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evommune Corporate Presentation August 2026
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Disclaimers 2 © Evommune, Inc. This presentation has been prepared by Evommune, Inc. (“we”, “us” or “our”) and contains forward-looking statements, including: statements about our expectations regarding the potential benefits, clinical activity and tolerability of our product candidates; our expectations with regard to the results of our clinical trials, preclinical studies and research and development programs, including the the potential therapeutic benefit of EVO756 and EVO301, the design, objectives, initiation, timing, progress and results of current and future preclinical studies and clinical trials of our product candidates, including the ongoing Phase 2 clinical trials for EVO756 and EVO301; anticipated cash runway; and continued advancement of our portfolio. These statements involve substantial known and unknown risks, uncertainties and other factors that may cause our actual results, levels of activity, performance or achievements to be materially different from the information expressed or implied by these forward-looking statements. We may not actually achieve the plans, intentions or expectations disclosed in our forward-looking statements, and you should not place undue reliance on our forward- looking statements. Actual results or events could differ materially from the plans, intentions and expectations disclosed in the forward-looking statements we make. These and other risks are described more fully in our Annual Report on Form 10-K for the year ended December 31, 2025 and our other filings with the Securities and Exchange Commission (the “SEC”) and our other documents subsequently filed with or furnished to the SEC. All forward-looking statements represent our views as of the date of this presentation. All forward-looking statements contained in this presentation speak only as of the date on which they were made. Except to the extent required by law, we undertake no obligation to update such statements to reflect events that occur or circumstances that exist after the date on which they were made. This presentation also contains estimates made by independent parties relating to industry market size and other data. These estimates involve a number of assumptions and limitations, and you are cautioned not to give undue weight on such estimates. We have not independently verified the accuracy or completeness of such information and we do not take any responsibility with the accuracy or completeness of such information. The trademarks included in this presentation are the property of the owners thereof and are used for reference purposes only.
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Evommune (EVMN) is Addressing Chronic Inflammation, a Global Healthcare Crisis © Evommune, Inc.3 1. https://www.ncbi.nlm.nih.gov/books/NBK493173/. 2. Wylezinski LS, et al. PMID: 30979036. 5Annual Direct Cost 2 $90B I&I Therapies Fail Patients >50% Deaths Worldwide 1 3 of 5 Experienced Team Distinct Mechanisms Portfolio Approach Evommune is Delivering Next Generation Therapies Substantial Burden on the Healthcare System Existing Treatment Options Have Critical Limitations Chronic Inflammation Destroys Lives
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5v Our Mission-Driven Approach to Treating Immune-Mediated Diseases © Evommune, Inc.4 Two Phase 2 Programs with Novel Approaches to Targeting Heterogeneous Diseases EVO756: Oral Therapy Targeting Mast Cells and Sensory Neurons EVO301: IL-18 Blockade for Multi - Pathway Immunomodulation Address critical gaps in care… Expansive Portfolio of Preclinical Programs Sensory NeuronMast Cell MRGPRX2 Nerves Mast Cells Novel Biologic Using the Fully Human IL-18 Binding ProteinAdaptive(Th2)Inflammation Innate Inflam m ation …Strategically select novel mechanisms with strong probability of success… … Steady cadence of new programs entering the clinic
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5 Mid-stage clinical company developing novel therapeutics for highly prevalent chronic inflammatory diseases Two clinically-validated programs in Phase 2: • EVO756 (oral MRGPRX2 antagonist) in atopic dermatitis and migraine • EVO301 (long-acting IL-18bp fusion protein) in atopic dermatitis Multiple clinical data readouts through 2028: • EVO756 Phase 2b top -line data in AD expected in September 2026, planned Phase 3 in 1H 2027 • EVO756 Phase 2b trial initiated in migraine in July 2026, top -line data expected in 2027 • EVO301 reported positive data in a Phase 2a in AD (Feb 2026), moving to Phase 2b in 2027 with subcutaneous formulation, data expected in 2028 Steady cadence of new programs entering the clinic in a broad range of inflammatory diseases , with next preclinical program entering the clinic in 2027 Proven and experienced leadership team has delivered almost 30 NDAs and BLAs ~$287 million of cash & investments as of June 30, 2026, with anticipated runway through 2028 © Evommune, Inc. Strong Cash Position with Potential to Unlock Significant Near-Term Value Creation across Multiple Milestones
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Proven and Experienced Leadership Team Has Delivered Almost 30 NDAs and BLAs © Evommune, Inc.6 Footnotes: Acquisition prices from press releases Luis Peña Founder, President & CEO Eugene Bauer, MD Founder, CMO Kyle Carver, MBA CFO Greg Moss, Esq CBO & CLO Jeegar Patel, PhD CSO Janice Drew, MPH Chief of Development Operations Lou Sehl, PhD SVP, Technical Operations Daniel Burge, MD SVP, Clinical Development Leadership in >25 Companies Key Roles in Almost 30 NDA / BLAs (Acquired by Eli Lilly for $1.1B) (Acquired by Sanofi for $1.9B) (Acquired by GlaxoSmithKline for $2.9B) (Acquired by LEO Pharma for $288M) (Acquired by Bristol Myers Squibb for $13.1B) (Acquired by Eli Lilly for $6.5B) (Acquired by Stiefel for $930M) (Acquired by Angiotech for ~$50M) Mark Jackson, MD SVP, Clinical Development
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Our Inflammation Portfolio © Evommune, Inc.7 Program / Target Indication Preclinical Phase 1 Phase 2 Phase 3 Next Anticipated Milestone EVO756 MRGPRX2 Atopic Dermatitis • Phase 2b data (September 2026) Migraine • Phase 2b trial initiated; Top -line data (2027) Other Indications • Phase 2 trial planning underway EVO301 IL-18BP Atopic Dermatitis • Positive Phase 2a POC: Full data to be presented at an upcoming medical meeting • Phase 2b trial planning underway Ulcerative Colitis • Phase 2 trial planning underway Other Indications • Phase 2 trial planning underway Advancing Multiple Preclinical Programs Toward Clinical Proof-of-Concept
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EVO756: Oral MRGPRX2 Antagonist First and Best-in-Class Dual Mechanism Modulates Both Peripheral Sensory Neurons and Mast Cells 8 © Evommune, Inc.
