Slides
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Altimmune R&D Day Pemvidutide: Designed to be the Treatment of Choice for Liver and Cardiometabolic Diseases MARCH 13, 2025
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Forward-looking Statements Safe-Harbor Statement This presentation has been prepared by Altimmune, Inc. ("we, " "us, " "our, " "Altimmune" or the "Company") and includes certain “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995, including statements regarding the timing of clinical development and funding milestones for our clinical assets, the timing of the IMPACT trial data readout, as well as statements relating to future financial or business performance, conditions, plans, prospects, trends, or strategies and other financial and business matters, and the prospects for commercializing or selling any product or drug candidates. In addition, when or if used in this presentation, the words “may, ” “could, ” “should, ” “anticipate, ” “believe, ” “estimate, ” “expect, ” “intend, ” “plan, ” “predict” and similar expressions and their variants, as they relate to the Company may identify forward-looking statements. The Company cautions that these forward-looking statements are subject to numerous assumptions, risks, and uncertainties, which change over time. Important factors that may cause actual results to differ materially from the results discussed in the forward-looking statements or historical experience include risks and uncertainties, including risks relating to: the potential impact of Pemvidutide in the indications of Alcohol Use Disorder ("AUD") and Alcohol Liver Disease ("ALD") and associated treatment needs and development plan, potential impacts such as delays in regulatory review, manufacturing and supply chain interruptions, adverse effects on healthcare systems and disruption of the global economy, the timing and reliability of the results of the studies relating to human safety and possible adverse effects resulting from the administration of the Company’s product candidates; our lack of financial resources and access to capital; clinical trials and the commercialization of proposed product candidates (such as marketing, regulatory, product liability, supply, competition, dependence on third parties and other risks) including in the new indications of AUD and ALD; the timing of regulatory applications and the regulatory approval process; and, the dependence on intellectual property. Further information on the factors and risks that could affect the Company's business, financial conditions and results of operations are contained in the Company’s filings with the U.S. Securities and Exchange Commission, including under the heading “Risk Factors” in the Company’s annual reports on Form 10-K and quarterly reports on Form 10-Q filed with the SEC, which are available at www.sec.gov. The statements made herein speak only as of the date stated herein, and any forward-looking statements contained herein are based on assumptions that the Company believes to be reasonable as of this date. The Company undertakes no obligation to update these statements as result of new information or future events. 2
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R&D Day Agenda 3 Introduction Pemvidutide for MASH: Upcoming Phase 2b Readout Pemvidutide for Obesity and its Comorbidities Introducing Two Additional High-Impact Indications • Alcohol Use Disorder (AUD) • Alcohol Liver Disease (ALD) Summary Vipin Garg, PhD Chief Executive Officer Altimmune, Inc. Scott Harris, MD Chief Medical Officer Altimmune, Inc. Louis Aronne, MD Weill Cornell Medical College Mazen Noureddin, MD, MHSc Houston Methodist Hospital Rohit Loomba, MD, MHSc University of California San Diego Today’s Speakers Sarah Browne, MD Vice President, Clinical Development Altimmune, Inc. Henry Kranzler, MD University of Pennsylvania
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Introduction Vipin Garg, PhD Chief Executive Officer Altimmune, Inc.
