Targeting the Lymph Nodes to AMPlify Immunotherapy Nasdaq: ELTX December 2024
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Disclaimers 3 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, including the potential durable clinical benefits and potential broad application 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. No forward-looking statement can be guaranteed, and actual results may differ materially from those projected. 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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 potential for broad cancer immunotherapy application 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 • Potential monotherapy adjuvant treatment for patients with high relapse risk mKRAS+ pancreatic (PDAC) and colorectal cancer (CRC) • Lymph node-targeted vaccine design for 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 elicit 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 • Alignment with FDA on key 7P Phase 3 study design parameters anticipated after Q4 2024 Type B meeting • 7P Phase 2 trial disease-free survival interim analysis expected in H1 2025 • End of Phase 2 FDA meeting expected in H2 2025 • Anticipate Phase 3 readiness in Q1 2026 Company Overview Clinical-stage biotech developing novel lymph node-targeted “off the shelf” cancer immunotherapies
• $33M in new capital raised – Company funded into the second quarter of 2025 past anticipated Phase 2 interim analysis • Pipeline of cancer vaccines and immunomodulators expands and advances • ELI-002 Phase 1/2 7-peptide updated Phase 1a data presented at AACR-Special Conference-Pancreatic Cancer • ELI-002 Phase 1/2 7-peptide updated Phase 1a data presented at SITC • FDA Type-B meeting expected to provide guidance for Phase 3 trial design • Phase 2 trial fully enrolled – 135 patients enrolled in 10 months in 27 clinical sites • AMPLIFY-201 Phase 1 2-peptide data presented December 12th at ESMO Immuno-Oncology Congress 2024 (“ESMO-IO”) in Dr. Shubham Pant (MD Anderson) podium presentation 5 H2 2024 Execution ELI-002 is now the most advanced off-the-shelf cancer vaccine in PDAC
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
7Pant, 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 Response5Subcutaneous injection1 Lymph Node Lymph node targeting3 Antigen Presenting Cell Delivery to immune cells4 Albumin-bound AMP T CellAlbumin-bound AMP Endogenous AlbuminAMP Tissue Injection Site Albumin binding2 • 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
8 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 PeptidePEG 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
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 + 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
10 Clinically advanced vaccine: PDAC Targeting 7 mKRAS driver mutations Lymph Node Targeting MOA Off-the-shelf simplicity, cost Robust T cell Response (CD4 + CD8) Monotherapy activity Potential durable clinical benefit Potential broad application for ~25% of human solid cancers expressing mKRAS Significant progress and investment in vaccine product development: • Moderna / Merck: KeyNote-942 • BioNTech / Roche: Autogene Cevumeran Validates potential for clinical value BUT • No lymph node targeting • Manufacturing is long + costly • Targets non-essential mutations • Combination with CPI needed FDA approvals for LUMAKRAS® & KRAZATI® validate target Mirati acquisition: $4.8B by BMS BUT Only affects 1 mutation (G12C), subject to multiple resistance mechanisms Limited duration of clinical benefit Lymph Node Targeted Vaccine vs Mutant KRAS Personalized Neoantigen VaccinesSmall Molecules Inhibiting Mutant KRAS ELI-002’s Differentiated Approach to mKRAS Therapy Validated mKRAS Target | Differentiated Vaccine Approach | Advanced Clinical Stage