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MRGPRX2 in Neuroinflammation and Mast Cell Activation © Evommune, Inc.9 Mast Cell MRGPRX2 Ligands Tissue Damage Sensory Neuron Vasodilation, Extravasation Immune Recruitment / Activation Sensory Neuron Activation Mast Cell Degranulation Itch / Pain / Cough Tissue Pathophysiology Clinical Manifestations Inflammatory Infiltrates Increased Mast Cell Numbers Innate Immunity Adaptive Immunity Tissue Remodeling Vascular Leak Neuronal Sensitivity Chronic Inflammation Erythema Hives Barrier Dysfunction Airflow Limitation Edema Angioedema Sensitivity to Chemicals / Foods MRGPRX2 Neuropeptides Mast Cell Mediators InflammatoryMediators
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EVO756: Broad Spectrum Oral Anti-Inflammatory Potential © Evommune, Inc.10 MRGPRX2 Expressed on Both Sensory Neurons and Mast Cells • Potent and highly selective small molecule • Oral convenience could drive adoption across multiple indications • Anticipate favorable safety and tolerability profile Potential First-Line Oral Across Several Specialties Mast Cell MRGPRX2 Nerves Mast Cells Sensory Neurons and Mast Cells Are Found in Close Proximity Sensory Neuron MRGPRX2
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EVO756: Differentiated Mechanism Across Multi-Billion-Dollar Markets Sequenced Expansion Across Underserved, Blockbuster Markets G7 prevalence estimates. CIndU = chronic inducible urticaria; AD = atopic dermatitis, Sources: Decision Resources DL&F; https://pmc.ncbi.nlm.nih.gov/articles/PMC9677261/, Novartis Investor Presentation (2026) treatment and eligibility figures per multiple published references. Future market estimates to be confirmed. LCM indications sized by moderate-to-severe populations.© Evommune, Inc.11 Future Target Population >95M Patients Today ~30M ~15M Migraine AD Initial Target Population Selected for unmet need, market size, and defined regulatory path ~45M Eligible Patients Expanding into High-Potential Indications Where Neuroinflammation Drives Disease IBS-D IC ~7M ~10M Asthma ~25M Food Allergy ~7M~1M CIndU >3M Chronic Pruritus
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EVO756 Clinical Development Overview © Evommune, Inc.12 CIndU = Chronic inducible urticaria; AD = Atopic dermatitis Trial Phase 1 Proof-of-Concept Phase 2 Phase 2b Phase 2b N 132 30 ~120 ~330 Indication Healthy Volunteers CIndU AD Migraine Key Takeaways • Well-tolerated across all doses • Clear target engagement in skin challenge • ~70% human skin penetration • PK supports full target coverage as low as 25mg BID • Well-tolerated across all doses • Complete responses as early as week 1 • Clear POC achieved with 70% FricTest responders • Similar activity at 50mg BID and 300mg QD doses Top-line Data Expected September 2026 Trial Initiated in July 2026, Top-line Data Expected 2027
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PART A: SAD Dosing N = 55 (41 active / 14 placebo) EVO756: Phase 1 Proof-of-Concept Trial Design and Summary Inclusion of Icatibant Skin Challenge Demonstrated EVO756 Target Engagement in Humans © Evommune, Inc.13 ECG = Electrocardiogram Cohort A1 1 mg Cohort A5 100 mg Cohort A4 30 mg Cohort A3 10 mg Cohort A2 3 mg Cohort A6 240 mg Cohort A7 500 mg Cohort B1 10 mg BID Cohort B3 100 mg BID Cohort B2 30 mg BID Cohort B4 240 mg BID Cohort B5 500 mg QD PART B: MAD Dosing N = 77 (58 active / 19 placebo) Included Skin Challenge at All Doses Pharmacokinetics Pharmacodynamics – Icatibant Skin Challenge Test Safety • Concentration dose proportional and linear • Half-life ranges from 8 - 12 hours • Tmax: 1 - 4 hours • Support QD and BID dosing • Clear target engagement • Dose dependent activity • All doses associated with response • Well-tolerated across all doses • No severe or serious adverse events • No clinically significant abnormal lab values • No clinically significant ECG abnormalities
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EVO756 PK Supports Full Target Coverage as Low as 25mg BID © Evommune, Inc.14 IC90 (mast cells) = 180 ng/mL Dose-Proportional • Linear concentration-dose relationship across SAD and MAD cohorts Half-Life: 8-12 Hours • Tmax 1–4 hours · supported both QD and BID dosing High Skin Penetration • ~70% tissue:plasma ratio in human skin 2-fold accumulation • 17% free drug ratio 0 2,250 4,500 6,750 9,000 0 4 8 12 16 20 24 25 mg BID 50 mg QD 150 mg QD 300 mg QD 50 mg BID Relative Plasma EVO756 Concentrations (ng/mL) Time (hours) IC90 Multiple of IC90 at Trough 5.1x 2.1x 1.2x Day 10 Median Concentrations