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1:1 POTENCY OF GLP -1 AND GLUCAGON GLP-1 Direct Effects on GI & Brain Appetite Inflammation Cravings Compelling data to-date support continued development in multiple indications Clinically meaningful weight loss Class-leading lean mass preservation Rapid and robust liver fat reduction Significant reductions in serum lipids Vision: Treatment of Choice for Liver and Cardiometabolic Diseases Pemvidutide: Novel GLP-1/Glucagon Dual Receptor Agonist 5 Energy expenditure Lipolysis Mobilization of liver fat Glucagon Direct effects on Liver Lipolysis Mobilization of Fat Energy Expenditure
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Breaking New Ground in Addressing Major Unmet Medical NeedsIntroducing Two Additional High-Impact Indications Alcohol Use Disorder (AUD) Compelling therapeutic potential in this highly prevalent indication Alcohol Liver Disease (ALD) Exciting commercial opportunity in large, underserved patient population Breaking New Ground in Addressing Major Unmet Medical Needs 6
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Pemvidutide: Pipeline in a Product STATUS / UPCOMING MILESTONES* Successful EOP2 meeting 4Q 2024 IMPACT Phase 2b topline data 2Q 25 Phase 2 trial initiation 2Q 25 Phase 2 trial initiation 3Q 25 PRECLINICAL PHASE 1 PHASE 2 PHASE 3 7 Obesity MASH AUD ALD *expected dates
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Pemvidutide for Obesity and its Comorbidities Sanford I. Weill Professor of Metabolic Research and Director of the Comprehensive Weight Control Center, Division of Endocrinology, Diabetes & Metabolism, Weill Cornell Medicine Louis Aronne, MD, FACP
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US OBESITY RATES (1990- 2030) 1 <20% 20-29% 30-39% 40-49% 50-59% 1990 2030 Obesity: A Growing Epidemic Nearly Half of All Americans will have Obesity by 2030 9
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58-75% MASLD4,5,6 15-36% MASH4,5,7 66-70% Dyslipidemia2,3 45-55% Hypertension2,8 Most Significant Comorbidities Relate to Lipid and Liver Fat Disorders Managing Comorbidities is Essential to Treating Obesity 10
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Muscle Preservation Some therapies result in as much as 40% lean mass loss Improved Tolerability High rates of discontinuation with lengthy dose titration Enhanced Effects on Lipid and Liver Fat Reductions Opportunity to further improve cardiovascular (CV) benefits Obesity Drugs: Unmet Medical Needs 11
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** p < 0.01 vs. no hepatic steatosis Patients with Liver Steatosis are at Higher Risk for CV Events CV Events Over 36 Months9 Incidence of Composite MACE (%) No Hepatic Steatosis Hepatic Steatosis 70% increase in risk Liver fat associated with 70% increase in MACE, independent of other CV risk factors or extent of atherosclerosis MACE = Major Adverse Cardiac Events 12
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13 >15% Weight Loss >75% Liver Fat Reduction 15-20% LDL-C Reduction Pemvidutide: Designed to Address Major CV Risk Factors
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Pemvidutide: MOMENTUM Phase 2 Clinical Data Summary
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Potential to optimize treatment with three active doses Over 30% of subjects lost ≥ 20% of body weight on 2.4 mg dose Placebo Pemvidutide 1.2 mg Pemvidutide 1.8 mg Pemvidutide 2.4 mg MOMENTUM Phase 2 Trial: Robust Weight Loss at All Doses 15 15 10 5 0 -5 -10 -15 -20 -25 -30 -35 Change in Weight from Baseline (%) 15 10 5 0 -5 -10 -15 -20 -25 -30 -35 15 10 5 0 -5 -10 -15 -20 -25 -30 -35 Change in Weight from Baseline (%) 15 10 5 0 -5 -10 -15 -20 -25 -30 -35
