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Corporate Presentation February 9, 2026
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© 2026 Enanta Pharmaceuticals, Inc. | This presentation contains forward-looking statements concerning our business, operations and financial performance and condition, as well as our plans, objectives and expectations for our research and development programs, our business and the industry in which we operate. Any statements contained herein that are not statements of historical facts may be deemed to be forward-looking statements. In some cases, you can identify forward-looking statements by terminology such as “aim,” “anticipate,” “assume,” “believe,” “contemplate,” “continue,” “could,” “due,” “estimate,” “expect,” “goal,” “intend,” “may,” “objective,” “plan,” “predict,” “potential,” “positioned,” “seek,” “should,” “target,” “will,” “would,” and other similar expressions that are predictions of or indicate future events and future trends, as well as other comparable terminology. These forward-looking statements include, but are not limited to, statements about overall trends, royalty revenue trends, research and clinical development plans and prospects, liquidity and capital needs and other statements of expectations, beliefs, future plans and strategies, anticipated events or trends, and similar expressions. These forward-looking statements are based on our management’s current expectations, estimates, forecasts and projections about our business and the industry in which we operate and our management’s beliefs and assumptions. These forward-looking statements are not guarantees of future performance or results and involve known and unknown risks, uncertainties and other factors that are in some cases beyond our control. As a result, any or all of our forward-looking statements in this presentation may turn out to be inaccurate. Please refer to the risk factors described or referred to in “Risk Factors” in Enanta’s most recent Annual Report on Form 10-K, and other periodic reports filed with the Securities and Exchange Commission. Enanta cautions investors not to place undue reliance on the forward-looking statements contained in this presentation. These statements speak only as of the date of this presentation, and Enanta undertakes no obligation to update or revise these statements, except as may be required by law. Forward Looking Statements Disclaimer 2
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© 2026 Enanta Pharmaceuticals, Inc. | Enanta Overview 3 Clinical-stage biotechnology company dedicated to creating small molecule drugs for virology & immunology indications STRONG CASH POSITION • Ongoing HCV royalties • $241.9M in cash at December 31, 2025 2 products approved with 3 Clinical-stage 3 Preclinical Founded: 1995 Public: 2013 WHOLLY OWNED PROGRAMS 3 CURED >1 million patients with Hepatitis C Virus All compounds discovered in house, leveraging deep expertise in medicinal chemistry, drug discovery & development
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© 2026 Enanta Pharmaceuticals, Inc. | *Fixed-dose antiviral combination contains glecaprevir and AbbVie's NS5A inhibitor, pibrentasvir. Marketed by AbbVie as MAVYRET® (U.S.) and MAVIRET® (ex-U.S.). **Continued development dependent on a future collaboration. ***Initial indications. Potential future indications include asthma, chronic inducible urticaria (CIndU), eosinophilic esophagitis (EoE); prurigo nodularis (PN), migraine and others. DISEASE TARGET DISCOVERY PRECLINICAL PHASE 1 PHASE 2 PHASE 3 MARKET Virology: Liver Hepatitis C Virus Protease Virology: Respiratory Respiratory Syncytial Virus N-Protein L-Protein COVID-19 3CL Protease Immunology: Type 2 Immune Diseases*** Chronic Spontaneous Urticaria (CSU) KIT Atopic Dermatitis (AD) STAT6 CSU/AD MRGPRX2 Zelicapavir High-Risk Adults EDP-235** SPRINT Zelicapavir Pediatrics Glecaprevir* Enanta Pipeline 4 EPS-3903 EDP-978 EDP-323 (challenge study)
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Virology: Respiratory Syncytial Virus
