
Corporate Presentation November 2026 © Evommune, Inc.

Disclaimers 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 potential therapeutic benefit of EVO756, EVO301, EVO646 and EVO570, the design, objectives, initiation, timing, progress and results of current and future preclinical studies and clinical trials of our product candidates, including the ongoing and planned Phase 2 clinical trials for EVO756, EVO301, EVO646 and EVO570; 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 to such estimates. We have not independently verified the accuracy or completeness of such information and we do not take any responsibility for 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. © Evommune, Inc.

Chronic Inflammation is a Global Healthcare Crisis © Evommune, Inc. 1. https://www.ncbi.nlm.nih.gov/books/NBK493173/. 2. Wylezinski LS, et al. PMID: 30979036. 3. GlobalData, 2023. 4. GlobalData, 2023 (US/EU5/JP forecasts). Annual Direct Cost2 $90B I&I Therapies Fail Patients >50% Deaths Worldwide1 3 of 5 Experienced Team Distinct Mechanisms Portfolio Approach Substantial Burden on the Healthcare System Treatments Have Critical Limitations Chronic Inflammation Destroys Lives Leaders behind ~30 approved NDAs and BLAs Novel approaches to heterogeneous diseases Multiple assets across multiple indications Evommune (EVMN) is Doing Something About It Patients Diagnosed with Immunological Disease3 234M 7% Advanced Therapies >$100B Sales4

A Broad Portfolio Progressing Multiple Opportunities © Evommune, Inc. 1. Moderate-to-severe atopic dermatitis, US adults; Chiesa Fuxench ZC, et al. J Invest Dermatol 2019. 2. US/EU5/JP 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). 3. Rheumatoid arthritis, global prevalence (17.6M); GBD 2021, Lancet Rheumatol 2023. 4. Evommune internal estimates based on initial potential indications. EVO756 | Oral MRGPRX2 EVO301 | IL-18 Biologic Focused on Innovative Targets with a High Probability of Success Targeting Sensory Neurons and Mast Cells in Migraine IL-18 Blockade for Multi-Pathway Immunomodulation Sensory Neuron Mast Cell Target Population: 30M2 Target Population: 6M1 EVO646 | Oral TLR7/8 Dual Mechanism for Autoimmune Disease Target Population: ~6M4 MRGPRX2 Novel Biologic Using the Fully Human IL-18 Binding Protein Adaptive (Th2) Inflammation Innate Inflammation Type I Interferon Pathway Pathogenic B-Cell Pathway Type I IFN Autoantibodies EVO570 | VAV1 Degrader Oral Molecular Glue Degrader for T- and B-Cell Disease Target Population: ~18M3 BCR CD19 TCR CD28 VAV1 Rac1 Rac1 GTP GDP GTP T-Cells B-Cells

Advancing Multiple Programs Toward Clinical Proof-of-Concept Program/Target Indication Preclinical Phase 1 Phase 2 Phase 3 EVO301 IL-18BP Atopic Dermatitis Ulcerative Colitis EVO756 MRGPRX2 Migraine EVO570 VAV1 MGD Rheumatoid Arthritis EVO646 TLR7/8 Antagonist Autoimmune Diseases Pipeline of Potential Best-in-Class and/or First-in-Class Assets © Evommune, Inc. Planned Phase 2b Initiation Mid-2027 Planned Phase 2a Initiation 1Q 2027 Phase 2b Top-line Anticipated 2H 2027 Phase 1 HV and Biomarker Data Late 2027 Phase 1 HV and Biomarker Data Mid-2027

Key Milestones Ahead For Evommune © Evommune, Inc. ~$290m Cash and Investments1, Current Runway Into 2H 2029 Championing Innovation for Chronic Inflammation EVO301 IL-18BP Plan to initiate Phase 2b in AD with subcutaneous formulation in mid-2027 Plan to initiate Phase 2a in UC in 1H 2027 EVO756 MRGPRX2 Antagonist Expect top-line data from Phase 2b migraine trial in 2027 EVO570 VAV1 MGD Expect Phase 1 HV biomarker data mid-2027 Plan to initiate Phase 2 program 2H 2027 EVO646 TLR7/8 Antagonist Plan to initiate Phase 1 in 1H 2027 Expect Phase 1 HV biomarker data in 2H 2027 1. Pro Forma: $262.3M cash, cash equivalents and investments as of September 30, 2026, plus net proceeds of approximately $28.0 million from the November PIPE financing.