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Drug Study Study Duration Lean Loss Ratio Pemvidutide MOMENTUM Phase 2 48 weeks 21.9%10 Semaglutide STEP-1 Phase 3 68 weeks 39.9%11 Tirzepatide SURMOUNT 1 Phase 3 72 weeks 26.0% 11 Retatrutide Obesity Phase 2 36 weeks 37.7%12 Lean Loss Ratio = Lean Loss (kg)/Total Loss (kg) Pemvidutide: Improved Quality of Weight Loss Class-leading Lean Mass Preservation Preferential Loss of Visceral Fat Subcutaneous Fat Visceral Fat -40 -30 -20 -10 0 -28.3% -15.6% -20.4% -8.8% LS Mean Change from Baseline (% ± SE) ** * placebo N=17 1.2 mg N=18 1.8 mg N=15 2.4 mg N=17 pemvidutide -40 -30 -20 -10 0 -19.5% -13.0% -11.5% -4.7% LS Mean Change from Baseline (% ± SE) placebo N=17 1.2 mg N=18 1.8 mg N=15 2.4 mg N=17 pemvidutide ** * p < 0.05 | ** p < 0.005 vs. placebo (analysis of covariance; ANCOVA) Visceral fat is a CV risk factor Note: These data are derived from different clinical trials at different points in time, with differences in trial design and patient populations. As a result, cross-trial comparisons cannot be made, and no head-to-head clinical trials have been conducted. 16
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Enhanced Lipid Reductions in Subjects with Elevated Baseline Levels Triglycerides > 150 mg/dL at Baseline Total Cholesterol > 200 mg/dL at Baseline LDL > 130 mg/dL at Baseline * p < 0.05 | ** p < 0.005 | *** p < 0.001 vs. placebo (ANCOVA) -80 -70 -60 -50 -40 -30 -20 -10 0 -55.8% -33.1% -36.3% -13.1% LS Mean Change from Baseline (% ± SE) * * *** placebo N=17 1.2 mg N=22 1.8 mg N=19 2.4 mg N=21 pemvidutide -30 -20 -10 0 -20.0% -18.5% -14.8% -4.4% ** *** *** placebo N=23 1.2 mg N=35 1.8 mg N=27 2.4 mg N=25 pemvidutide 17 -40 -30 -20 -10 0 ** * placebo N=15 1.2 mg N=22 1.8 mg N=21 2.4 mg N=17 pemvidutide -2.4% -12.1% -21.8% -17.4%
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Robust weight loss with continued linear weight loss trajectory on 2.4 mg at Week 48 Quality of Weight Loss Class-leading lean mass preservation Weight Loss Serum Lipids and Liver Fat Significant reductions in risk factors for CV disease Active dose without titration, ideal for PCP setting Tolerability Gastrointestinal adverse event rates similar to other incretin agents Dose Titration Safety No MACE events, no imbalances in cardiac arrythmias across treatment groups, no CV safety study required Pemvidutide: Differentiated Profile for the Treatment of Obesity and its Comorbidities 18
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Pemvidutide for MASH: Upcoming Phase 2b Data Readout Professor of Medicine, Lynda K. and David M. Underwood Center for Digestive Disorder Department of Medicine, Sherrie and Alan Conover Center for Liver Disease & Transplantation, Houston Methodist Hospital Mazen Noureddin, MD, MHSc
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The Rising Prevalence of MASH . . 16.5M 27.5M 0 5 10 15 20 25 30 2015 2030 Prevalence (M) 63% increase Projected MASH Prevalence in the US (2030)13 Projected MASH Prevalence by Stage (2030)13 3.9M 9.0M 6.1M 4.5M 3.5M 20 F0 F1 F2 F3 F4
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1 Significant Comorbidities Associated with MASH Addressing Comorbidities Essential for Comprehensive MASH Treatment14 21
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Projected Liver and CV-Related 10-year Mortality in F2/F3 MASH15 1.0% 4.0% 5.2% 9.7% 0.0% 2.0% 4.0% 6.0% 8.0% 10.0% 12.0% 14.0% 16.0% F2 F3 Liver-Related Mortality CV-Related Mortality 22 Ideal MASH Therapy Would Address Both Liver and CV Disease Cumulative 10 Year Mortality
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MASH Resolution Fibrosis Improvement Both Endpoints 0 10 20 30 40 50 60 70 Liver Fat Reduction Drives MASH Improvement16 Weight Loss Benefits MASH Outcomes17 Response Rate (%) > 50% reduction > 30% reduction < 30% reduction Liver Fat Reduction and Weight Loss are Critical to Effective MASH Treatment 23 0 10 20 30 40 50 60 70 80 90 100 Weight Loss Proportion of Patients (%) Regressed Stabilized Worsened < 5% ≥ 10% 10% 45% 45% 81% 19% Proportion of Patients (%) Regressed Stabilized Worsened
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Pemvidutide: MASLD Phase 1b Clinical Data Summary