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0 1 2 3 4 Mean FricTest Score (0-4) Week 0 Week 4 Week 10 Week 12 Positive Phase 2 CIndU Data Validated EVO756 Activity Robust Efficacy at Week 4 Competitive with Omalizumab and Barzolvolimab © Evommune, Inc.15 For illustrative purposes only. Not a head-to-head comparison. Differences exist between trial designs and study characteristics, and caution should be exercised when comparing across trials. Sources: Evommune clinical data (observed), competitor data from Maurer et al. (2017), Maurer et al., ACAAI (2024) • Symptomatic dermographism (N=30) • Open-label, within-patient controlled • 50 mg BID and 300 mg QD over 4 weeks • FricTest: standardized friction provocation test (0 –4) FricTest Response Complete Response at Week 4 across both doses (8 of 27 patients · FricT est score = 0) ≥1-point improvement at Week 4 (19 of 27 patients) EVO756 50mg BID EVO756 300mg QD Omalizumab 150 mg Q4W Omalizumab 300 mg Q4W Barzolvolimab 150 mg Q4W Barzolvolimab 300 mg Q8W Clinical Improvements Over Time 30% 70%
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5v Safety Summary Well Tolerated Across All Evaluated Dosing Levels © Evommune, Inc.16 Evommune clinical data; ALT = alanine aminotransferase; AST = aspartate aminotransferase; 1. The two subjects in the 300 mg QD cohort with AEs of increased ALT and AST had asymptomatic transaminase elevations that were greater than ten times the upper limit of normal at four weeks, which were not present at baseline, week 1 or week 2 and later returned to baseline. Other liver tests, including bilirubin and alkaline phosphatase were within normal limits. Both of these subjects had confounding factors that may have contributed to these elevations. 300 mg QD N = 11 50 mg BID N = 19 ALT/AST Increased 2 (18%)1 – Gastroenteritis 1 (9%) 1 (5%) Pruritus 1 (9%) 1 (5%) Summary of Treatment Emergent Adverse Events Occurring in >1 Patient EVO756 was Generally Well Tolerated No serious adverse events No treatment discontinuations due to adverse events
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EVO756 Phase 2b Dose Selection Rationale Understanding of Dose Response Evolved During CIndU Study, Guiding Phase 2b Trial Doses © Evommune, Inc.17 • Active across all icatibant doses • 10 μg/mL icatibant dose is most relevant comparison based on patient biopsies • Suggests potential activity as low as 10 mg BID PK/PD Modeling • Refined model to predict IC90 coverage at trough • Suggested complete coverage as low as 25 mg BID • High tissue penetration in human skin (~70%) • Strong activity in 300 mg QD dose provided confidence to explore lower doses • 50 mg BID dose had similar activity EVO756 Phase 2 CIndU Results HV Icatibant Skin Challenge Selection of Phase 2b Doses Potential for large therapeutic window; driving approach to dose-ranging trials
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18 EVO756 in Atopic Dermatitis (AD) © Evommune, Inc.
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MRGPRX2 is Only Dual MOA: Targeting Inflammatory Lesions and Neuroinflammation 19 Strong Scientific Rationale for EVO756 in ADExpect Benefit on Neuroinflammation and Mast Cell Aspects of AD © Evommune, Inc. Pathway activation in disease and preclinical evidence of Mrgprb2/X2 involvement Strong translational validation Broad therapeutic potential MOA likely effective across patient endotypes Direct effect on sensory neurons Rapid impact on itch Dual mechanism impacting key inflammatory pathways Neuroinflammatory and mast cell disease Sensory NeuronMast Cell MRGPRX2 Nerves Mast Cells
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AD Still Has No First-Line Oral Option No Current Oral Therapy Combines Lesion Control, Itch Relief, and Tolerability © Evommune, Inc.20 G7 prevalence estimates. Sources: Clarivate “Migraine: Disease Landscape and Forecast” (2026), AHS guidelines for migraine prevention eligibility, Buse et al. (2024), Silberstein et al. (2015), Cohen et al. (2024), Coppola et al. (2025), Sakai et al. (2022). Targeted-Therapy Eligible Patients EVO756 – Promising First-Line Candidate Designed to Deliver on All Three: Oral Dosing Preferred ROA 1 Differentiated Activity MOA Targets Lesions + Itch 2 Well-Tolerated Profile Supports Broad Use 3 15M~
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CytoReason Collaboration: in silico AD Model Identifies and Validates Opportunities Beyond IL-4/IL-13 © Evommune, Inc.21 MRGPRX2 Signature Generation Computational Engine Clinical Anchoring in silico AD Model From RNAseq of in vitro human mast cells activated with MRGPRX2 ligands with/without EVO756 Integration of MRGPRX2 signature, 24 RNAseq datasets, >2,000 of human skin biopsies Model calibration against EASI scores and Dupilumab response data Acts as digital twin by integrating high-dimensional molecular data with real world clinical endpoints In collaboration with