• PDAC (33) or CRC (6) patients treated after local surgery and chemotherapy yet with minimal residual disease (Adjuvant setting) • Phase 1 trials included dose-ranging for both peptide and adjuvant components of ELI-002 • Data from both trials have shown: • ELI-002 was well tolerated at all dose levels, with no DLTs or SAEs observed • 10mg AMP CpG with 4.9mg 7 AMP peptides identified as RP2D (median 113X T cell fold change) • ELI-002 generates a robust mKRAS-specific T cell response (CD4+ and CD8+) • ELI-002 generates T cell response correlating with a reduction in tumor biomarker levels • ELI-002 induces Antigen Spreading at RP2D with immune response targeting personal tumor antigens • Strength of ELI-002 T cell response correlating with a reduction in the risk of progression or death • Preliminary Phase 1 (AMPLIFY-201) study of ELI-002 2P including RFS outcome published in Nature Medicine January 2024 • Follow-up Phase 1 (AMPLIFY-201) data highlighting RFS and OS to be presented at ESMO-IO December 2024 11 ELI-002 Summary of Phase 1 Clinical Trials 39 patients treated in two Phase 1 trials with ELI-002 monotherapy (2 AMP peptides + AMP CpG) & (7 AMP peptides + AMP CpG)
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
13 20-Months Follow-up Boost (4 doses over 4 weeks) Prime (6 doses over 8 weeks) Complete Local Therapy (e.g., Surgery, Chemo) E L I - 0 0 2 M O N O T H E R A P Y : N C T 0 4 8 5 3 0 1 7 Pancreatic Ductal Adenocarcinoma (PDAC) Colorectal Cancer (CRC) n=20 n=5 mKRAS G12D / R – aligned to 2 peptide formulation 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, 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 EnrollmentMonotherapy (no chemo, CPI combo) Phase 1AELI-002 2PAMPLIFY-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*
14 • 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 6 17 7 25 8 23 9 24 5 101113141215182216201921 -100 -75 -50 -25 0 25 50 75 100 28 0 90 38 22 -2 6 -2 8 -2 8 -4 3 -4 4 -4 7 -5 0 -7 6 -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) P P P P P P C P P P P P P P P C P P P P P C P C CTumor 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 DKRAS Biomarker D G12D R G12R P PDAC C CRC ctDNA CEA / CA19-9 -9 -1 1 -1 8 -2 S S SS * -2 -1 1 -1 7 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/ClearanceTumor Biomarker Responses Pant, O’Reilly, et al. Nature Medicine. 2024 Phase 1AELI-002 2PAMPLIFY-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 Fo ld C ha ng e fr om B as el in e 2 15 • 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-ChangesmKRAS T Cell Responses Baseline Max Respo se 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 1AELI-002 2PAMPLIFY-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 f rom baseline) Be st O ve ra ll Bi om ar ke r R es po ns e (% o f Ba se lin e) ✱✱ 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 Phase 1AELI-002 2PAMPLIFY-201: T Cell Fold-change Predicts Tumor Biomarker Response All patients with T cell responses over the median showed tumor biomarker response
17 Phase 1AELI-002 2PESMO-IO UPDATE: Full Cohort (n=25) vs PDAC Subgroup (n=20): Median follow up has increased to 19.7 months vs 8.5 months in Pant et al., 2024 Nature Med Median RFS times similar for the full cohort and PDAC subgroup: Data cut-off Sept 24, 2024 Full Cohort (n=25)Relapse-free Survival: Re la ps e- fr ee S ur vi va l Months No. at Risk 25 16 11 9 7 7 3 1 0 Median RFS: 16.33 Months Re la ps e- fr ee S ur vi va l Months No. at Risk 20 11 7 5 5 5 3 1 0 Median RFS: 15.31 Months PDAC Subgroup (n=20)Relapse-free Survival: Median follow-up for study: 19.7 months Pant, et al. ESMO-IO Annual Meeting. 2024