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© 2026 Enanta Pharmaceuticals, Inc. | RSV Burden Estimates2 (2024 - 2025 U.S.) Respiratory Syncytial Virus (RSV) 6 Causes severe lung infections, including bronchiolitis (infection of small airways in the lungs) and pneumonia. Leading cause of hospitalization in infants.1 No safe and effective treatments are currently approved. 1. CDC RSV In Infants and Young Children. 2. CDC Preliminary Estimates of RSV Burden for 2024-2025; for period: 10/1/24-9/27/25 3. Terlizzi EP et al. NCHS Data Brief. 2020; Age 60+ 4. CDC Influenza Vaccination Coverage, Adults 65+ Populations at higher risk for severe illness • Pediatrics (infants and young children) • High-risk adults (e.g.; >65 yrs, COPD, asthma, CHF) • Immunocompromised (e.g.; HIV, transplant) up to 6.8M up to 370K up to 24K Outpatient visits Hospitalizations Deaths Significant Unmet Need for Antivirals • Adult vaccines have sub-optimal adoption – Not recommended for all FDA-approved patient groups – Vaccine adoption for elderly: ~35% (shingles3) to <50% (flu4) • Pediatric prophylaxis only provides passive immunity; will shift first infection to next season – Antibody approach has a low barrier to resistance • Breakthrough infections can occur despite prophylaxis Growing Momentum for RSV Diagnosis, Enabling a Test-to-Treat Model
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© 2026 Enanta Pharmaceuticals, Inc. | Zelicapavir High-Risk Adult Phase 2b Study Age ≥65 years Chronic heart or lung disease (e.g. COPD, CHF, asthma) Positive Phase 2b Results Zelicapavir Pediatric Phase 2 Study Infants and young children Positive Phase 2 Results RSV Development Goal: Treatment for Patients at High-Risk for Severe RSV Infection 7 Leading portfolio of RSV replication inhibitors with potential for first-in-disease (zelicapavir) and best-in-disease (EDP-323) treatments and ability for combination High-risk populations have reduced RSV immunity, resulting in a higher and longer duration of viral load and greater disease severity
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© 2026 Enanta Pharmaceuticals, Inc. | • Only N-inhibitor in clinical development for RSV – Replication inhibitor: shuts down the production of new virions (vs. fusion inhibitors which block viral entry) • Granted Fast Track designation by the FDA • Strong preclinical profile – Nanomolar potency against RSV-A and RSV-B – Antiviral potency across all clinical isolates tested – High barrier to resistance – Synergistic activity and no cross-resistance with other drug mechanisms (e.g. L-inhibitors) • Favorable safety and efficacy profile in clinical studies – Challenge study showed statistically significant (p<0.001) reduction in viral load and clinical symptoms – Well-tolerated in more than 700 people dosed Zelicapavir (EDP-938): N-Protein Inhibitor for RSV 8 RSV
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© 2026 Enanta Pharmaceuticals, Inc. | • Primary Objective: Time to resolution** of RSV LRTD symptoms (RiiQTM symptom scale) – Shortness of breath, wheezing, coughing, coughing up phlegm • Secondary Objectives: PROs, MAVs, virology, antibiotic use, bronchodilator use, corticosteroid use, hospitalization, ICU, mechanical ventilation, all cause mortality, PK & safety Zelicapavir Phase 2b High-Risk Adult Study: Design & Objectives 9 Double-Blind Treatment Phase 5 days Placebo (QD) 800mg (QD)* Day 1 Day 33Day 5 186 adults with at least one of the following: • COPD • Congestive heart failure • Asthma • Age ≥65 28 Day Follow-up *Equivalent to 600mg suspension dosage form used in challenge study; **Resolution: all symptoms mild or absent COPD: chronic obstructive pulmonary disease; LRTD: lower respiratory tract disease; PROs: patient reported outcomes; MAVs: medically attended visits; ICU: intensive care unit; PK: pharmacokinetics; QD: once-daily • Patients enrolled within 72 hours of symptom onset • Proportion of patients aged 65-74 years or those with asthma capped at 20% of the total population HR3 = ~80% of the population with CHF, COPD, or age >75 First proof-of-concept Phase 2 high-risk adult outpatient study with positive clinical signal
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© 2026 Enanta Pharmaceuticals, Inc. | Zelicapavir Phase 2b High-Risk Adult Study: Faster Time to Complete Symptom Resolution Across Multiple RiiQ Measures 10 13.0 16.0 18.9 15.0 18.9 21.012.5 13.8 15.3 12.0 12.2 13.8 0 2 4 6 8 10 12 14 16 18 20 LRTD 4 Symptoms All RSV 13 Symptoms Total RiiQ 29 Parameters LRTD 4 Symptoms All RSV 13 Symptoms Total RiiQ 29 Parameters Placebo Zelicapavir 3.0d (20%) 3.6d (19%) Median days to complete symptom resolution by RiiQ 2.2d (14%) 6.7d (35%) 0.5d (4%) Efficacy Population HR3 Population* *HR3 Population: Patients with CHF, COPD, or age >75; LRTD: lower respiratory tract disease 7.2d (34%)