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Predictive Modeling Reveals MRGPRX2 as a Core to AD Pathophysiology © Evommune, Inc.22 Magenta = Th2 signatures; Teal = Itch / Neuroinflammation signatures, Green = Th22 signatures, Blue = Th17 signatures Broad reach may enable EVO756 to potentially outperform IL-4/-13–restricted approaches In collaboration with
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MRGPRX2 Captures Core IL-4/-13 Biology and Broader Disease Drivers Shared Biology • MRGPRX2 and IL-4/-13 signatures capture both Th2 inflammation and neuroinflammation Differentiated Coverage • MRGPRX2 uniquely captures “white space” biology, including cellular proliferation and barrier pathways • MRGPRX2 molecular signature remains expressed in non- responders to IL-4/-13 standard of care Implications • Complementary—not redundant—mechanism • Potential to expand efficacy beyond current standard of care © Evommune, Inc.23 In collaboration with
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Phase 2b Dose-Ranging Trial in AD Top-Line Data Expected September 2026 © Evommune, Inc.24 EASI = Eczema Area and Severity Index; vIGA = Validated Investigator Global Assessment; Pruritus-NRS = Pruritus Numerical Rating Scale; BSA = Body Surface Area; BL = Baseline. Trial identifier: NCT07150845 Primary Endpoint • % change in EASI from BL at Week 12 Key Secondary Endpoints • EASI-50, EASI-75, and EASI-90 • Change in vIGA • Change in Pruritus -NRS • Proportion of patients achieving ≥4 point reduction in Pruritus -NRS • Change in BSA affected Exploratory Biomarkers • Patient subtyping • Pharmacodynamics & disease severity 5v BL W14 Adults with Moderate-to-Severe Atopic Dermatitis (N = 120) Randomized, Double-Blind, Placebo-Controlled Trial Follow-up Screening Enrollment End of Trial W12 EVO756, Dose 1 EVO756, Dose 2 EVO756, Dose 3 Placebo
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© Evommune, Inc.25 EVO756 in Migraine
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MRGPRX2 is a Novel Migraine Target with Potential to Address Neuroinflammatory and Mast Cell Drivers of Migraine 26 Strong Scientific Rationale for EVO756 in Migraine © Evommune, Inc. MRGPRX2 is expressed in human trigeminal neurons and meningeal mast cellsDisease-Relevant Expression in vivo headache models support pathogenic role for MRGPRX2 Preclinical Validation Translational Insights Multiple MRGPRX2 ligands induce migraine in humans mAb inhibition of MRGPRX2 ligand (PACAP) shows clinical benefitClinical Proof-of-Concept
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EVO756: Targeting Major Unmet Need in Migraine Prevention © Evommune, Inc.27 G7 eligible patients estimated. Sources: Clarivate “Migraine: Disease Landscape and Forecast” (2026), AHS guidelines for migraine prevention eligibility, Buse et al. (2024), Silberstein et al. (2015), Cohen et al. (2024), Coppola et al. (2025), Sakai et al. (2022). G7 Patients Eligible for Preventative Therapy EVO756 – Defining the Next Wave of Preventatives Oral Dosing Preferred ROA 1 Novel Dual Mechanism Targets neurons + mast cells; Blocks 3 migraine triggers (PACAP, VIP , Substance P) 2 First-Line Potential AHS now recommends targeted therapies first-line 3 30M~
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High Demand for Preventative Migraine Therapy © Evommune, Inc.28 Sources: Clarivate “Migraine: Disease Landscape and Forecast” (2026), AHS guidelines for migraine prevention eligibility, Bus e et al. (2024), Silberstein et al. (2015), Cohen et al. (2024), Coppola et al. (2025), Sakai et al. (2022). Note: Sales represent 7 Major Markets (US, EU5, Japan); Percent of patients by therapy type exceeds 100% due to co -prescribing; % patient numbers by therapy reflect US patient breakdown. Prevention Drives ~50% of $25B Migraine Market 0 10 20 30 WW Sales ($B) 10.2 9.3 2026 13.0 12.7 2030 $19.5 $25.7 Acute Prophylaxis >75M People Living with Migraine Worldwide ~30M Global Patients Eligible for Preventative Therapy Most Patients Remain on Legacy Preventives — Targeted Therapies Drive Sales 0 40 80 120% Patients 5% 13% 20% 36% 9% 30% 113% >$8B in 2026 NSAIDs/Analgesics Calcium Channel Blockers Tricyclic Antidepressants Beta Blockers Antiepileptics Neurotoxin CGRPs
