted vaccine design: potent immunogenicity, durable CD4+ and CD8+ T cell responses, increased T cell cytotoxic function, and antigen spreading to target personalized tumor mutations ELI - 002 Clinical Data (39 pts across two Phase 1 a trials) • Elicits mKRAS specific T cell response ~100x increase over baseline at the phase 2 dose without any DLTs or SAEs • T cell responses include generation of CD4+ helper and CD8+ killer cells, formation of a pool of memory cells, and ability to el icit T cell response to personal tumor neoantigens (antigen spreading) • mKRAS specific T cell response correlates with reductions in tumor biomarker and reduced risk of relapse or death ELI - 002 Next Steps • ‘7P Phase 1a preliminary disease - free survival data 3Q 2024 • ‘2P Phase 1a updated recurrence - free survival and T cell response data 4Q 2024 • ‘7P Phase 2 trial e nrollment anticipated to be completed (135 patients) in 4Q 2024 • ‘7P Phase 2 trial disease - free survival interim analysis expected in 1Q 2025 Company Overview Clinical - stage biotech developing novel lymph node - targeted immunotherapies

• Elicio is harnessing the natural power of the immune system with AMP technology , to deliver therapeutic payloads directly to the lymph nodes, enhancing the immune system’s cancer - fighting capabilities. • Our targeted - delivery approach generates a robust immune response that amplifies cancer fighting T cells, for the treatment of cancers • Proper education, multiplication, and activation in the lymph nodes is critical for preparing disease - fighting immune cells to resolve disease • Numerous key immune cells, including antigen - presenting cells, and T cells are organized in the lymph nodes – the primary site where the immune response is generated to fight cancers • The lymph nodes , known as the “command center” of the immune response play a vital role in detecting threats to our health and coordinating the buildup of protective immune responses • Lymph nodes collect and filter lymphatic fluid for signs of danger, including traces of cancer or infectious pathogens 5 Previous cancer vaccine efforts have not generated a sufficient T cell response to be an effective immunotherapy. We believe accessing the lymph nodes is critical to generate the robust immune response for effective immuno - oncology. Lymph Nodes T Cell Response Amphiphile (AMP) Technology Engaging the Lymph Node A critical component to activating the immune response in the fight against cancer

6 • Expansion • Phenotype • Effector Function • Anti - tumor Activity Response Coordination The Immune “School House” Numerous Immune Cells APC : T Cell Interaction T Cell Response Lymph Node Lymph Nodes: Eliciting a Robust T Cell Response Immune biology in the Lymph Nodes directs the development of anti - tumor immunity

7  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 B lood Lymph Small Molecules Large Molecules (e.g. Albumin) Blood Vessel Lymph Vessel L ymph Nodes Blood Circulation Tissue Injection Site Targeting Immunity in the Lymph Nodes The Amphiphile (AMP) Technology Harnessing the untapped potential of the lymph nodes for immunotherapy

8 Pant, et al. Nature Medicine 2024; Liu, et al. Nature 2014; Moynihan, et al. Nature Medicine 2016; Ma, et al. Science 2019 » APC Activation » T Cell Expansion and Activation Immune Response 5 Subcutaneous injection 1 Lymph Node Lymph node targeting 3 Antigen Presenting Cell Delivery to immune cells 4 Albumin - bound AMP T Cell Albumin - bound AMP Endogenous Albumin AMP Tissue Injection Site Albumin binding 2 • Expansion • Persistence • Effector function • Phenotype • Metabolic function MOA: AMP Locates to Lymph Node Orchestrating Immunity AMP technology capable of delivering payloads to lymph nodes generating robust immune response