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© 2026 Enanta Pharmaceuticals, Inc. | Symptoms Measured by RiiQ • Faster time to complete resolution of all RSV symptoms to absent – About a week reduction in the HR3 population (for all 13 RSV symptoms and total RiiQ) • No effect on time to resolution of RSV symptoms to mild, including primary endpoint (time to resolution of LRTD subset of symptoms to mild in the efficacy population) • Improvement in RSV 13-symptom score* in HR3 population – Day 9 (p=0.0403) and Day 14 (p=0.0247) Symptom Resolution Measured by PGI-S • 2-day faster median time to improvement in efficacy (p=0.0446) and HR3 population (p=0.0465) Zelicapavir Phase 2b High-Risk Adult Study: Symptom Summary for Zelicapavir Compared to Placebo 11 *post-hoc analysis RiiQ: Respiratory Infection Intensity and Impact Questionnaire; PGI-S: Patient Global Impression of Severity; HR3 Population: Patients with CHF, COPD, or age >75; LRTD: lower respiratory tract disease
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© 2026 Enanta Pharmaceuticals, Inc. | • Lower hospitalization rate for patients treated with zelicapavir • One death on placebo; no deaths on zelicapavir Zelicapavir Phase 2b High-Risk Adult Study: Hospitalization and Death Endpoints 12 Placebo Zelicapavir All-cause-hospitalizations 5.0% (3/60) 1.7% (2/115) RSV-associated hospitalizations* • Investigator attribution • Post-hoc attribution 5.0% (3/60) 5.0% (3/60) 0% (0/115) 0.9% (1/115) *72yo man on zelicapavir was hospitalized on study day 21 for influenza infection after RSV symptoms had completely resolved on day 11; Investigator and Enanta deemed hospitalization not related to RSV *74yo woman on zelicapavir was hospitalized on study day 7 for infective exacerbation of asthma; Investigator deemed hospitalization not related to RSV; Enanta deemed hospitalization related to RSV
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© 2026 Enanta Pharmaceuticals, Inc. | Zelicapavir Phase 2b High-Risk Adult Study: Virology Results for Zelicapavir Compared to Placebo 13*HR3 Population: Patients with CHF, COPD, or age >75 • Larger viral load decline at the end of treatment (Day 5) – Efficacy Population: 0.6 log – HR3 population: 0.7 log • Greater proportion of patients with undetectable viral load at the end of treatment – Efficacy Population: 23.5% (27/115) vs 10.0% (6/60) (p=0.0198) – HR3 Population: 23.9% (22/92) vs 10.0% (5/50) (p=0.0292) • Faster median time to undetectable viral load – Efficacy Population: 4 days – HR3 Population: 5 days
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© 2026 Enanta Pharmaceuticals, Inc. | • Zelicapavir demonstrated compelling results on multiple clinically meaningful and potential registrational endpoints measuring different aspects of RSV disease ✓ Up to one week improvement in complete RiiQ symptom resolution ✓ Statistically significant improvement in PGI-S ✓ Lower hospitalization rate • Robust antiviral effect • Well-tolerated, with a favorable safety profile Zelicapavir Phase 2b High-Risk Adult Study: Conclusions 14RiiQ: Respiratory Infection Intensity and Impact Questionnaire; PGI-S: Patient Global Impression of Severity Data support advancement of zelicapavir into Phase 3 study of high-risk adults
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© 2026 Enanta Pharmaceuticals, Inc. | • First zelicapavir pediatric study: safety and dose selection • Signal finding in different patient populations to inform a potential registration-enabling trial – Age: ≥28 days to <6 months and ≥6 months to ≤36 months – Time from symptom onset to treatment – Hospitalized or outpatient Zelicapavir Phase 2 Pediatric Study: Design & Objectives 15 ~90 patients dosed in 2 age cohorts: • ≥28 days to <6 months • ≥6 months to ≤36 months Double-Blind Treatment Phase 5 days Part 1: MAD vs Placebo Part 2: Selected dose from Part 1 vs Placebo Day 1 Day 5 Day 28 23 Day Follow-up Primary Objectives of Study • Overall: Antiviral activity of zelicapavir across all patients • Part 1: Safety and PK • Part 2: Antiviral activity
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© 2026 Enanta Pharmaceuticals, Inc. | • Viral load decline of 0.88 log at Day 3 and 1.18 log at Day 5 Zelicapavir Phase 2 Pediatric Study: Prespecified mITT-3 Population: RSV PCR Viral Load 16 1 3 5 9 14 Study Day -6 -5 -4 -3 -2 -1 0 LSMean Viral Load (log10 copies/mL) (+/-SE) Placebo N=(10) EDP-938 N=(28) LS Mean Viral Load Change from Baseline (+/-SE) (log10 copies/mL) Study Day Zelicapavir (n=28) Placebo (n=10) Δ = -0.88 Δ = -1.18 Δ = -0.57 Δ = -0.20 mITT-3: patients randomized within 3 days of symptom onset