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Advanced Treatments Class Route of Administration CGRP Oral QD Oral EOD IV SC SC SC Neurotoxin IM Innovation in Migraine Prevention Has Been Limited to CGRPs © Evommune, Inc.29 Source: Qulipta Prescribing Information from pivotal trial in chronic migraine patients. Limited Therapeutic Diversity • Only CGRP inhibitors and neurotoxin Inadequate Efficacy • ~45% of patients do not achieve 50% improvement Tolerability Challenges Remain • CGRPs associated with constipation, hypertension, Raynaud’s, nausea, allergic and injection site reactions High Unmet Need in Migraine Prevention Migraine Burden Persists Despite Oral CGRP Therapy 13.8 12.3 0 3 6 9 12 15 Monthly Migraine Days (On Treatment) Placebo Qulipta Preventive Innovation has Clustered Around a Single Target (CGRP) • Many chronic patients still experience >12 monthly migraine days on treatment
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MRGPRX2: Positioned to Address Neuronal and Mast Cell Drivers of Migraine © Evommune, Inc.30 Source: Evommune internal data (trigeminal neurons; in situ hybridization on human tissue samples), PMID: 40712576 (meningeal mast cells) Expression Confirmed in Disease-Relevant Tissues MRGPRX2 nuclei Trigeminal Ganglia Meningeal Mast Cells MRGPRX2 Mediates Neuropeptide Signaling Associated with Migraine (PACAP, VIP, Substance P) Meningeal Mast Cells: Perivascular cells in the dura responsive to PACAP, VIP, and Substance P Trigeminal Neurons: Primary sensory neurons mediating migraine pain Meninges Trigeminal Afferents
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PACAP Triggers Migraine via MRGPRX21 as Primary Receptor in vivo © Evommune, Inc.31 1. Mrgprb2 is rodent homologue. 2. In grams, measured via Orbital von Frey assessment. Source: Internal Evommune data. Confirms data published in PMID: 37516794. Facial withdrawal threshold2 • in vivo data support functional role of MRGPRX2 1 signaling in migraine Time After PACAP Administration 1 PACAP injected directly to meninges of wild type and knockout models Facial withdrawal threshold used as functional pain readout Knockout of MRGPRX21 Reduced PACAP-Induced Migraine Symptoms MRGPRX2 Ligand PACAP Induces Headache in vivo 2
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MRGPRX2 Ligands Induce Migraine in Humans PACAP , VIP , Substance P are Known MRGPRX2 Agonists © Evommune, Inc.32 Note: Data shown from PACAP -38; PACAP-27 also induces migraine. Sources: Adapted from PMID19052139, PMID34357396, PMID37009867, Al-Khazali et al., (2026). Note that there have been multiple studies inducing headache/migraine with ligands and experimental paradigms / r esults differed. Data shown represent cumulative observations pooled across multiple trials and cannot support definitive conclusions. PACAP, VIP, Substance P Infusion all Induce Migraine-Like Headache in Migraineurs PACAP-Induced Headaches More Closely Recapitulate Migraine Features vs. CGRP 58 71 81 5 10 0 25 50 75 100% Patients PACAP VIP Substance P 0 Drug PBO • Similar to CGRP, which induces migraine in ~2/3 patients CGRP PACAP 0 25 50 75 100 Associated with Migraine in Subset of Patients Difference (absolute) 39% 0% 5% -11% 25% 28% 31% Flushing Warm Sensation Finger Tingling Facial Puffing Jaw Pain Dizziness Premonitory Symptoms % Patients
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PACAP Likely Induces Migraine in Humans Through MRGPRX2 as Primary Receptor © Evommune, Inc.33 1. Trigeminal sensory neurons, brainstem pain circuits, hypothalamus, cortex, thalamus. Note: In addition to MRGPRX2 PACAP b inds PAC1, VPAC1, VPAC2, but PAC1 inhibition (Amgen’s AMG301: PAC1 blocking mAb.) does not show therapeutic benefit in migraine. Sources: PMID: 33231 489, PMID: 39085771, PMID: 37706270. PACAP Impact in Migraine Is Primarily through MRGPRX2 PACAP MRGPRX2 PAC1 PACAP Receptor Relevant Tissue Expression Preclinical Evidence? Clinical Validation In Migraine? PAC1 Neurons1 Limited VPAC1 VPAC2 Cranial vessels Neurons (?) Limited Not evaluated MRGPRX2 Mast Cells Sensory Neurons TBD VPAC1 VPAC2 ?X
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Inhibition of MRGPRX2 Ligand PACAP Achieves CGRP-Like Efficacy in Migraine Prophylaxis © Evommune, Inc.34 Note: Lundbeck’s bocunebart is a humanized mAb that neutralizes PACAP. Results above from Phase 2 a study in migraine prophylaxis (HOPE; N=237; single IV administration of bocunebart in patients that were a mix of episodic and chronic migraineurs). Source: Clinicaltrials.gov NCT05133323. Direct comparisons cannot be made in the absence of head -to-head trials because of differences in trial design, patient population and other factors. Lundbeck’s Bocunebart Reduced Monthly Migraine Days by ~2 Second Neuropeptide Axis Validated in Migraine Prevention PACAP likely acts through MRGPRX2 as a key neuropeptide trigger of migraine attacks Antibody blockade reduced migraine frequency in controlled clinical study Effect size falls within range observed for approved CGRP therapies • Magnitude of benefit consistent with marketed CGRP inhibitors -6.2 -4.2 -9 -6 -3 0 Mean Change in Monthly Migraine Days Bocunebart (IV) Placebo