AMP Platform Technology 9 Cancer Vaccines Immunotherapy / Combinations CAR - T Cell Adoptive Therapy TCR - T Cell Adoptive Therapy Infectious Disease Vaccines Lymph Node Delivery Adjuvants Lung - specific Delivery Mucosal Delivery (NALT) Autoimmunity Versatile | Simple | Clinical stage 2014 Liu Nature 2016 Moynihan Nature Medicine 2018 Moynihan Cancer Immunology Research 2019 Ma Science 2021 Rakhra Science Immunology 2021 Steinbuck Science Advances 2021 Li J Immunology 2022 Dasari Nature Communications 2022 Hartwell Science Translational Medicine 2022 Seenappa NPJ Vaccines 2023 Ma Cell 2023 Zhang Nature Biomedical Engineering 2024 Drakes Cancer Immunology Research 2024 Pant Nature Medicine Applications MOA

10 ELI - 007 (Mutant BRAF - Peptide Vaccine) ELI - 008 (p53 Hotspot Mutant - Peptide Vaccine) In preclinical models, ELI - 007 and ELI - 008 have shown strong induction of tumor antigen - specific T cell responses Preclinical Data presented at AACR 2024. Posters can be found here . Similar to KRAS, p53 mutations are present in a broad spectrum of cancer types accounting for >30% of solid tumors BRAF - mutations are highly prevalent in melanoma, colorectal and thyroid cancer existing in 8% of solid tumors representing up to 1.5 million cancer incidences worldwide each year • ELI - 007 is an investigational multi - valent lymph node – targeted AMP peptide vaccine comprised of the V600E and V600K mutant antigens, developed to target BRAF gene mutations. • In preclinical models, AMP - immunization generated robust in vivo immune responses yielding strong T cell activation against mBRAF epitopes. • Lymph node - targeted AMP - vaccination resulted in a 19 - fold increase in immune response after only 3 doses and a 42 - fold increase after 5 doses when compared to conventional comparator vaccines. • ELI - 008 is an investigational multi - valent lymph node – targeted AMP peptide vaccine comprised of the several p53 mutant antigens, developed to target hotspot p53 gene mutations. • In preclinical models, AMP - immunization generated robust immune responses yielding strong T cell activation against common p53 hot spot mutations (R248W, R248Q, R175H, R273H, R273C, R282W, G245S, Y220C, C135Y, R158H, H214R). • For multiple p53 mutations, ELI - 008 demonstrated a several - hundred - fold increase over conventional comparator vaccines. AMP Technology has the potential to address several mutations Preclinical programs funded by Gastro - Intestinal (GI) Research Foundation

11 ELI - 002 G12X G13X Peptide Composition 2P D R 7P 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 ELI - 002 Composition Lymph node targeted therapeutic vaccine candidate comprised of AMP - peptides and AMP - CpG

12 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, 2 021), 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 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 Cancer Total incidence: ~62k Other KRAS mutations The mKRAS Opportunity ELI - 002 targets the 7 most common KRAS mutations driving 25% of solid tumors

13 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’s Differentiated Approach to mKRAS Early mKRAS - targeting efforts in the clinic, while promising, leave significant white space

ELI - 002 2P: 2 - Peptide (2P) Formulation Phase 1A: Adjuvant Dose Ranging 0.1mg to 10mg doses First - in - human Study: mKRAS G12D or G12R - expressing, Adjuvant treatment of MRD+ PDAC and CRC

15 20 - Months Follow - up Boost (4 doses over 4 weeks) Prime (6 doses over 8 weeks) Complete Local Therapy (e.g., Surgery, Chemo) ELI - 002 MONOTHERAPY: NCT04853017 Pancreatic Ductal Adenocarcinoma (PDAC) Colorectal Cancer (CRC) n=20 n=5 x mKRAS G12D / R – aligned to 2 peptide formulation x No radiographic evidence of disease (NED) x 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, 25 evaluable at database cutoff (9/6/2023) • 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 Basket Trial Enrollment Monotherapy (no chemo, CPI combo) Phase 1A ELI - 002 2P AMPLIFY - 201 Study Overview 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 Published in Nature Medicine * Preliminary Phase 1 (AMPLIFY - 201) study of ELI - 002 2P published in Nature Medicine January 2024 Pant, et al. Lymph - node - targeted, mKRAS - specific amphiphile vaccine in pancreatic and colorectal cancer: the phase 1 AMPLIFY - 201 trial. Nature Medicine. 2024. https://doi.org/10.1038/s41591 - 023 - 02760 - 3 *