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0 10 20 30 40 50 60 70 80 90 100 0% 30.8% 53.8% 45.5% 0% 61.5% 84.6% 72.7% 5.6% 76.9% 92.3% Proportion of Subjects (%) 0.0% placebo N=18 1.2 mg N=14 1.8 mg N=13 2.4 mg N=11 pemvidutide 0.0% 100.0% placebo N=18 1.2 mg N=14 1.8 mg N=13 2.4 mg N=11 pemvidutide placebo N=18 1.2 mg N=14 1.8 mg N=13 2.4 mg N=11 pemvidutide **** **** **** *** **** **** *** ** * Pemvidutide: Up to 76.4% Reduction of Liver Fat Relative Reduction at Week 24 Responder Analyses at Week 24 *** p < 0.001 vs. placebo (ANCOVA) * p < 0.05 | ** p < 0.005 | *** p < 0.001 | **** p < 0.0001 vs. placebo (Cochran-Mantel-Haenszel; CMH) 50% Reduction Normalization (≤5% LFC) 30% Reduction 0 10 20 30 40 50 60 70 80 90 14.0% 56.3% 75.2% 76.4% LS Mean Change from Baseline (% ± SE) *** *** *** placebo N=18 1.2 mg N=14 1.8 mg N=13 2.4 mg N=11 pemvidutide 25
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PEMVIDUTIDE 1.8 mg 95% relative reduction in liver fat in a patient with high liver fat (normalization within 24 weeks) Baseline 32.3% Week 24 1.7% MASLD Ph1b Case Example: Near Complete De-Fatting of Liver with Pemvidutide 26 PDFF %
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ALT Reductions 27 -40 -30 -20 -10 0 -2.2 -13.3 -13.7 -15.2 -3.1 -17.0 -17.7 -20.6 LS Mean Change from Baseline (IU/L ± SE) pemvidutide ** ** ** placebo N=19 1.2 mg N=16 1.8 mg N=15 2.4 mg N=14 pemvidutide placebo N=13 1.2 mg N=7 1.8 mg N=10 2.4 mg N=9 * * * * p < 0.05 | ** p < 0.005 vs. placebo (mixed model for repeated measures; MMRM) All Subjects Subjects w/ Baseline ALT ≥ 30IU/L Significant Reduction in ALT, a Marker of Liver Inflammation
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cT1: A Marker of Increased CV Risk Elevated cT1 is associated with an increased Hazard Ratio (HR) for CV events18 cT1 is an MRI-derived biomarker of liver disease activity; data from UK Biobank 800 ms = upper limit of normal cT1 Relaxation Time (ms) HR (95% CI) Range Cardiovascular Events: Hospitalization 1.27 1.18-1.37 Atrial Fibrillation 1.3 1.12-1.51 Heart Failure 1.3 1.08-1.58 Any Cardiac Event 1.14 1.03-1.26 All-cause Mortality 1.19 1.02-1.38 28 cT1 Responder Rates at Week 12 ** p < 0.005 | *** p < 0.001 vs. placebo (CMH) 0 10 20 30 40 50 60 70 80 90 100 85.7%83.3% 87.5% 0% Proportion of Subjects with 80 ms Reduction in cT1 (%) ******** 0.0% placebo N=11 1.2 mg N=8 1.8 mg N=6 2.4 mg N=7 pemvidutide Sub-study analysis cT1 signal is reduced in over 80% of subjects
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Magnitude of Liver Fat Reduction Correlates with MASH Resolution & Fibrosis Improvement Level of Liver Fat Reduction19 > 50% reduction > 30% reduction < 30% reduction MASH Resolution Fibrosis Improvement Both Endpoints Response Rate (%) >75% liver fat reduction at week 24 Pemvidutide 29
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Class-Leading Liver Fat Reduction among MASH Agents Pbo 28 mg 50 mg Pbo 30 mg (QW) 44 mg (Q2W) Pbo 4.8 mg 6.0 mg Pbo 2.5 mg (QD) 10 mg (QOD) Pbo 80 mg 100 mg Pbo 1.2 mg 1.8 mg 2.4 mg Note: These data are derived from different clinical trials at different points in time, with differences in trial design and patient populations. As a result, cross-trial comparisons cannot be made, and no head-to-head clinical trials have been conducted. Sema 1 mg 10 mg Pemvidutide QW (GLP-1/GCG) 24wk Phase 1b Efruxifermin QW (FGF21) 24wk Phase 2b Efinopegdutide QW (GLP-1/GCG) 24wk Phase 2a Survodutide QW (GLP-1/GCG) 48wk Phase 2 Semaglutide QD* (GLP-1) 48wk Phase 1 Resmetirom QW (THR-β) 52wk Phase 3 Pegozafermin QW & Q2W (FGF21) 24wk Phase 2b VK2809 QD & QOD (THR-β) 52wk Phase 2b Pbo 0.4 mg* Please see Appendix for data sources 30 Tirzepatide QW (GLP-1/GIP) 52wk Phase 2 Pbo 10 mg 15 mg
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Pemvidutide has the Potential to be a Complete Solution for MASH Liver Effect Weight Loss Pemvidutide 1:1 GLP-1/Glucagon Optimal Therapeutic Effect GLP-1/GIP THR-β FGF21 31 Significant weight loss, modest liver effect Insignificant weight loss, modest liver effect Rapid liver effects, insignificant weight loss
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Pemvidutide: IMPACT Phase 2b Topline Data Readout 2Q 2025