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3 Neuropeptides that Trigger Migraine Signal Through MRGPRX2 Neuropeptide Preclinical Evidence Induced Headache in Humans Clinical Validation PACAP VIP TBD Substance P TBD MRGPRX2 Inhibition May Offer Broader Migraine Benefit than Targeting PACAP Alone © Evommune, Inc.35 Note that PACAP also binds PAC1, VPAC1, VPAC2, but PAC1 inhibition does not show therapeutic benefit in migraine. PACAP VIP Substance P MRGPRX2
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EVO756 Potently (low nM) Inhibits PACAP, Substance P and VIP-Induced MRGPRX2 Activation in vitro © Evommune, Inc.36 All assays (agonists) run at ≥EC80. Primary skin MC: CD63; similar experiment run on primary skin mast cells with CD107a with similar results. EVO756 Inhibits PACAP and SP-Induced Primary Human Mast Cell Activation in vitro EVO756 Inhibits Migraine Relevant Endogenous Ligands in X2-CHO Cells 0.0001 0.001 0.01 0.1 1 10 100 -40 -20 0 20 40 60 80 100 120 PACAP 1-38 VIP Substance P PACAP 1-27 EVO756 (μM) % Inhibition 0.001 0.01 0.1 1 10 100 -50 0 50 100 150 Substance P PACAP SP and PACAP with Skin Primary MCs EVO756 (μM) % Inhibition
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Phase 2b Dose-Ranging Trial in Migraine Prophylaxis Top-line Data Expected in 2027 © Evommune, Inc.37 BL = Baseline; CFB = change from baseline; MMD = monthly migraine days; MHD = monthly headache days; QoL = quality of life BL Adults with Refractory Migraine ≥6 Days/Month (N ≈ 330) Screening Enrollment W12 EVO756, Dose 1 EVO756, Dose 2 Placebo Randomized, Double-Blind, Placebo-Controlled Trial Primary Endpoint • Mean CFB in MMD Key Secondary Endpoints • ≥50%, ≥75% reduction in MMD • CFB in MHDs and MMD • CFB in monthly acute migraine medication use Exploratory Endpoints • Patient subtyping • Changes in biomarkers • Change in migraine-specific QoL Exploring daily doses up to100 mg
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EVO301: Best-in-Class IL-18BP Fusion Protein Long-Acting Serum Albumin-Binding Injectable Therapeutic Fusion Protein Designed to Neutralize IL-18 Signaling 38 © Evommune, Inc.
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EVO301 Could Command Substantial Market Share in the Potentially $60B+ AD Market as a Clearly Differentiated Biologic © Evommune, Inc.39 Sales from Evaluate Pharma may represent projections. 1. At maintenance. 2. From ’25-’26. Sales in $M Class Route of Administration 1 Launch Year 2025 WW Sales 2025 US Sales Projected Growth2 Projected Peak WW AD Sales in $M IL-4/-13 Q2W SubQ 2017 $12,496 $9,234 +9% $17,423 (2030) IL-13 Q2W SubQ 2021 $1,508 $1,421 +22% $2,469 (2030) IL-13 Q4W or Q8W SubQ 2024 $533 $274 +72% $2,625 (2032) IL-31 Q8W SubQ 2024 $339 $172 +91% $2,759 (2032) Four Marketed AD Biologics Currently ~$15B, Projected to be ~$25B by 2032
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10 20 30 0 50 60 40 Proven Playbook, Larger Market: AD Projected to Reach ~$60B 40 Per Evaluate Pharma (May represent projections and not actual sales); “Year 1” for AD represents 2017 (year of Dupixent launch); “Year 1” for Psoriasis represents 2004 (year of Enbrel launch in plaque psoriasis); 1. Total estimated prevalence in adult and pediatric populations from Decision Resources DL&F; 2. Total estimated prevalence in adult and pediatric populations; Estimated per psoriasis.org, datacenter.aecf.org, Armstrong et al. (2021), Paller et al. (2018), Tannenbaum et al. (2022), Helmick et al. (2014), Rosario-Jansen et al. (2025). Note this slide contains registered trademarks not owned by Evommune. AD market size from Evaluate and internal analyses. 10 of 14 Psoriasis Advanced Therapies Became Blockbusters — And AD Has ~5x the Patients Atopic Dermatitis Mod-to-Sev Patients ≈ 29M 1 AD Today: Concentrated, Early in Market Expansion Psoriasis Mod-to-Sev Patients ≈ 5.6M 2 $12.5B Dupixent (IL-4/-13) $ 1.5B Adbry (IL-13) $ 1.0B Rinvoq (JAK1) $ 0.5B Ebglyss (IL-13) $ 1.8B Other $10.6B Skyrizi (IL-23) $ 4.2B Tremfya (IL-23) $ 2.4B Stelara (IL-12/-23) $ 5.3B Cosentyx (IL-17A) $ 2.5B Taltz (IL-17A) $ 1.4B Bimzelx (IL-17A/F) $ 0.8B Humira (TNFα) $ 0.2B Enbrel (TNFα) $ 0.1B Remicade (TNFα) $ 2.0B Otezla (PDE4) $ 0.2B Cimzia (TNF) $ 0.3B Nemluvio (IL-31) $ 0.3B Cibinqo (JAK1) $ 1.0B Ilumya (IL-23) $ 0.3B Sotyktu (TYK2) $ 0.2B Siliq (IL-17R) $ 1.0B Other Global Sales ($B) © Evommune, Inc. Y1 Y2 Y3 Y4 Y5 Y6 Y7 Y8 Y9 Y10 Y11 Y12 Y13 Y14 Y15 Y16 Y17 Y18 Y19 Y20 Y21 Y22