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© 2026 Enanta Pharmaceuticals, Inc. | • In a post-hoc analysis, zelicapavir reduced the time to complete symptom resolution by 1.6 days and sustained resolution by 3.7 days compared to placebo Zelicapavir Phase 2 Pediatric Study: RSV Signs/Symptoms by ReSViNET 17 ReSViNET: Respiratory Syncytial Virus Network. 1. All 7 symptoms were mild or absent; 2. All 7 symptoms were absent and patient was not hospitalized; 3. All 7 symptoms were absent, remained absent, and patient was not hospitalized. Symptom Resolution (ReSViNET) Zelicapavir (n=69) Placebo (n=27) Difference Median time to symptom resolution1 (protocol-defined) (95% CI) 3.0 days (2.0-3.8) 2.7 days (1.0-4.1) 0.3 days Median time to complete resolution2 (post hoc) (95% CI) 7.0 days (5.9-8.0) 8.6 days (5.0-12.0) -1.6 days Median time to sustained resolution3 (post hoc) (95% CI) 7.0 days (6.0-8.2) 10.7 days (5.2-13.0) -3.7 days
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© 2026 Enanta Pharmaceuticals, Inc. | • Well-tolerated, with favorable safety profile – No adverse events leading to treatment discontinuation or study withdrawal • Antiviral effect observed for the primary and secondary virology endpoints in overall population • Viral load decline of 1.4 log at the end of treatment in Part 2 • Viral load decline of 1.2 log at Day 5 observed in prespecified subset of patients randomized within 3 days of symptom onset • RSV Signs/Symptoms – ReSViNET: Reduced the time to complete symptom resolution – RESOLVE-P: Trend toward greater sign/symptom reduction with zelicapavir in a small dataset Zelicapavir Phase 2 Pediatric Study: Conclusions 18 Primary Objectives of Study ✓Overall: Antiviral activity of zelicapavir across all patients ✓Part 1: Safety and PK ✓Part 2: Antiviral activity Data support further clinical development of zelicapavir in pediatrics
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© 2026 Enanta Pharmaceuticals, Inc. | • Direct-acting antiviral targeting the L-protein – Replication inhibitor: shuts down the production of new virions (vs. fusion inhibitors which block viral entry) • Granted Fast Track designation by the FDA • Sub-nanomolar potency against RSV-A and B • Protects mice in a dose-dependent manner from RSV infection • Potential to be used alone or in combination – Additive to synergistic activity with zelicapavir – No cross resistance expected with other mechanisms • Phase 1 indicated 200mg or 600mg once-daily as potential safe and efficacious doses EDP-323: RSV L-Protein Inhibitor 19 . RSV
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© 2026 Enanta Pharmaceuticals, Inc. | • Highly statistically significant reductions in Viral Load AUC measured by qRT-PCR compared to placebo – No statistically significant difference between the two EDP-323 dosing regimens; 600mg and 200mg (with 600mg loading dose) EDP-323: Robust Antiviral Effect in Human Challenge Model Primary Efficacy Endpoint: 85-87% ↓ in Viral Load AUC by qRT-PCR 20 Viral Load (Log10 copies/mL) Mean (±SE) 26 26 26 26 26 26 26 26 26 26 26 26 26 26 15 12 10 6 4 1 23 23 23 23 23 23 23 23 23 23 23 23 23 23 17 16 10 5 4 2 30 30 30 30 30 30 30 30 30 30 30 30 30 30 19 18 11 8 6 4 Number of Subjects EDP-323 High dose EDP-323 Low dose Placebo 0 1 2 3 4 5 6 7 8 9 Time (Days) 0 1 2 3 4 5 6 Mean (±SE) Viral Load (Log₁₁ copies/mL) Placebo (N=30) EDP-323 Low dose (N=23) EDP-323 High dose (N=26) Time (days) EDP-323 High Dose EDP-323 Low Dose % AUC Reduction (vs pbo) 84.93% 87.48% P-value <0.0001 <0.0001 VL AUC: viral load area under the curve (hours x log10 copies/mL); qRT-PCR: quantitative reverse transcriptase polymerase chain reaction; SE: standard error
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© 2026 Enanta Pharmaceuticals, Inc. | EDP-323: Robust Antiviral Effect in Human Challenge Model Secondary Efficacy Endpoint: 97-98% ↓ in VL AUC by Viral Culture 21 Viral Load (Log10 PFU/mL) Mean (±SE) 26 26 26 26 26 26 26 26 26 26 26 26 26 26 15 12 10 6 4 1 23 23 23 23 23 23 23 23 23 23 23 23 23 23 17 16 10 5 4 2 30 30 30 30 30 30 30 30 30 30 30 30 30 30 19 18 11 8 6 4 Number of Subjects EDP-323 High dose EDP-323 Low dose Placebo 0 1 2 3 4 5 6 7 8 9 Time (Days) 0.0 0.5 1.0 1.5 2.0 2.5 3.0 Mean (±SE) Viral Load (Log₁₁ PFU/mL) Placebo (N=30) EDP-323 Low dose (N=23) EDP-323 High dose (N=26) • Highly statistically significant reductions in infectious VL AUC measured by quantitative culture compared to placebo – No statistically significant difference between the two EDP-323 dosing regimens; 600mg and 200mg (with 600mg loading dose) EDP-323 High Dose EDP-323 Low Dose % AUC Reduction (vs pbo) 98.32% 97.26% P-value <0.0001 <0.0001 Time (days) VL AUC: viral load area under the curve (hours x log10 copies/mL); PFU: plaque forming units; SE: standard error