EVO301: Potential Best-in-Class IL-18BP Fusion Protein Long-Acting Serum Albumin-Binding Injectable Therapeutic Fusion Protein Designed to Neutralize IL-18 Signaling © Evommune, Inc.

IL-36 IL-33 EVO301 Mechanism of Action © Evommune, Inc. Inflammation Lichenification ITCH IL-17C IL-18 IL-31 Nemluvio EVO301 Camoteskimab TL1A Afimkibart Innate Immunity Macrophage NK Cell Mast Cell Dendritic Cell Basophil Eosinophil ILC2 IL-23 IL-22 IL-17A TH17 Cell IL-12 IFN-γ Approved In Development IL-18 + Co-Signaling Cytokine Rinvoq Cibinqo STAT STAT P P JAK P JAK P KT-621 PF-08049820 IL-2 IL-4 IL-13 Th2 Cell Ebglyss Adbry Zumilokibart Dupixent IL-12/ IL-15/ IL-3 IL‑18 is released from the skin barrier and, alongside other cytokines, contributes to innate immunity and Th1 (IFN-γ), Th2 (IL‑4, IL‑13) and Th17 (IL‑17) responses EVO301 and camoteskimab target IL‑18, which plays a role across several AD inflammatory pathways at once Approved agents block single pathways: IL‑31, IL‑4/IL‑13 or JAK signaling Treg Rezpeg TH1 Cell EVO301 Blocks IL-18, a Cytokine Active Across Multiple AD Inflammatory Pathways

IL-18 Blockade Clinically Validated: Safe, Long-Term & Effective © Evommune, Inc. Human Data SupportLong-Term IL-18 Inhibition IL-18BP Is the Basis of EVO301 Mechanism IL-18BP is the body’s natural IL-18 brake1 Tolerated for years, incl. in children2 Human Genetics No AD, infections or other disease with IL-18 loss of function3 People with undetectable IL-18 live normal lifespans4 Clinical Safety No treatment-related safety signals No conjunctivitis in 4 IL-18 programs5,6 Sources: ¹Dinarello et al., Front Immunol (2013). ²Canna et al., J Allergy Clin Immunol (2017); Gabay et al., Ann Rheum Dis (2018). ³Belkaya et al., J Exp Med (2019). ⁴Dominy et al., J Allergy Clin Immunol (2026). ⁵Ellis et al., Allergy (2025). ⁶Evommune EVO301 top-line results (2026). Efficacy Shown Across3 IL-18 Programs Tadekinig alfa IL-18BP, AB2 Bio Still’s Ph2: 11 of 22 responded by Week 32 Ph3 ongoing in NLRC4/XIAP2 Camoteskimab anti-IL-18, Apollo AD Ph2a: met primary EASI endpoint7 ~80% EASI reduction, open-label7 Aletekitug anti-IL-18, GSK AD Ph1b: EASI −68% vs. −33% placebo5 Single IV dose, Week 125 Data from separate studies, not head-to-head. Source: ⁷Apollo Therapeutics camoteskimab Ph2a press release (Sept 2025).

EVO301 in Atopic Dermatitis (AD) Neutralizing IL-18 to address the Th2 and non-Th2 inflammation that drives AD © Evommune, Inc.