18 Phase 1AELI-002 2PESMO-IO Relapse-Free Survival UPDATE: RFS Prolonged - no relapse or death in 10/13 (77%) of above median T cell group Data cut-off (DCO): September 24, 2024 • 10/13 in the above median T cell group have not relapsed or died • Favorable RFS stratified by T cell response was maintained relative to prior analysis: • Median RFS not reached for above median T cell Responders • Median RFS 4.01 months for below median T cell Responders • HR 0.226, P = 0.0184 • 77% reduction in Risk of Progression or Death due to any cause in above median T cell Responders to ELI-002 DCO September 24, 2024 Relapse-free Survival: Re la ps e- fr ee S ur vi va l Months T Cell Response No. at Risk ≥ Median 13 12 9 7 5 5 3 1 0 < Median 12 4 2 2 2 2 0 Median RFS: Not Reached Median RFS: 4.01 Months ≥ Median T Cell Response (n=13) < Median T Cell Response (n=12) DCO 06-Sept-2023 24-Sept-2024 Median RFS (Months) ≥ Median T Cell Not Reached Not Reached < Median T Cell 4.01 4.01 HR (95% CI) 0.142 0.226 (0.0321, 0.6278) (0.0552, 0.9277) P-value 0.0167 0.0184 ELI-002 2P Relapse-free Survival Median follow-up for study: 19.7 months Pant, et al. ESMO-IO Annual Meeting. 2024
19 Phase 1AELI-002 2POVERALL Survival in FULL COHORT AND SUBGROUPS Full Cohort (n=25) Overall Survival; mOS 28.94 mo is longer than historical for PDAC, CRC not yet estimable DCO September 24, 2024 Overall Survival: O ve ra ll Su rv iv al Months No. at Risk 25 25 23 23 22 20 13 6 2 2 1 1 0 Median OS: 28.94 Months Median Follow-up: 19.70 Months Data cut-off (DCO): September 24, 2024; NR= not reached • Median RFS for full cohort and PDAC, CRC subgroups are similar • Median OS for full cohort and PDAC, CRC subgroups are identical • mOS longer than MRD+ PDAC e.g. 17 mo from resection, Groot et al., 2019. Clin Cancer Res 25:4973 Cohort Full (n=25) PDAC (n=20) CRC (n=5) Median RFS (months) 16.33 15.31 16.33 Median OS (Months) 28.94 28.94 NR Median Follow-up (Months) 19.7 19.5 23.2 ELI-002 2P Relapse-free and Overall Survival Pant, et al. ESMO-IO Annual Meeting. 2024
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
21 32-Months Follow-up Boost (4 doses over 4 weeks) Prime (6 doses over 8 weeks) Complete Local Therapy (e.g., Surgery, Chemo) E L I - 0 0 2 M O N O T H E R A P Y : N C T 0 5 7 2 6 8 6 4 Pancreatic Ductal Adenocarcinoma (PDAC) Colorectal Cancer (CRC) n=13 n=1 Includes: mKRAS G12D/R/V/C/A/S/G13D No radiographic evidence of disease (NED) 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 EnrollmentMonotherapy (no chemo, CPI combo) Phase 1AELI-002 7PAMPLIFY-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
0 5 10 15 20 25 30 100 200 300 Fo ld -c ha ng e fr om b as el in e 22 • 100% of patients showed T cell responses • 4.9 mg dose group selected for Phase 2 • Median fold change = 113.3x • 85.7% 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 period. ELI-002 7P: Data cutoff 24-Sep-24 AMPLIFY-201 T Cell Fold-Changes by Dose LevelmKRAS T Cell Responses Baseline Max Response Direct Ex Vivo T Cell Response Average Median 4.9 mg 113.8 113.3 1.4 mg 11.3 9.3 All 71.1 18.5 T Cell ResponseDose = Phase 2 Dose Phase 1AELI-002 7PAMPLIFY-7P: T Cell Responses 100% of patients with robust T cell response 7P RP2D Median 113.3x
23 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 18.5 113.3 CD4 + CD8 T cells 59% 75.0% 85.7% Response to 7 mKRAS Antigens 52.4% 50.0% 71.4% Response to Tumor Antigen 81% 83.3% 100% • ELI-002 7P data based on n=12 Patients (1.4 mg, n=5; 4.9 mg, n=7) • 100% T cell Response Rate (n=12) • 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 24-Sep-24 Phase 2 Dose = Phase 2 Dose Phase 1AELI-002 7PAMPLIFY-7P: T Cell Responses Phase 2 Dose generates higher immune response than seen with ELI-002 2P