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© 2026 Enanta Pharmaceuticals, Inc. | • Well-tolerated with safety profile similar to placebo • Primary and key secondary efficacy endpoints achieved with high statistical significance at both dose levels compared to placebo: ✓ Reduction in viral load of 85-87% ✓ Reduction in viral culture of 97-98% ✓ Alleviation of clinical symptoms by 66-78% EDP-323 Phase 2a RSV Challenge Study: Conclusions 22 Data support further clinical development of EDP-323
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Immunology
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© 2026 Enanta Pharmaceuticals, Inc. | Building Enanta’s Immunology Portfolio: Focusing on Best-in-Disease Treatments 24 Exploit novel biology to select targets with potential in multiple indications Leverage innovative chemistry to develop best-in-class small molecule drugs Clinical, genetic, or pathway validation to link target to disease Yet to be drugged, drugged by injectables or suboptimal orals Predictive biomarkers or early clinical signals derisk development Differentiated value proposition; Large market opportunity Strong Target Rationale Clear Means to Differentiation Expedited Clinical Path to POC Significant Unmet Need
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© 2026 Enanta Pharmaceuticals, Inc. | Immunology Portfolio: Multiple Targets Addressing Type 2 Immune Diseases 25 Potential Indications: Atopic Dermatitis, Asthma, CSU, CIndU, COPD, EoE, PN, CRSwNP, Migraine, Others Degranulation Granules neuropeptidesantimicrobial peptides xenobiotics MRGPRX2 MRGPRX2 Inhibition KIT receptor P P PP PP Mast cell activator Mast cell activator KIT Inhibition MRGPRX2KIT STAT6 MRGPRX2 Inhibition prevents activation and degranulation in mast cells KIT Inhibition blocks cell survival signal resulting in apoptosis and cell death STAT6 Inhibition impedes type 2 inflammation JAK1 JAK3/ TYK2 STAT6 STAT6 STAT6 STAT6 IL-4/13 IL-4R C/IL-13R1 STAT6 STAT6 IL-4/IL-13 mAb Gene Transcription Type 2 Inflammation P P P P P P STAT6 Inhibition CSU: chronic spontaneous urticaria; CIndU: chronic inducible urticaria, CRSwNP: chronic rhinosinusitis with nasal polyps; EoE: eosinophilic esophagitis, PN: prurigo nodularis
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© 2026 Enanta Pharmaceuticals, Inc. | Explore Expansion Fast PoC Urticaria AD Asthma, COPD CRSwNP, ARC, EoE, PN TBD Total $40B $>120B Indications / 2032F Market Potential1• Type 2 inflammation is characterized by overproduction of IL-4, IL-5, IL-13, and IgE which recruits and activates Th2 CD4 T cells, B cells, mast cells, eosinophils, and basophils • Potential to treat broad patient populations across numerous disease areas Immunology Portfolio: Addressing unmet need in multiple Type 2 immune-driven diseases 26 AD: Atopic Dermatitis; ARC: Allergic Rhinoconjunctivitis; COPD: Chronic Obstructive Pulmonary Disease; CRSwNP: Chronic Rhinosinusitis with Nasal Polyps; EoE: Eosinophilic Esophagitis; PN: Prurigo Nodularis Source: 1. Evaluate Pharma, © Evaluate Ltd, September 2025, www.evaluate.com $80B
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© 2026 Enanta Pharmaceuticals, Inc. | Chronic Spontaneous Urticaria (CSU): KIT and MRGPRX2 Inhibitor Initial Focus for Clinical Proof of Concept 27 Angioedema 1. Kaplan A et al. Allergy. 2023; 78(2): 389–401. 2. Yosipovitch et al. Dermatol Ther. 2023; 13(8): 1647–1660. 3. H1 antihistamines up to 4x standard dose. Hives Itch Erythema• Severely debilitating, chronic inflammatory skin disease – Driven by mast cell activation, triggering release of inflammatory mediators1 – Quality of life impacts beyond the skin: sleep disturbances, fatigue, irritability, anxiety and depression2 • Affects ~0.5-1% of the global population1 • Substantial unmet need for efficacious oral agent – ~50% not controlled with antihistamines1,3
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© 2026 Enanta Pharmaceuticals, Inc. | Atopic Dermatitis (AD): STAT6 Inhibitor Initial Focus for Clinical Proof of Concept 28 1. Silverberg JI et al. Annals of Allergy, Asthma & Immunol. 2018. 2. Asthma and Allergy Foundation of America: https://aafa.org/asthma-allergy-research/our-research/atopic-dermatitis- in-america/. 3. Market share ($) from Evaluate Pharma, © Evaluate Ltd, September 2024, www.evaluate.com 4.Prescribing Information for RINVOQ & CIBINQO • Chronic dermatological disease characterized by dry, red, inflamed, irritated and itchy skin – Driven by Th2 immune dysregulation1 – Quality of life impacts beyond the skin: limited lifestyle, avoidance of social interaction and impacted activities1 • 7.3% of U.S. adults, ~40% have moderate-severe symptoms2 • Significant need for efficacious and safe oral agents – Market dominated by mAb (IL-4/13) – Oral JAKi use <10%3 • Boxed warning: serious infections, mortality, malignancy, major adverse cardiac events, thrombosis4