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33 1.2 mg weekly (N~38) 1.8 mg weekly (N~76) Key endpoints Primary MASH resolution and fibrosis improvement Secondary Weight Loss (WL) Noninvasive tests (NITs) Placebo weekly (N~76) Week48 WL/NITs IMPACT Phase 2B Biopsy-driven F2/F3 MASH Trial Topline Data 2Q 2025 Week24 Liver Biopsy/WL/NITs Screening/Randomization
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IMPACT Phase 2b Trial: Designed for Success 34 34 Large Sample Size Greater Liver Fat Reduction Biopsy Re-Reads and the use of 3 Readers Increased Study Power Greater Biopsy Responses Minimize the Placebo Response
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Pemvidutide: A Foundational Therapy for MASH 35 If successful, pemvidutide would become: The first incretin-based agent to achieve statistical significance on fibrosis improvement at 24 weeks The first therapeutic candidate in any class to achieve statistically significant fibrosis improvement AND meaningful weight loss at 24 weeks
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Q&A Vipin Garg, PhD Chief Executive Officer Altimmune, Inc. Scott Harris, MD Chief Medical Officer Altimmune, Inc. Louis Aronne, MD Weill Cornell Medical College Mazen Noureddin, MD, MHSc Houston Methodist Hospital Rohit Loomba, MD, MHSc University of California San Diego Henry Kranzler, MD University of Pennsylvania
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Pemvidutide: Compelling Opportunities in Additional Indications Scott Harris, MD Chief Medical Officer Altimmune, Inc.
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Pemvidutide Treatment Could Halt Progression of AUD to ALD Up to 28.1M patients have AUD20 AUD5+/day First-in-class candidate in development to address alcohol misuse and liver inflammation, with added promise of weight loss Pemvidutide: Positioned to Address Significant Unmet Needs in AUD & ALD 38 Up to 6.6M patients have ALD21 ALD
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Pemvidutide: Attractive Profile for Both Physicians and Patients 75% of HCPs very likely to prescribe pemvidutide (N=24) HCPs are eager to prescribe… 84% of patients with AUD and ALD would use if prescribed (N=200) …and patients are ready to start Product profile demonstrating reductions in alcohol craving and liver inflammation was compelling to HCPs and patients Weight loss and serum lipid improvements viewed as additional positive attributes 39Altimmune-sponsored third-party market research
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Phase 2b Topline Results Q2 2025 MASH Phase 2 Start Q2 2025 AUD Phase 2 Start Q3 2025 ALD Obesity impacts the progression of MASH and ALD22 Alcohol impacts the progression of MASH, AUD and ALD23 Pemvidutide: Optimized for Steatotic Liver Diseases and their Primary Causes 40
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Pemvidutide: Alcohol Use Disorder (AUD) Henry Kranzler, MD Karl E. Rickels Professor of Psychiatry; Director, Center for Studies of Addiction University of Pennsylvania Perelman School of Medicine Breaking Barriers to Treatment
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0 5 10 15 20 25 30 Prevalence (M) Only 2.0% of patients drug-treated AUD Population Treated Drug-treated 28.1M 552K2.2M AUD: One of the Largest Known Healthcare Treatment Gaps20 42
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Alcohol Use Disorder (AUD) Only 3 approved medications, which are decades old Many limitations with current treatment options Poor treatment compliance with current therapies Opportunity to Address Cravings, Improve Liver Health and Promote Weight LossAUD Field is Ripe for Innovation 43
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Surgeon General Advisory January 2025 AUD: Significant Societal Burden 7th Leading cause of death and disability globally due to alcohol24 $249B Total cost of alcohol misuse in the US in 201025 44 Alcohol is 3rd leading cause of preventable cancer after tobacco and obesity