16 • Waterfall displays best response of ctDNA or serum tumor biomarker • Most patients (84%, 21/25) showed decline from baseline in ctDNA or CEA/CA19 - 9 levels • 24% of patients (6/25) showed complete clearance of ctDNA • Responses observed in PDAC and CRC, mKRAS G12D and G12R • Responses observed despite prior splenectomy (S annotated) * Patient biopsied, exhibited T cell infiltration and continued study treatment S Patient underwent splenectomy Data cutoff 6 - Sept - 23 1 2 3 4 6177258239245101113141215182216201921 -100 -75 -50 -25 0 25 50 75 100 2 8 0 9 0 3 8 2 2 - 2 6 - 2 8 - 2 8 - 4 3 - 4 4 - 4 7 - 5 0 - 7 6 - 1 0 0 - 1 0 0 - 1 0 0 - 1 0 0 - 1 0 0 - 1 0 0 B e s t O v e r a l l B i o m a r k e r R e s p o n s e ( % o f B a s e l i n e ) 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 Pant, O’Reilly, et al. Nature Medicine. 2024 Phase 1A ELI - 002 2P AMPLIFY - 201: Tumor Biomarker Response Robust responses observed across tumor types and KRAS mutations with ELI - 002 monotherapy

Baseline Max Response 0 5 10 20 30 40 50 450 F o l d C h a n g e f r o m B a s e l i n e 2 17 • T cells detectable by standard direct ex vivo FluoroSpot and flow cytometry, with no expansion required • 84% of patients showed T cell responses; 100% at the RP2D (10 mg) • 58x average fold - change in T cell numbers from baseline (median 12.75; range 2 - 423x) • 59% of patient responses included both CD4 and CD8 T cells • De novo T cell priming and memory cell expansion • Responses were observed across diverse HLA backgrounds Responses shown are best overall responses vs baseline for each patient at any timepoint during the assessment period. Data cutoff 6 - Sept - 23 Median = 12.75x AMPLIFY - 201 T Cell Fold - Changes mKRAS T Cell Responses Baseline Max Response Direct Ex Vivo T Cell Response 0.1 mg 0.5 mg 2.5 mg 5.0 mg 10.0 mg Pant, O’Reilly, et al. Nature Medicine. 2024 Phase 1A ELI - 002 2P AMPLIFY - 201: Immune Response 84% of patients generated mKRAS - specific T cells directly ex vivo ; 100% at RP2D

Clearance Reduction Non - Responder ≥Median <Median -100 0 100 200 300 T Cell Response (Fold change from baseline) B e s t O v e r a l l B i o m a r k e r R e s p o n s e ( % o f B a s e l i n e ) ✱✱ 18 • 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 Phase 1A ELI - 002 2P AMPLIFY - 201: T Cell Fold - change Predicts Tumor Biomarker Response All patients with T cell responses over the median showed tumor biomarker response

19 • 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 Data cutoff 6 - Sept - 23 AMPLIFY - 201: Majority of Above Median T Cell Responders Include CD4 and CD8 T cells Above median mKRAS - specific T cell response correlated to improved clinical outcome Phase 1A ELI - 002 2P

0 3 6 9 12 15 18 0 25 50 75 100 Months R e l a p s e - f r e e S u r v i v a l ( % ) 20 • At a median follow up of 8.5 months, median RFS was not reached for above median T cell responders 1 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 RFS was 16.3 months ≥ 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 Pant, O’Reilly, et al. Nature Medicine. 2024 Phase 1A ELI - 002 2P AMPLIFY - 201: Above Median T Cell Responders Median RFS Significantly Prolonged 86% reduction in the risk of progression or death in above median T cell responders