24 • 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 1AELI-002 7P 4.9 mg1.4 mg 7P Antigen Dose Level 0 1 2 3 4 5 6 7 8 9 10 # of P er so na liz ed Tu m or N eo an tig en s A ss ay ed fo r T c el l R es po ns e Immunogenic Non-immunogenic
25 • 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 / ClearanceTumor Biomarker Responses -100 -75 -50 -25 0 25 50 75 100 10 0 10 0 86 74 -1 9 -2 4 -4 5 -6 4 -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 -1 3 * 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 early 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 PTumor 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 1AELI-002 7PAMPLIFY-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 IIData cutoff 18-Dec-23
> Median < Median -100 0 100 200 T Cell Response (Fold change f rom baseline) Be st O ve ra ll Bi om ar ke r R es po ns e (% o f B as el in e) ✱ Clearance Reduction Non-Responder 26 • Strength of T cell response to ELI-002 is correlated to tumor biomarker response • 100% (6/6) of the above median T cell group respond to ELI-002; in the below median group 33% (2/6) respond to ELI-002* • 71.4% (5/7) 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 = 0.0260) Tumor Biomarker data cutoff 18- Dec-23; T cell biomarker data cutoff 24-Sep-24 mKRAS T Cell Response Tumor Biomarker Response Best Overall Tumor Biomarker Response ≥ Median < Median P = 0.0260 *10 patients had both immunogenicity and biomarker data available at data cutoff. Phase 1AELI-002 7PAMPLIFY-7P: T Cell Response Drives Tumor Biomarker Response All patients with T cell responses above median showed tumor biomarker response
0 12 24 36 48 60 0 25 50 75 100 Weeks on Study D is ea se -f re e Su rv iv al (% ) 27 Phase 1AELI-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 were free from disease progression as of the data cutoff date ELI-002 7P Disease-free Survival Data cutoff 23-May-24
28 • 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 1AELI-002 7PAMPLIFY-7P: Safety ELI-002 was well tolerated at all dose levels with no DLTs observed Amph-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
ELI-002 7P: 7-Peptide (7P) Formulation Phase 2: 135 PDAC Patients Randomized 2:1
mKRAS: Expanded Antigen Coverage G12D / R / V / C / A / S / G13D 30 C L I N I C A L S T U D Y O V E R V I E W : N C T 0 5 7 2 6 8 6 4 Includes: mKRAS G12D/R/V/C/A/S/G13D Up front resectable Stage I, II or III disease (PDAC) Complete R0/R1 resection Radiographic NED status within 6 months following completion of locoregional treatment 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 SchemaMonotherapy (no chemo, CPI combo) Phase 2 enrollment complete; interim analysis expected in 1H 2025 Phase 2ELI-002 7PELI-002 Randomized Phase 2 PDAC, n=135 patients 2:1 Randomized, Open Label Study with 10 DFS endpoint
Published Preliminary Phase 1a Data in Nature Medicine Antigen spreading and expanded immunogenicity data (AACR) Updated RFS and OS response data (ESMO- IO: 4Q 2024) Preliminary Phase 1 T Cell and biomarker response (ASCO) T cell and Antigen Spreading (SITC) Complete 135 patient Phase 2 enrollment (4Q 2024) FDA Type B Meeting Phase 2 DFS Interim Analysis (expected 1H 2025) End of Phase 2 FDA Meeting (expected 2H 2025) Phase 3 readiness to initiate pivotal ELI-002 P3 PDAC study Initiate ELI-002 Phase 1B Colorectal Cancer study Initiate ELI-002 combination studies in metastatic MSS CRC; Neo-adjuvant PDAC Advance ELI-007 BRAF and ELI-008 p53 vaccines into Phase 1 ELI-002 and ELI-004 partnerships and collaborations 31 ELI-002 2P Phase 1 Study ELI-002 7P Phase 1/2 Study 2025/2026 Growth Initiatives Key Milestones Achieved and Growth Initiatives 2025-2026
Targeting the Lymph Nodes to AMPlify Immunotherapy Nasdaq: ELTX December 2024