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Both EBGLYSS and NEMLUVIO, Launched in 2024, Projected for $2.5B+ Global Sales EBGLYSS and NEMLUVIO Launches in AD Outpacing Historical Psoriasis Launches, Highlighting Need for New Options in AD © Evommune, Inc.41 Sources: IQVIA, based on New to Brand prescriptions. 0 3 6 9 12 1 2 3 4 5 6 7 8 9 10 11 12 Months Post-Launch U.S. Monthly TRX (000s) Ebglyss Nemluvio Bimzelx Skyrizi
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Biologic Pathway Adaptive Inflammation Innate Inflammation Skin Barrier (IL-22)TH2 TH1 TH17 IL-18 DUPIXENT® EBGLYSS® ADBRY® NEMLUVIO® EVO301 Addresses Limitations of Existing Biologics; Demonstrating Ability to Impact Multiple Drivers of AD, While Being Well Tolerated © Evommune, Inc.42 Green = impacts biological pathway; Red = negative effect. Broader inflammatory signaling of IL-18 can address endotypes not fully captured by Th2- targeted therapies — enabling potential for broader patient coverage and efficacy
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IL-18 Immune Rebalancing: Modulate Innate and Adaptive Inflammation for Potential Disease Remission © Evommune, Inc.43 PAMPs: Pathogen-associated molecular patterns; DAMPs: Damage-associated molecular patterns Chronic Inflammation Tissue Pathophysiology Clinical Manifestations Inflammatory Infiltrates Inflammatory Cytokines Autoimmunity AngiogenesisTh1, 2, 17 Differentiation Barrier Dysfunction Infection Tissue Damage Pathogen Clearance IL-18BP Therapeutic Approach Involved in Innate and Adaptive Immune Processes IL-18 producing cells IL-18 responding cells Stromal/mesenchymal IL-18 Epithelial Endothelial CD4 T NKCD8 TMacrophage Dendritic cell Dendritic cellMacrophage Dysbiosis Tissue InjuryInfection DAMPs*PAMPs* IL-18R1 IL-18RAP No ResponseActivation IL-18IL-18BP Epithelial Barrier
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Atopic Dermatitis & PsoriasisRheumatoid Arthritis Inflammatory Bowel Disease IL-18 Plays Key Role Across Multiple Chronic Inflammatory Diseases Cardiovascular Multiple Sclerosis CNS Heart GI Joints Skin 44 © Evommune, Inc.
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EVO301: Long-Acting IL-18BP Neutralizer Designed for Tissue Targeting SAFA and IL-18BP Fused Via Peptide Linker for Extended Neutralization of IL-18 Activity © Evommune, Inc.45 SAFA - Anti-Serum Albumin Fab-Associated. HSA – Human Serum Albumin SAFABODY is a trademark of AprilBio Co., Ltd. Free IL-18 IL-18 IL-18 BP SAFA Peptide linker Albumin SAFAbody Platform Technology • T½ extension: FcRn-mediated recycling of HSA • Efficient tissue distribution: – Smaller size (MW ~65 kD) and HSA binding IL-18 Binding Protein (IL-18BP) • High binding affinity and specificity • Native fully human sequence
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EVO301 Phase 2a Proof of Concept Trial Design © Evommune, Inc.46 EASI = Eczema Area and Severity Index; vIGA = Validated Investigator Global Assessment; BSA = Body Surface Area; BL = Baseline; PBO = Placebo. Trial identifier: NCT06723405 Screening Randomization 2 Active : 1 PBO End of Trial BL W12W4 Adults with Moderate-to-Severe Atopic Dermatitis (N = 70) Randomized, Double-Blind, Parallel Group, Placebo-Controlled Trial AD Population • EASI ≥16 • vIGA ≥3 • BSA ≥10% Primary Endpoint • Percent change from EASI at Week 12 (Bayesian) Pharmacokinetics Target EngagementW8 EVO301: 5 mg/kg IV Placebo Dosing day Dosing day W2
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EVO301 Achieved the Primary Endpoint Phase 2a Proof-of-Concept Trial in Moderate-to-Severe Atopic Dermatitis 47 • Highly statistically significant EASI reductions at weeks 4, 8, and 12 versus placebo • 34% and 33% placebo adjusted improvement in EASI at week 8 and 12, respectively • 23% of patients achieved IGA 0/1 at week 12 versus 0% placebo • Well-tolerated, with no treatment related serious or severe adverse events reported • Corresponding reductions in secondary endpoints, as well as key Th2 and non Th2 cytokines • Pharmacokinetics (PK) continues to support a Q4 week dosing regimen © Evommune, Inc. Phase 2a Profile Supports Potential Best-in-Class Monotherapy in Atopic Dermatitis