21 • T cells detectable by standard direct ex vivo FluoroSpot and flow cytometry, with no expansion required • 68% of evaluated patients (13/19) developed increased cytotoxic CD4 + T cell responses targeting mKRAS • ELI - 002 vaccination induces development of central and effector memory phenotype mKRAS Cytotoxic CD4 + T Cell Response Responses shown are best overall responses vs baseline for each patient at any timepoint during the assessment period. Direct Ex Vivo T Cell Response Baseline Week 9 Phase 1A ELI - 002 2P AMPLIFY - 201: ELI - 002 Amplifies Cytotoxic mKRAS - specific CD4 + T cells Induced mKRAS - specific CD4 + T cells develop enhanced cytotoxic function, memory phenotype 0 5 5 15 25 800 1500 2200 F o l d c h a n g e f r o m b a s e l i n e 2 Responses shown are best overall responses vs baseline for each patient at any timepoint during the assessment period. Cytotoxic CD4 + T Cell Fold - Changes Baseline Week 9 0.1 mg 0.5 mg 2.5 mg 5.0 mg 10.0 mg 0 20 40 60 80 % C D 4 + T c e l l s CM EM TEMRA Naive CD4 + T cell Memory Baseline Week 9 (Post Prime)

0 20 40 60 80 100 % C D 8 + T c e l l s 0 5 5 20 35 50 200 400 F o l d c h a n g e f r o m b a s e l i n e 2 22 • T cells detectable by standard direct ex vivo FluoroSpot and flow cytometry, with no expansion required • 84% of evaluated patients (16/19) developed increased cytotoxic CD8 + T cell responses targeting mKRAS • ELI - 002 vaccination induces development of TEMRA phenotype mKRAS Cytotoxic CD8 + T Cell Response 22 Responses shown are best overall responses vs baseline for each patient at any timepoint during the assessment period. Cytotoxic CD8 + T Cell Fold - Changes Direct Ex Vivo T Cell Response 0.1 mg 0.5 mg 2.5 mg 5.0 mg 10.0 mg CM EM TEMRA Naive CD8 + T cell Memory Baseline Week 9 (Post Prime) Baseline Week 9 Phase 1A ELI - 002 2P AMPLIFY - 201: ELI - 002 Amplifies Cytotoxic mKRAS - specific CD8 + T cells Induced mKRAS - specific CD8 + T cells develop enhanced cytotoxic function, memory phenotype

1 2 3 4 4 4 4 5 5 0 1 2 3 4 5 6 7 8 9 10 # o f P e r s o n a l i z e d T u m o r N e o a n t i g e n s A s s a y e d f o r T c e l l R e s p o n s e 23 • ELI - 002 2P vaccination led to expansion of T cell responses targeting passenger mutations alongside mKRAS driver mutations in a majority of evaluable patients • T cells detectable by standard direct ex vivo FluoroSpot and flow cytometry, with no expansion required • 67% of evaluated patients (6/9) developed increased T cell responses targeting personalized tumor neoantigens • 100% at RP2D 10.0 mg CpG adjuvant dose • Polyfunctional CD4 and CD8 T cells Antigen Spreading to Personal Tumor Neoantigens A MPLIFY - 201: ELI - 002 Stimulates Antigen Spreading Expansion of T cells specific to personalized tumor antigens not targeted by vaccination AMP - CpG Adjuvant Immunogenic Non - immunogenic Phase 1A ELI - 002 2P Cohort 1 2 3 4 4 4 4 5 5 Dose (mg) 0.1 0.5 2.5 5.0 10.0

24 • No Grade 3/4 TEAEs, no CRS, no DLTs at time of data cutoff (6 - Sept - 2023) • 12/25 (48%) had Grade 1 or 2 AEs • 4/25 (16%) 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 Term a 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 Phase 1A ELI - 002 2P AMPLIFY - 201: Safety & Tolerability ELI - 002 was well tolerated at all dose levels, with no DLTs or SAEs