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Immunology: KIT Inhibitor
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© 2026 Enanta Pharmaceuticals, Inc. | KIT Inhibitors Offer Potential for Differentiated Efficacy 30 • Mast cells: primary driver of inflammation in skin, and implicated in multiple allergic diseases – Urticaria, asthma, prurigo nodularis (PN) and others • KIT: well-characterized receptor tyrosine kinase critical for regulating mast cell activity • KIT inhibitors: potential for best-in-disease efficacy – Directly reduces quantity of mast cells through apoptosis and depletion, addressing key disease driver – Current therapy reduces mast cell activator levels or downstream mediators, but not mast cells directly – Positive proof-of-concept in urticaria and PN with anti-KIT mAb
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© 2026 Enanta Pharmaceuticals, Inc. | • EDP-978 selected as clinical candidate – Inhibits KIT with nanomolar potency in both binding and cellular assays – Demonstrates sub-nanomolar activity in vivo – Highly selective for KIT versus other kinases – Good in vitro and in vivo ADME properties • Well-absorbed with good plasma exposure across preclinical species • No GSH adducts (or reactive metabolites) detected in vitro or in vivo, minimizing metabolic/safety issues • Low drug-drug interaction potential via CYP inhibition or induction • Excellent metabolic stability with once-daily dosing potential in human • File IND in 1Q 2026 and report Phase 1 data in 4Q 2026 Goal of Oral KIT Inhibitor Program: Develop Best-in-Class Treatment for Mast Cell Mediated Diseases 31
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© 2026 Enanta Pharmaceuticals, Inc. | • Nanomolar inhibition in cellular assays with an EC50 of 1.6 – 3.4nM EDP-978 Exhibits Potent Inhibition of KIT In Vitro and In Vivo 32 *M-07e and UT-7 cells endogenously express KIT; Ba/F3 cells are engineered to express KIT Binding or Cellular Assay* EC50 (nM) KINOMEscan Kd 0.3 M-07e Phosphorylated KIT 1.6 UT-7 Cell Proliferation 2.8 KIT Ba/F3 Cell Proliferation 3.3 CD34+ Derived Mast Cell Degranulation 3.4 • Inhibits SCF-mediated histamine release in mice with an EC50 (free drug) of 0.25nM **KIT binding to its ligand SCF (Stem Cell Factor) in vivo triggers mast cell degranulation with histamine release 10-1 100 101 102 0 25 50 75 100 125 150 EDP-978 (nM) free Histamine (% Vehicle) In Vivo Mast Cell Degranulation Degranulation Histamine Release**SCF Challenge (injection) KIT Inhibitor (oral delivery) P P PP PP KIT SCF
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© 2026 Enanta Pharmaceuticals, Inc. | S(10) @ 1 μM: selectivity score at a concentration of 1 μM; CSF1R: colony stimulating factor 1 receptor; PDGFRA/B: platelet-derived growth factor receptor alpha/beta; FLT3: FMS-like tyrosine kinase 3 • Greater than 200-fold selectivity for KIT over other KIT family members EDP-978 Demonstrates Good Selectivity for KIT 33 Selectivity EDP-978 S(10) @ 1 µM 0.02 CSF1R* >200x PDGFRα* >900x PDGFRβ* >800x FLT3 Kd >30,000x *Cellular selectivity calculated as ratio of EC50 in kinase dependent Ba/F3 cells
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Immunology: STAT6 Inhibitor
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© 2026 Enanta Pharmaceuticals, Inc. | • Th2 dysregulation drives allergic and autoimmune diseases including atopic dermatitis and asthma – Characterized by IL-4 & IL-13 overproduction • STAT6: transcription factor responsible for IL-4/IL-13 signaling, which drives a Th2 dominant phenotype – STAT6 gain-of-function variants result in severe atopic dermatitis1 – STAT6 loss-of-function protects against type 2 high asthma2 – Inhibition of the IL-4/13 pathway is clinically validated • STAT6 inhibitors: potential for an “oral DUPIXENT” – Blocks IL-4/13 signaling pathway – Reduces inflammation in Th2 driven preclinical models – No oral therapy selectively targeting IL-4/13 pathway available STAT6 Inhibitors Offer Potential for an “Oral DUPIXENT®” 351. Suratannon et al. J Allergy Clin Immunol. 2023. 2. Kristjansdottir et al. J Allergy Clin Immunol. 2024. JAK1 JAK3/ TYK2 STAT6 STAT6 STAT6 STAT6 IL-4/13 IL-4R C/IL-13R1 STAT6 STAT6 Gene Transcription Type 2 Inflammation P P P P P P IL-4/IL-13 mAb STAT6 Inhibition