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In addition to managing underlying alcohol misuse patients with AUD require therapies to address comorbidities Cardiometabolic Comorbidities 66% are overweight or have obesity27 90% will develop liver steatosis 26 45% have hypertension 28 23% have hyperlipidemia 28 AUD Patients Have Significant Comorbidities 45
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Decades Since Last Approved AUD Medication Disulfiram (Antabuse®) 1949 Naltrexone (Revia®) Naltrexone ER (Vivitrol®) Acamprosate (Campral®) 1994 2004 2006 Limitations of Current Agents Administration and compliance challenges Small effect size Fail to improve other important risk factors (e.g., metabolic / obesity) Lack of Innovation and High Burden of Disease Create Major Unmet Need 46
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Pemvidutide Suppresses Alcohol Intake in Preclinical Model vehicle Hamster Free-Choice Model 0 2 4 6 8 10 12 14 16 18 20 0 10 20 30 40 50 60 70 80 90 100 Day % Alcohol Intake per Day (Alcohol/Total Volume) pemvidutide 10 nmol/kg 47Water and 15% ethanol solution
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Pemvidutide: Phase 2 AUD Trial Design Randomized, double-blind, placebo-controlled trial of ~ 100 subjects with obesity and moderate to severe AUD according to DSM-5 48 Screening/Randomization Key endpoints Primary Change in heavy drinking days Week 24 Secondary Change in biomarkers of alcohol consumption Weight loss placebo weekly (N~50) Week 1 4 Weeks 4 Weeks 1.2 mg 1.8 mg 2.4 mg weekly (N~50)
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Pemvidutide: Alcohol Liver Disease (ALD) A Critical Health Challenge Professor of Medicine, Chief, Division of Gastroenterology and Hepatology Director, MASLD Research Center, University of California at San Diego Rohit Loomba, MD, MHSc
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50 Result of chronic, excessive alcohol use Similar to MASH, disease progression begins with liver steatosis, which may lead to fibrosis, and ultimately cirrhosis Patients have high rates of progression to cirrhosis Complications of ALD can lead to high short-term morbidity/mortality ALD is Caused by Alcohol Misuse Alcohol Liver Disease
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51 Alcohol Liver Disease Up to 6.6 million Americans affected by ALD No approved treatments; few in development Obesity significantly accelerates disease progression and leads to worse outcomes ALD: Critical Need for Drugs that Improve Liver Health and Reduce Alcohol Consumption
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Obesity Potentiates Alcohol-Related Liver Mortality22 0 2 4 6 8 10 12 14 16 18 20 Baseline (B) B + Obesity (O) B + O + Alcohol Interaction Relative Risk 17.3 10 1.91 For heavy drinkers, increasing BMI increases all-cause disease mortality Baseline Risk Excess Obesity Risk Excess Alcohol Risk Excess Interaction Risk Obesity Significantly Increases Risk of Poor Alcohol- Related Liver Outcomes 52
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Relative Liver Fat Reduction at Week 24 Improved Liver Inflammation cT1 Responder Rates at Week 24 Significant Reductions in ALT Subjects w/ Baseline ALT ≥ 30IU/L *** p < 0.001 vs. placebo (ANCOVA) * p < 0.05 | ** p < 0.005 vs. placebo (Fisher’s Exact Test) * p < 0.05 vs. placebo (MMRM) Placebo 1.2 mg Pemvidutide 1.8 mg Pemvidutide 2.4 mg Pemvidutide Rationale for Use in ALD: Fat-Associated Inflammation Drives both MASH and ALD 0 10 20 30 40 50 60 70 80 90 100 0% 85.7% 75.0% Proportion of Subjects (%) 100.0% ** * * placebo N=6 1.2 mg N=7 1.8 mg N=4 2.4 mg N=2 pemvidutide 0.0% 0 10 20 30 40 50 60 70 80 90 14.0% 56.3% 75.2% 76.4% LS Mean Change from Baseline (% ± SE) *** *** *** placebo N=18 1.2 mg N=14 1.8 mg N=13 2.4 mg N=11 pemvidutide -40 -30 -20 -10 0 -3.1 -17.0 -17.7 -20.6 LS Mean Change from Baseline (IU/L ± SE) * * * placebo N=13 1.2 mg N=7 1.8 mg N=10 2.4 mg N=9 pemvidutide 53