ELI - 002 7P: 7 - Peptide (7P) Formulation Phase 1A: Peptide Dose Ranging 1.4mg or 4.9mg doses First - in - human Study: mKRAS G12x or G13D - expressing, Adjuvant treatment of MRD+ PDAC and CRC

26 32 - Months Follow - up Boost (4 doses over 4 weeks) Prime (6 doses over 8 weeks) Complete Local Therapy (e.g., Surgery, Chemo) ELI - 002 MONOTHERAPY: NCT05726864 Pancreatic Ductal Adenocarcinoma (PDAC) Colorectal Cancer (CRC) n=13 n=1 x Includes: mKRAS G12D/R/V/C/A/S/G13D x No radiographic evidence of disease (NED) x High risk of relapse (MRD+ ctDNA /serum biomarkers) Key Criteria 1 - 2 months 2 months Safety Maximum Tolerated Dose (MTD) or RP2D ctDNA /serum biomarker change from baseline Immunological Responses Disease Free Survival (DFS) Endpoints 14 patients enrolled across 2 dose cohorts, 12 biomarker evaluable at database cutoff (Dec 18, 2023) • Advanced: 7 (50%) had stage III • Pre - treated: All received prior chemo and surgery, 29% had prior radiation Baseline Characteristics Basket Trial Enrollment Monotherapy (no chemo, CPI combo) Phase 1A ELI - 002 7P AMPLIFY - 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

Baseline Max response 0 5 10 15 20 25 50 100 150 200 F o l d c h a n g e f r o m b a s e l i n e 27 • 100% of patients showed T cell responses • 4.9 mg dose group selected for Phase 2 • Median fold change = 109.2x • 66.7% with CD4 and CD8 T cells • T cells detectable by standard direct ex vivo FluoroSpot and flow cytometry, with no expansion required Responses shown are best overall responses relative to baseline for each patient at any timepoint during the assessment perio d. ELI - 002 7P: Data cutoff 18 - Dec - 23 AMPLIFY - 201 T Cell Fold - Changes by Dose Level mKRAS T Cell Responses Baseline Max Response Direct Ex Vivo T Cell Response Average Median 4.9 mg 99.2 109.2 1.4 mg 11.3 9.3 All 59.2 23.6 T Cell Response Dose = Phase 2 Dose Phase 1A ELI - 002 7P AMPLIFY - 7P: T Cell Responses 100% of patients with robust T cell response 7P RP2D Median 109.2x

28 ELI - 002 2P (Nat Med) ELI - 002 7P (All) ELI - 002 7P (4.9 mg) Response Rate 84% 100% 100% Median Fold Change 12.8 23.6 109.2 % CD4 + CD8 T cells 59% 63.6% 66.7% Response to 7 mKRAS Antigens 52.4% 45.5% 66.7% Response to Tumor Antigen 81% 72.7% 83.3%  ELI - 002 7P data based on n=11 Patients (1.4 mg, n=5; 4.9 mg, n=6)  100 % T cell Response Rate (n=11)  ELI - 002 7P 4.9 mg shows increased:  Median Fold Change  CD4 + CD8 Response Rate  Response Rate for all 7 mKRAS Antigens  Response Rate to Patient Tumor Antigen ELI - 002 2P vs ELI - 002 7P 4.9 mg Responses shown are best overall responses vs baseline for each patient at any timepoint during the assessment period. ELI - 002 2P: Data cutoff 6 - Sept - 23 ELI - 002 7P: Data cutoff 18 - Dec - 23 Phase 2 Dose = Phase 2 Dose Phase 1A ELI - 002 7P AMPLIFY - 7P: T Cell Responses Phase 2 Dose generates higher immune response than seen with ELI - 002 2P