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© 2026 Enanta Pharmaceuticals, Inc. | Goal of Oral STAT6 Inhibitor Program: Develop Best-in-Class Oral STAT6 Inhibitors 36 • EPS-3903 selected as development candidate – Favorable in vitro and in vivo ADME properties supporting once daily dosing – Inhibits STAT6 with nanomolar potency in both binding and cellular assays – Highly selective for STAT6 versus other STATs – Rapid, continuous and complete (>90%) inhibition of pSTAT6 after oral dosing in mice – In vivo efficacy comparable to dupilumab or an anti-mouse IL-4/IL-13 antibody in multiple disease models of asthma (ovalbumin, house dust mite) and atopic dermatitis (MC903) • Initiated IND-enabling activities with goal of IND filing in 2H 2026
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© 2026 Enanta Pharmaceuticals, Inc. | EPS-3903 Demonstrates Potent Activity 37 Cellular Assay (IL-4/IL-13 Induced) EPS-3903 EC50 (nM) Upadacitinib EC50 (nM) pSTAT6 (hPBMC) 4 10 Cell Proliferation (TF-1) 8 16 TARC (hPBMC) 16 20 Periostin (primary bronchial cells) 3 11 • EPS-3903 exhibits nanomolar inhibition in biochemical (Kd = 0.4 nM) and cellular assays – Inhibits phosphorylation of STAT6 and STAT6-mediated cellular proliferation – Prevents production of STAT6-driven biomarkers of type 2 inflammation TF-1: human erythroleukemic cell line, dependent on STAT6 signaling for cell growth Upadacitinib: JAK Inhibitor hPBMC: human peripheral blood mononuclear cells ; pSTAT6: phosphorylated STAT6; TARC: thymus and activation-regulated chemokine 1 100 10000 0 25 50 75 100 125 Inhibitor [nM] % inhibition EPS-3903 Upadacitinib PBMC pSTAT6 % Inhibition Compound, nM hPBMC pSTAT6
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© 2026 Enanta Pharmaceuticals, Inc. | EPS-3903 Displays Good Selectivity 38 pSTAT1 pSTAT2 pSTAT3 pSTAT4 pSTAT5 pSTAT6 EPS-3903 >5000 >5000 >5000 >5000 >5000 4 Upadacitinib (JAK Inhibitor) 1 8 24 195 16 10 Selectivity in hPBMCs EC50 (nM) pSTAT: phosphorylated STAT; hPBMCs: human peripheral blood mononuclear cells • No inhibition of other STATs observed in human PBMCs • Greater than 1000x biochemical selectivity for STAT6 over other STATs • Selectivity much improved compared to JAK inhibitors
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© 2026 Enanta Pharmaceuticals, Inc. | • In vivo STAT6 target engagement after a single oral dose • Rapid, complete and continuous (>90%) inhibition of phosphorylated STAT6 sustained for 24 hours EPS-3903 Results in Complete Inhibition of pSTAT6 in Mouse Model 39pSTAT6: phosphorylated STAT6 NS=not statistically different 24 hours post-oral dose in IL-4-stimulated mouse whole blood - low mid high 0 20 40 60 80 100 120 % pSTAT6 Induction EPS-3903: ↓76% ↓90% ↓95% NS
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© 2026 Enanta Pharmaceuticals, Inc. | EPS-3903 Shows Comparable Efficacy to Dupilumab in a House Dust Mite (HDM) Challenge Asthma Model 40pSTAT6: phosphorylated STAT6; BALF: bronchioalveolar lavage fluid; TARC: thymus and activation-regulated chemokine; BQL: below quantification limit • HDM model in transgenic mice expressing human IL-4/IL-4Rα triggers allergic airway inflammation that mimics key aspects of asthma EPS-3903 efficacy comparable to dupilumab • >90% inhibition of pSTAT6 in lung • Decreased type 2 inflammation – BALF Eosinophils, TARC, Serum IgE – Improved histological scoring • Reduced bronchiolar hyperplasia, inflammatory infiltrates, airway wall thickness - - low high IgG4 Dupilumab 0 50 100 150 200 Cell number (X104) BALF Eosinophils HDM-Challenged ** * EPS-3903 - - low high IgG4 Dupilumab 0 500 1000 1500 2000 ng/ml BALF TARC HDM-Challenge ** * EPS-3903 - - low high IgG4 Dupilumab 0 50 100 150 % of HDM Vehicle Lung pSTAT6 HDM-Challenged BQL EPS-3903 BQL BQL - - low high IgG4 Dupilumab 0 1000 2000 3000 4000 ng/ml Serum IgE HDM-Challenged EPS-3903 BQL BQL BQL *p<0.05 vs Corresponding Vehicle
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© 2026 Enanta Pharmaceuticals, Inc. | • MC903 model in transgenic mice expressing human IL-4/IL-4Rα triggers TSLP-mediated systemic inflammation with increased B-cell activity EPS-3903 efficacy comparable to dupilumab • >90% inhibition of pSTAT6 in skin and spleen • Robust decrease in serum IgE EPS-3903 Demonstrates Comparable Efficacy to Dupilumab in a MC903-Driven Atopic Dermatitis Mouse Model 41 *p<0.05 vs Corresponding Vehicle - - low high IgG4 Dupilumab 0 50 100 150 200 % of MC903 Vehicle Spleen pSTAT6 MC903-Challenge ** * EPS-3903 - - low high IgG4 Dupilumab 0 25 50 75 100 125 150 % of MC903 Vehicle Skin pSTAT6 MC903-Challenged ** * EPS-3903 - - low high IgG4 Dupilumab 0 200 400 600 ng/ml Serum IgE MC903-Challenged EPS-3903 BQL BQL BQL