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Pemvidutide: Phase 2 ALD Trial Design 54 Screening/Randomization Other Key Endpoints Weight loss Change in alcohol consumption 4 Weeks 4 Weeks 1.2 mg 1.8 mg 2.4 mg weekly (N~50) placebo weekly (N~50) Randomized, double-blind, placebo-controlled trial of ~ 100 subjects with obesity and ALD Week48Week24 Key eligibility Primary Endpoints Change in LSM Additional Endpoints Change in LSM Weight loss Change in alcohol consumption • Liver Stiffness Measurement (LSM) (10 to ≥ 18.5 kPa) • BMI ≥ 25 kg/m2 • Heavy alcohol consumption
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Pemvidutide Could Integrate AUD/ALD Care Current Treatment Paradigm Potential Future Treatment Paradigm AUD Patient ALD Patient AUD Patient ALD Patient 55 Pemvidutide unifies treatment Streamlined management across specialties, including PCPs Holistic treatment of AUD, ALD, and associated cardiometabolic conditions Treatment limited No approved treatments Managed by addiction specialist Managed by liver specialist ALD goes untreated AUD goes untreated
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Pemvidutide Vision: A Transformational Therapy Across Related Diseases 56 Designed to cover the spectrum of steatotic liver disease and its primary causes MASH ALD AUDObesity
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Q&A Vipin Garg, PhD Chief Executive Officer Altimmune, Inc. Scott Harris, MD Chief Medical Officer Altimmune, Inc. Louis Aronne, MD Weill Cornell Medical College Mazen Noureddin, MD, MHSc Houston Methodist Hospital Rohit Loomba, MD, MHSc University of California San Diego Sarah Browne, MD Vice President, Clinical Development Altimmune, Inc. Henry Kranzler, MD University of Pennsylvania
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Altimmune R&D Day Summary Vipin Garg, PhD Chief Executive Officer Altimmune, Inc.
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Milestones and Near-Term Catalysts Q2NOV Successful FDA EOP2 meeting for obesity Q4 File INDs in AUD and ALD Q2 Q4Q3 H1 2026: Initiate MASH Phase 3 Registrational Trial 2024 2025 Initiate Phase 2 AUD trial IMPACT Phase 2b 24-week topline data Initiate Phase 2 ALD trial FDA EOP2 meeting for MASH 59
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A Complete Solution MASH AUD ALD Pemvidutide Vision: Transformational Therapy Across Multiple Indications 60 Treating the Comorbidities OBESITY Major Cause of Liver Damage No Approved Therapies
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Thank You
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Appendix: References 1. Ward ZJ et al. Projected US State-Level Prevalence of Adult Obesity and Severe Obesity. N Engl J Med. 2019;381:2440-50. doi: 10.1056/NEJMsa1909301 2. Bays, Harold, et. al. (2013) Obesity, adiposity, and dyslipidemia: A consensus statement from the National Lipid Association. Journal of Clinical Lipidology 7(4):304–383 3. Lim Y, Boster J. Obesity and Comorbid Conditions. [Updated 2023 Feb 8]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; https://www.ncbi.nlm.nih.gov/books/NBK574535/ 4. Quek, Jingxuan, et. al. (2023) Global prevalence of non-alcoholic fatty liver disease and non-alcoholic steatohepatitis in the overweight and obese population:. The Lancet Gastroenterology & Hepatology 8(1):20-30. 5. Vernon, G, et. al. (2011) Systematic review: the epidemiology and natural history of non-alcoholic fatty liver disease and non-alcoholic steatohepatitis in adults. Aliment Pharmacol Ther 34:274–285. 6. Le, Michael, et. al. (2022) 2019 Global NAFLD Prevalence: A Systematic Review and Meta-analysis. Clinical Gastroenterology and Hepatology 2022;20:2809–2817 7. Dufour, Jean-François, et. al. (2021) The global epidemiology of nonalcoholic steatohepatitis (NASH) and associated risk factors–A targeted literature review. Endocrine and Metabolic Science 3. 8. Pantalone KM, et al. Prevalence and recognition of obesity and its associated comorbidities. BMJ Open 2017;7:e017583. doi:10.1136/ bmjopen-2017-017583 9. Adapted from Meyersohn et al. Association of Hepatic Steatosis with Major Adverse Cardiovascular Events, Independent of Coronary Artery Disease. Clin Gastroenterol Hepatol. 