29 • ELI - 002 7P vaccination led to expansion of T cell responses targeting passenger mutations alongside mKRAS driver mutations in a majority of evaluable patients • T cells detectable by standard direct ex vivo FluoroSpot and flow cytometry, with no expansion required • 70% of evaluated patients (7/10) developed increased T cell responses targeting personalized tumor neoantigens • 100% at RP2D 4.9 mg peptide antigen dose • Polyfunctional CD4 and CD8 T cells Antigen Spreading to Personal Tumor Neoantigens AMPLIFY - 7P: ELI - 002 Stimulates Antigen Spreading Expansion of T cells specific to personalized tumor antigens not targeted by vaccination Phase 1A ELI - 002 7P 4.9 mg 1.4 mg 7P Antigen Dose Level 0 1 2 3 4 5 6 7 8 9 10 # o f P e r s o n a l i z e d T u m o r N e o a n t i g e n s A s s a y e d f o r T c e l l R e s p o n s e Immunogenic Non - immunogenic

30 • 71% (5/7) of patients in the 4.9 mg dose had biomarker decline • 40% (2/5) of patients in the 1.4 mg dose had biomarker decline • 14% (1/7) PDAC patients at 4.9 mg dose had complete clearance • Response may deepen over time (some patients not yet finished boosters) Amph - Peptides - 7P Dose 1.4 mg 4.9 mg AMPLIFY - 201 Waterfall Plot: Biomarker Reduction / Clearance Tumor Biomarker Responses -100 -75 -50 -25 0 25 50 75 100 1 0 0 1 0 0 8 6 7 4 - 1 9 - 2 4 - 4 5 - 6 4 - 1 0 0 B e s t O v e r a l l B i o m a r k e r R e s p o n s e ( % o f B a s e l i n e ) * * 9 - 11 - 13 * Represents percent change > 100%; data display at maximum 100% Two (2) pts not included in this analysis. Pt 111 - 002 had insufficient post - baseline biomarker data; pt 107 - 002 d/c treatment ea rly due to non - treatment related AE KRAS variant post - analysis: 107001 G12D, 106001 G12V, 110004 G12D, 117001 G12D P P P P P P C P P P P P Tumor Type KRAS Biomarker P PDAC C CRC ctDNA CEA / CA19 - 9 V D D D D R D D V D D V G12 G13 = Phase 2 Dose Phase 1A ELI - 002 7P AMPLIFY - 7P: Tumor Biomarker Responses Waterfall reflects superiority of 4.9 mg AMP - Peptide 7P dose level A B C DP DQ DR HLA I HLA II Data cutoff 18 - Dec - 23

≥Median <Median -100 0 100 200 300 T Cell Response (Fold change from baseline) Median = 17.3 B e s t O v e r a l l B i o m a r k e r R e s p o n s e ( % o f B a s e l i n e ) P = 0.0317 Clearance Reduction Non - Responder 31 • Strength of T cell response to ELI - 002 is correlated to tumor biomarker response • 100% (5/5) of the above median T cell group respond to ELI - 002; in the below median group 40% (2/5) respond to ELI - 002* • 80% (4/5) of the 4.9 mg dose cohort are in the above median T cell group, including a complete responder • Statistically significant, p - value per Mann Whitney Test ( P = 0.0317) Data cutoff 18 - Dec - 23 mKRAS T Cell Response Tumor Biomarker Response Best Overall Tumor Biomarker Response ≥ Median < Median P = 0.0317 *10 patients had both immunogenicity and biomarker data available at data cutoff. Phase 1A ELI - 002 7P AMPLIFY - 7P: T Cell Response Drives Tumor Biomarker Response All patients with T cell responses above median showed tumor biomarker response