10 20 30 0 50 60 40 Proven Playbook, Larger Market: AD Could Reach ~$60B © Evommune, Inc. 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. 3. Kymera Therapeutics perspective piece: <1M of ~42M AD patients worldwide receive dupilumab. 4. Apogee Therapeutics 10-K: >20% of patients discontinue Dupixent within six months. Atopic Dermatitis Mod-to-Sev Patients ≈ 29M 1 AD Today: <1 in 40 patients worldwide on Dupixent3 1 in 5 stop within 6 months4 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 (TNFα) $ 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 New Entrants Will Grow the AD Market Global Sales ($B) Y1 Y2 Y3 Y4 Y5 Y6 Y7 Y8 Y9 Y10 Y11 Y12 Y13 Y14 Y15 Y16 Y17 Y18 Y19 Y20 Y21 Y22 40% of Psoriasis Patients Have Cycled Through 3+ Biologics, AD Needs Many More Options 10 of 14 Psoriasis Advanced Therapies Became Blockbusters AD Has ~5x the Patients

EVO301 Has Potential to Command Substantial Market Share in AD Market © Evommune, Inc. Sales from Evaluate Pharma may represent projections (accessed Sept 2026). 1. At maintenance. 2. From ’25-’26. 3. Global atopic dermatitis therapeutics market, projected at $29.5B by 2033 from $15.4B in 2024 (7.5% CAGR); Astute Analytica, Feb 2026. Sales in $M Class Route of Administration1 Launch Year 2025 WW Net Sales 2025 US Net Sales Projected CAGR2 Projected Peak WW AD Net Sales in $M IL-4/-13 Q2W SubQ 2017 $12,496 $9,234 +9% $18,787 (2030) IL-13 Q2W SubQ 2021 $532 $422 +5% $691 (2030) IL-13 Q4W or Q8W SubQ 2024 $408 $274 +24% $2,318 (2033) IL-31 Q8W SubQ 2024 $339 $172 +33% $3,312 (2033) Top AD Biologics Currently ~$17B Worldwide, Projected to be ~$30B by 20333

EVO301 Has Multi-Billion Dollar Potential © Evommune, Inc. Source: Evommune 2036 estimates based on Evaluate Pharma (2032), Datamonitor (2033) data ~$100B Market IL-18-Driven Diseases 2L+ Advanced Therapy AD Biologic-experienced / inadequate responders 1L Advanced Therapy AD Initiating advanced systemic therapy Expand into IL-18 Diseases Secure Access Advance to 1L AD Market Expansion Moderate-to-Severe AD Eligible for advanced therapies AD, UC, CD + adjacent pipeline expansion EVO301 has the potential to become a foundational therapy in atopic dermatitis and other IL-18 driven diseases Patients ~6M Patients ~700K Patients ~2.0M Patients ~2.3M ~$60B Market

EVO301: Long-Acting IL-18 Neutralizer Designed for Tissue TargetingSAFA and IL-18BP Fused Via Peptide Linker for Extended Neutralization of IL-18 Activity © Evommune, Inc. 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 kDa) and HSA binding IL-18 Binding Protein (IL-18BP) High binding affinity and specificity Native fully human sequence No binding to anti-inflammatory IL-37 Only Long-Acting IL-18BP in Development, Differentiated From IL-18 mAbs in Size, Binding Affinity and Targeting

Therapy Adaptive Inflammation Innate Inflammation Skin Barrier (IL-22) No Conjunctivitis Signal Th2 TH1 TH17 EVO301 DUPIXENT® EBGLYSS® ADBRY® NEMLUVIO® EVO301 Matches Biologics on Th2, Then Goes Beyond ItClinically Validated Modulation of Th2 and Non-Th2 Inflammation © Evommune, Inc. Green = impacts biological pathway; Red = negative effect. EVO301 biomarker data: see slide 22 Demonstrated Ability to Impact Multiple Drivers of AD Broader inflammatory signaling of IL-18 can safely address endotypes not fully captured by Th2-targeted therapies