2021 July; 19(7): 1480-1488 https://pmc.ncbi.nlm.nih.gov/articles/PMC7855524/pdf/nihms-1614732.pdf 10. Pemvidutide data from MRI MOMENTUM sub-study 11. Harris C, Obesity Week 2023 12. Wilding JPH. N Engl J Med. 2021 Mar 18;384(11):989-1002 13. Estes C, et. al. Modeling the epidemic of nonalcoholic fatty liver disease demonstrates an exponential increase in burden of disease. Hepatology. 2018 Jan;67(1):123-133. doi: 10.1002/hep.29466 14. Younossi et al. (2016) North America Prevalence. Hepatology 64(1):73 Supplement (http://onlinelibrary.wiley.com/doi/10.1002/hep.28431/suppinfo) 15. Chattwal et al. Analysis of a Simulation Model to Estimate Long-term Outcomes in Patients with Nonalcoholic Fatty Liver Disease. JAMA Network Open. 2022;5(9):e2230426. doi:10.1001/jamanetworkopen.2022.30426 16. Adapted from Loomba, European Association for the Study of the Liver, International Liver Conference, 2020, analysis of Phase 2 resmetirom study (Harrison SA, Lancet 2019) 17. Adapted from Vilar-Gomez et al. Weight Loss Through Lifestyle Modification Significantly Reduces Features of Nonalcoholic Steatohepatitis. Gastroenterology 2015;149:367-378 18. Roca-Fernandez. (2023) Liver disease is a significant risk factor for cardiovascular outcomes – A UK Biobank study. Journal of Hepatology Volume 79 Issue 5 Pages 1085-1095 19. Adapted from Loomba, European Association for the Study of the Liver, International Liver Conference, 2020, analysis of Phase 2 resmetirom study (Harrison SA, Lancet 2019) Slide 30 Data Sources: • Pemvidutide: Phase 1b NAFLD Study Topline Results Extension • Efinopegdutide: EASL Congress 2023, Manuel Romero-Gomez Presentation • Efruxifermin: Harrison et al. “Safety and efficacy of once-weekly efruxifermin versus placebo in non-alcoholic steatohepatitis (HARMONY): a multicentre, randomised, double-blind, placebo-controlled, phase 2b trial.” The lancet. Gastroenterology & hepatology vol. 8,12 (2023): 1080-1093. doi:10.1016/S2468-1253(23)00272-8 • Survodutide: Sanyal, Arun J et al. “A Phase 2 Randomized Trial of Survodutide in MASH and Fibrosis.” The New England journal of medicine vol. 391,4 (2024): 311-319. doi:10.1056/NEJMoa2401755 • Tirzepatide: Loomba et al. “Tirzepatide for Metabolic Dysfunction-Associated Steatohepatitis with Liver Fibrosis.” The New England journal of medicine vol. 391,4 (2024): 299-310. doi:10.1056/NEJMoa2401943 • Semaglutide: Flint et al. “Randomised clinical trial: semaglutide versus placebo reduced liver steatosis but not liver stiffness in subjects with non-alcoholic fatty liver disease assessed by magnetic resonance imaging.” Alimentary pharmacology & therapeutics vol. 54,9 (2021): 1150-1161. doi:10.1111/apt.16608 • VK2809: Company Release June 3, 2024 • Pegozafermin: Corporate Presentation March 2025 • Resmetirom: Harrison et al. “A Phase 3, Randomized, Controlled Trial of Resmetirom in NASH with Liver Fibrosis.” The New England journal of medicine vol. 390,6 (2024): 497-509. doi:10.1056/NEJMoa2309000 62
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Appendix: References (Cont’d) 20. SAMHSA 2023 NSDUH Survey 21. Calculated based on Amonker S, et. al. Hepatol Commun. 2023;7:e0133. https://doi.org/10.1097/HC9.0000000000000133 22. Patra et al. Impact of body mass and alcohol consumption on all-cause and liver mortality in 240,000 adults in the United States. Drug and Alcohol Review (September 2021), 40, 1061–1070 23. Desalegn et al. Impact of alcohol use on liver disease outcomes. Clinical Liver Disease. 2024;23:e0192. 24. GBD 2016 Alcohol Collaborators. Lancet 2018; 392: 1015–35 25. https://www.hhs.gov/surgeongeneral/reports-and-publications/alcohol-cancer/index.html 26. Osna et al. Alcoholic Liver Disease: Pathogenesis and Current Management. Alcohol Research Current Reviews 27. Raza et al. Burden of high-risk phenotype of heavy alcohol consumption among obese US population: results from NHANES 1999-2020. Lancet Vol 23, July, 2023 28. AshaRani PV, et.al. Prevalence and Correlates of Physical Comorbidities in Alcohol Use Disorder (AUD): a Pilot Study in Treatment-Seeking Population. Int J Ment Health Addict. 2022 Jan 23:1-18 63