32 • No DLT observed, No CRS or T cell Toxicities • Most common TRAE (>20%) were Fatigue (28.6%; all Gr1) and Malaise (21.4%; all Gr1) • One (1) pt had SAE (107 - 002) 1.4 mg dose non - treatment related intestinal obstruction resulted in hospitalization and w/d from treatment • No dose modification • No TRAE leading to death ELI - 002 7P Safety / Tolerability Phase 1A ELI - 002 7P AMPLIFY - 7P: Safety ELI - 002 was well tolerated at all dose levels with no DLTs AMP - Peptide 7P Dose 1.4 mg n=6 4.9 mg n=8 Overall n=14 Adverse Event Term a Patients with Any Related TEAE, n (%) 5 (83.3) 6 (75.0) 11 (78.6) Fatigue 3 (50.0) 3 (37.5) 6 (42.9) Malaise 1 (16.7) 2 (25.0) 3 (21.4) Diarrhea 1 (16.7) 2 (25.0) 3 (21.4) Abdominal Distension 2 (33.3) 0 2 (14.3) Abdominal Pain 1 (16.7) 1 (12.5) 2 (14.3) Patient Summary KRAS Mutation DDDDV 13D DDDDRVVV Dose Limiting Toxicity 0 0 0 Biomarker Reduction / Clearance 2 / 5 (40) 5 / 7 (71) 7 / 12 (58) b T cell Response 6 / 6 (100) 5 / 5 (100) 11 / 11 (100) c TEAE: Treatment Emergent Adverse Event a Preferred terms per the Medical Dictionary for Regulatory Activities, version 25.0 b Measured among 12 evaluable patients as of the data cut off: December 18, 2023 c Measured among 11 evaluable patients as of the data cut off: December 18, 2023

33 AMPLIFY - 7P: Preliminary Phase 1 Disease - free Survival Improved DFS observed at 4.9mg Phase 2 dose versus 1.4 mg dose Phase 1A ELI - 002 7P 0 12 24 36 48 60 0 25 50 75 100 Weeks on Study D i s e a s e - f r e e S u r v i v a l ( % ) 4.9 mg (n = 8) P = 0.0939 1.4 mg (n = 6) HR: 0.186 (0.024 – 1.436) Median DFS: not reached Median DFS: 12.57 weeks 4.9 mg AMP - Peptide Dose versus 1.4 mg dose level 6 mo 12 mo No. at Risk 1.4 mg 6 3 2 1 0 4.9 mg 8 7 4 2 1 0 Data cutoff 24 - May - 24 • AMP - Peptide - 7P 4.9 mg dose: • Median DFS not reached • Associated with 8 1 % decreased risk of disease progression and death compared to 1.4 mg (P = 0.0939) ELI - 002 7P Disease - free Survival

0 12 24 36 48 60 0 25 50 75 100 Weeks on Study D i s e a s e - f r e e S u r v i v a l ( % ) 34 Phase 1A ELI - 002 7P Supervised by Median T cell Fold Change 6 mo 12 mo Median DFS: not reached Median DFS: not reached ≥ Median T Cell Response (n = 6) < Median T Cell Response (n = 6) No. at Risk 6 6 5 3 1 0 6 4 1 0 AMPLIFY - 7P: Preliminary Phase 1 Disease - free Survival Improved DFS associated with above median T cell response • Induction of above median mKRAS - specific T cell responses by ELI - 002 7P associated with decreased risk of disease progression and death compared to below median T cell response • All patients with above median T cell responses are free from disease progression ELI - 002 7P Disease - free Survival Data cutoff 24 - May - 24

0 12 24 36 48 60 0 25 50 75 100 Weeks on Study D i s e a s e - f r e e S u r v i v a l ( % ) 35 Phase 1A ELI - 002 7P 6 mo 12 mo Median DFS: not reached Supervised by Biomarker Response Median DFS: 11.00 weeks AMPLIFY - 7P: Phase 1 Disease - free Survival Improved DFS associated with biomarker response Biomarker Response (n = 7) Biomarker Non - response (n = 5) No. at Risk 7 7 5 3 1 0 5 2 0 • Tumor biomarker reduction or clearance after ELI - 002 7P treatment a ssociated with decreased risk of disease progression and death compared to below median T cell response • All patients with tumor biomarker reduction or clearance are free from disease progression ELI - 002 7P Disease - free Survival Data cutoff 24 - May - 24