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Phase 2a Trial in AD Met Primary Outcome Measure (Bayesian) © Evommune, Inc.48 EASI: Eczema Area and Severity Index, SD: standard deviation, HPD: high posterior density % Change in EASI at Week 12: Protocol Success Criterion Met Statistic EVO301 versus Placebo Success Criterion: Posterior Probability of Difference < -8% 75% Trial Results: Posterior Probability of Difference < -8% 99.8% Posterior Mean Difference -32 95% HPD Interval for Difference in Mean -47, -15
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-75 -50 -25 0 Week 2 Phase 2a Trial in AD Demonstrated Statistically Significant Efficacy Across Time Points © Evommune, Inc.49 Week 0 Week 4 Week 8 Week 12 % Average Change in EASI ↓ Dosed at Weeks 0 and 4 Placebo EVO301 * * % Change in EASI by Study Visit *p<0.01 ↓ % Average change in EASI is LS Mean -22 -18 -16 -22 -30 -41 -50 -55 ↓ *
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IL-18BP IL-31IL-13IL- 4 / IL-13 Two Doses of EVO301 Demonstrated Comparable Activity at 12 Weeks to Dose-Optimized Marketed Biologics at 16 Weeks © Evommune, Inc.50 For illustrative purposes only. Not a head-to-head comparison. Differences exist between trial designs and study characteristics, and caution should be exercised when comparing across trials. Sources: Silverberg et al. (2016), Silverberg et al. (2023), Wollenberg et al. (2020), Ruzicka et al. (2017). Placebo-Adjusted % Improvement from Baseline in EASI Dose-Optimized Products # Doses: 2 8 8 8 8 8 8 3 33 35 36 38 34 23 35 14 0 15 30 45 EVO301 EVO301-AD001 Phase 2a 12 week N = 70 5 mg/kg IV Dupixent® SOLO 1 Phase 3 16 week N=671 600 mg W0 300 mg Q2W Dupixent® SOLO 2 Phase 3 16 week N=708 600 mg W0 300 mg Q2W Ebglyss ADVOCATE 1 Phase 3 16 week N=424 500 mg W0, W2 250 mg Q2W Ebglyss ADVOCATE 2 Phase 3 16 week N=427 500 mg W0, W2 250 mg Q2W Adbry® ECZTRA 1 Phase 3 16 week N=802 300 mg Q2W Adbry® ECZTRA 2 Phase 3 16 week N=794 300 mg Q2W Nemluvio® Phase 2a 12 week N=264 2 mg/kg QW4
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0 4 8 12 16 20 24 ↑ Week 0 ↑ Week 4 Week 8 Week 12 vIGA Response Phase 2a Trial in AD: Early Clinical Signal in vIGA 0/1 Response © Evommune, Inc.51 vIGA: Validated Investigator’s Global Assessment Visit EVO301 Placebo Week 4 4.2% 0% Week 8 12.5% 0% Week 12 22.9% 0% vIGA Response (≥2-point improvement and a score of 0 or 1) ↑ Dosed at Weeks 0 and 4 Placebo EVO301
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Safety Summary Over 12 Week Trial Period EVO301 Was Well Tolerated © Evommune, Inc.52 No Clinically Significant Lab Abnormalities. No Conjunctivitis Reported (as is Common with Other Biologics in AD) EVO301 Placebo Total N=48 N=22 N=70 Patients with ≥1 Adverse Event (AE) 30 (62.5%) 16 (72.7%) 46 (65.7%) Patients with ≥1 Treatment Related AE 5 (10.4%) 3 (13.6%) 8 (11.4%) Patients with a Related Serious or Severe AE 0 0 0 AEs Leading to Study Discontinuation 0 0 0 AEs > 5% in Either Arm EVO301 Placebo Total Upper respiratory tract infection 10 (20.8%) 4 (18.2%) 14 (20.0%) Atopic dermatitis 10 (20.8%) 9 (40.9%) 19 (27.1%) Headache 8 (16.7%) 3 (13.6%) 11 (15.7%) Nasopharyngitis 4 (8.3%) 0 4 (5.7%) Viral upper respiratory tract infection 3 (6.3%) 2 (9.1%) 5 (7.1%) Dizziness 3 (6.3%) 1 (4.5%) 4 (5.7%) Fatigue 3 (6.3%) 0 3 (4.3%)
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EVO301 Subcutaneous Formulation Exposure Consistent with IV © Evommune, Inc.53 Comparable Nonclinical Serum Exposure Key PK Parameters Parameters 10 mg/kg (N = 3/group) Intravenous (IV) Subcutaneous (SC) Cmax (g/mL) 343 90 AUC (g•hr/mL) ~27,000 ~27,000 Tmax (hr) 0.83 72 T1/2 (hr) 101 168 0 1 2 3 4 5 6 7 0.1 1.0 10.0 100.0 1,000.0 Time (weeks) Concentration ( g/mL) IC90 (CD4+ T Cells) SC IV
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5v Planned EVO301 Phase 2b Dose-Ranging Trial in AD Trial Initiation Expected Mid-2027 © Evommune, Inc.54 EASI = Eczema Area and Severity Index; vIGA = Validated Investigator Global Assessment; Pruritus-NRS = Pruritus Numerical Rating Scale; BSA = Body Surface Area; BL = Baseline, QoL = Quality of Life Q4W = Every four week dosing, Q2W = Every two week dosing, LD = Loading Dose. Primary Endpoint • % CFB in EASI at Week 16 Key Secondary Endpoints • EASI-50, EASI-75, and EASI-90 • Change in vIGA • Change in Pruritus -NRS • Proportion of patients achieving ≥4 point reduction in Pruritus -NRS • Change in BSA affected Exploratory & Biomarkers • QoL • Biomarkers • Target Engagement BL W16 Adults with Moderate-to-Severe Atopic Dermatitis (N ≈ 180) Randomized, Double-Blind, Placebo-Controlled Trial Screening Enrollment End of Trial W10 EVO301: Dosing Regimen 1 EVO301: Dosing Regimen 2 EVO301: Dosing Regimen 3 Placebo W2 W6W4 W8 W12 W14 Plan to explore Q2W and Q4W Regimens
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Thank You! 55 © Evommune, Inc.