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© 2026 Enanta Pharmaceuticals, Inc. | Day 1 Day 2 EPS-3903 Leads to Continuous, Complete STAT6 Pathway Blockade 42 • Proven modality with ability to optimize ADME and eliminate metabolic liabilities • High selectivity minimizes off-target effects Merits of Small Molecule Inhibitors • Fast reversibility in case of adverse events • Straightforward PK/PD modeling Drug Exposure EPS-3903 provides continuous drug exposure above the EC90 EPS-3903 Degrader EC90 EPS-3903100% Degrader Time EPS-3903 completely suppresses STAT6 over a 24-hour period Target/ Pathway Suppression PK: pharmacokinetics, PD: pharmacodynamics 0%
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Immunology: MRGPRX2 Inhibitor
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© 2026 Enanta Pharmaceuticals, Inc. | • Mast Cells: primary driver of inflammation in skin, and implicated in multiple allergic diseases – Urticaria, asthma, prurigo nodularis (PN) and others • MRGPRX2: non-canonical GPCR expressed predominantly on mast cells – Agonism leads to degranulation and release of inflammation mediating components • MRGPRX2 Inhibitors: potential for strong efficacy with best-in-disease safety – Non-depleting mast cell modulation – Includes IgE-independent pathways MRGPRX2 Inhibitors Offer Potential for Strong Efficacy and Best-in-Disease Safety Profile 44MRGPRX2: Mas-related G-protein coupled receptor member X2 Degranulation Granules neuropeptides antimicrobial peptides xenobiotics MRGPRX2 Inhibition MRGPRX2 MRGPRX2 Inhibition prevents activation and degranulation in mast cells
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© 2026 Enanta Pharmaceuticals, Inc. | MRGPRX2: Evidence for a Key Role in Chronic Spontaneous Urticara 451. Fujisawa 2014 2. Shtessel 2021 • Patients with CSU have more MRGPRX2 expressing mast cells and a greater response to MRGPRX2 agonist
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© 2026 Enanta Pharmaceuticals, Inc. | • Novel, oral inhibitors of MRGPRX2 being optimized in discovery stage • Prototypes being optimized with goal of selecting development candidate in 2H 2026 Goal of Oral MRGPRX2 Inhibitor Program: Develop Best-in-Class Treatment for Mast Cell Mediated Diseases 46 Inhibits MRGPRX2 with nanomolar potency in cellular assays Prevents skin mast cell activation in mouse model Highly selective for MRGPRX2 versus other GPCRs Favorable in vitro and in vivo ADME properties supporting once daily dosing
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© 2026 Enanta Pharmaceuticals, Inc. | • Nanomolar inhibition in cellular assays with an EC50 of 1 – 2nM Prototype MRGRPX2 Inhibitor Exhibits Potent Inhibition In Vitro and In Vivo 47 Cells stimulated with MRGPRX2 agonist Cortistatin-14 LAD2 Cells: human mast cell line capable of histamine release (degranulation) Cellular Assay EC50 (nM) LAD2 Cells (β-hexosaminidase release) 1.7 LAD2 Cells (Histamine Release) 2.1 Primary Human Skin Mast Cells (β-hexosaminidase release) 1.2 • Prevents skin mast cell activation in humanized MRGPRX2 mice1 1. Cortistatin-14 binding to MRGPRX2 triggers mast cell degranulation resulting in vascular permeability, allowing blue dye to leak into tissues Cortistatin-14*MRGPRX2 Agonist (and Evans Blue Dye) MRGPRX2 Inhibitor (oral delivery) Degranulation Vascular permeability MRGPRX2 Vehicle Prototype Vehicle Prototype 0 10 20 30 Skin Dye Relative Evans Blue Cortistatin14PBS # * Relative Evans Blue Dye
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© 2026 Enanta Pharmaceuticals, Inc. | Prototype MRGRPX2 Inhibitor Demonstrates Potent Activity Across Multiple Agonists 48 Agonist β-hexosaminidase EC50 (nM) Cortistatin-14 1.7 Vasoactive intestinal peptide 0.6 PACAP1-38 1.9 Substance P 1.0 LL37 2.3 Icatibant 0.7 Chlorpromazine 0.7 • Potent inhibition of degranulation in LAD2 cells across endogenous and exogenous MRGPRX2 ligands MRGPRX2 Neuropeptides Cortistatin-14 Substance P PACAP1-38 Antimicrobial Peptides LL-37 Exogeneous Icatibant Chlorpromazine Vancomycin Peptide Hormones VIP PAMP1-12
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© 2026 Enanta Pharmaceuticals, Inc. | Respiratory Syncytial Virus Align with FDA on adult Phase 3 design and registration path in 2Q 2026 Prepare for a Phase 3 study of zelicapavir in high-risk adults in 2H 2026 Explore business development opportunities for RSV assets 2026 Key Catalysts 49 KIT Program File IND for EDP-978 in 1Q 2026 Report Phase 1 data for EDP-978 in 4Q 2026 STAT6 Program File IND for EPS-3903 in 2H 2026 MRGPRX2 Program Nominate development candidate in 2H 2026 Virology Immunology
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