36 AMPLIFY - 7P: Preliminary Phase 1 Disease - free Survival Favorable overall DFS observed Phase 1A ELI - 002 7P 0 12 24 36 48 60 0 25 50 75 100 Weeks on Study D i s e a s e - f r e e S u r v i v a l ( % ) 6 mo 12 mo Median DFS: not reached All Patients (n = 14) No. at Risk ELI - 002 - 7P 14 10 6 3 1 0 • Full Phase 1 Cohort: • Median DFS not reached ELI - 002 7P Disease - free Survival Data cutoff 2 4 - May - 24

ELI - 002 7P: 7 - Peptide (7P) Formulation Phase 2: 135 PDAC Patients Randomized 2:1

x mKRAS : Expanded Antigen Coverage G12D / R / V / C / A / S / G13D 38 CLINICAL STUDY OVERVIEW: NCT05726864 x Includes: mKRAS G12D/R/V/C/A/S/G13D x Up front resectable Stage I, II or III disease (PDAC) x Complete R0/R1 resection x Radiographic NED status within 6 months following completion of locoregional treatment x MRD agnostic (biomarker +/ - included) Phase 2: Key Criteria Primary Endpoint: Disease Free Survival Tumor Biomarker Response (biomarker subset) Overall Survival, Safety, iRECIST Overall Response Rate Exploratory: Immunogenicity Endpoints ELI - 002 7P 8wk immunization (1,2,3,4,6,8) 8wk observation, 4wk boosting Observation: SOC n~90 n~45 R 2:1 Crossover @ PD Schema Monotherapy (no chemo, CPI combo) Phase 2 interim analysis expected in 1Q 2025 Phase 2 ELI - 002 7P ELI - 002 Randomized Phase 2 PDAC, n=135 patients 2:1 Randomized, Open Label Study with 1 0 DFS endpoint

x Published Preliminary Phase 1a Data in Nature Medicine x Antigen spreading and expanded immunogenicity data (AACR) □ Updated RFS and T Cell response data (4Q 2024) x Preliminary Phase 1 T Cell and biomarker response (ASCO) □ Complete 135 patient Phase 2 enrollment (4Q 2024) □ Phase 2 DFS Interim Analysis (1Q 2025) □ Initiate ELI - 002 Phase 1B Colorectal Cancer study □ Advance ELI - 007 / ELI - 008 into Phase 1 39 ELI - 002 2P Phase 1 Study ELI - 002 7P Phase 1/2 Study Growth Initiatives Key Milestones and Growth Initiatives 2024 - 2025

Targeting the Lymph Nodes to AMPlify Immunotherapy Nasdaq: ELTX June 2024

 

 

v3.24.1.1.u2

Document and Entity Information	Jun. 27, 2024
Cover [Abstract]
Document Type	8-K
Amendment Flag	false
Document Period End Date	Jun. 27, 2024
Entity File Number	001-39990
Entity Registrant Name	Elicio Therapeutics, Inc.
Entity Central Index Key	0001601485
Entity Incorporation, State or Country Code	DE
Entity Tax Identification Number	11-3430072
Entity Address, Address Line One	451 D Street, 5th Floor
Entity Address, City or Town	Boston
Entity Address, State or Province	MA
Entity Address, Postal Zip Code	02210
City Area Code	857
Local Phone Number	209-0050
Title of 12(b) Security	Common Stock, $0.01 par value per share
Trading Symbol	ELTX
Security Exchange Name	NASDAQ
Entity Emerging Growth Company	true
Entity Ex Transition Period	false
Written Communications	false
Soliciting Material	false
Pre-commencement Tender Offer	false
Pre-commencement Issuer Tender Offer	false

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