EVO301 Phase 2a Proof-of-Concept Trial DesignOne dose, administered twice © Evommune, Inc. EASI = Eczema Area and Severity Index; vIGA = Validated Investigator Global Assessment; BSA = Body Surface Area; BL = Baseline; PBO = Placebo. Trial identifier: NCT06723405 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 baseline in EASI at Week 12 (Bayesian) Pharmacokinetics Target Engagement Screening Randomization 2 Active : 1 PBO End of Trial BL W12 W4 W8 EVO301: 5mg/kg IV Placebo Dosing day Dosing day W2

EVO301 Achieved the Primary EndpointPhase 2a Proof-of-Concept Trial in Moderate-to-Severe Atopic Dermatitis (N=70) © Evommune, Inc. 34% placebo-adjusted EASI improvement at week 8 (33% at week 12) 23% of patients achieved vIGA 0/1 at week 12 vs 0% on placebo Highly significant EASI reductions vs placebo at weeks 4, 8, and 12 No treatment-related serious or severe AEs No conjunctivitis Biomarkers and secondary endpoints moved with EASI PK supports at least Q4-week dosing Phase 2a Profile Supports Potential Best-in-Class Monotherapy in Atopic Dermatitis With one dose, administered twice, comparable to dose-optimized marketed biologics

Rapid, Robust and Durable Separation from PlaceboOne dose, administered twice © Evommune, Inc. Week 2 Week 0 Week 4 Week 8 Week 12 % Average Change in EASI * * ↓ % Average change in EASI is LS Mean -22 -18 -16 -22 -30 -41 -50 -55 * ↓ Dosed at Weeks 0 and 4 Placebo (n=22) EVO301 (n=48) *p<0.01 ↓ Off Drug Period EASI Improvement Kept Deepening for 8 Weeks After the Last Dose (-41% to -55%)

EVO301 Demonstrated Comparable Activity at 12 Weeks to Dose-Optimized Marketed Biologics at 16 Weeks © Evommune, Inc. IL-18 IL-31 IL-13 IL-4 / IL-13 For illustrative purposes only. Not a head-to-head comparison. Differences exist between trial designs and trial 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); Nemluvio Ph2b + TCS: Silverberg et al., JACI (2020), 30mg arm, week 24. Placebo-Adjusted % Improvement from Baseline in EASI Dose-Optimized Products # Doses: 2 8 8 8 8 8 8 3 6 EVO301 EVO301-AD001 Phase 2a 12 week N = 70 5mg/kg IV Dupixent® SOLO 1 Phase 3 16 week N=671 600mg W0 300mg Q2W Dupixent® SOLO 2 Phase 3 16 week N=708 600mg W0 300mg Q2W Ebglyss ADvocate 1 Phase 3 16 week N=424 500mg W0, W2 250mg Q2W Ebglyss ADvocate 2 Phase 3 16 week N=427 500mg W0, W2 250mg Q2W Adbry® ECZTRA 1 Phase 3 16 week N=802 300mg Q2W Adbry® ECZTRA 2 Phase 3 16 week N=794 300mg Q2W Nemluvio® Phase 2a 12 week N=264 2mg/kg Q4W Nemluvio® Phase 2b + TCS 24 week N=226 30mg Q4W EVO301: Single Dose Administered Twice, Already Comparable to Marketed Biologics

EASI-75 Response Continued to Rise After the Last DoseRapid, Durable and Increasing Responses with Just One Dose, Administered Twice © Evommune, Inc. Week 2 Week 0 Week 4 Week 8 Week 12 Patients Achieving EASI-75 EASI-75 = ≥75% improvement in EASI. EVO301 vs placebo: p=0.148 (Wk 8), p=0.069 (Wk 12). 0% 0% 5% 9% 8% 19% 19% 29% ↓ Dosed at Weeks 0 and 4 Placebo (n=22) EVO301 (n=48) p=0.069 at Week 12 ↓ Off Drug Period PBO-Adjusted EASI-75 Reached 20% at Week 12, 8 Weeks After the Last Dose ↓

EVO301 Ph2a EASI-75 Matches Lebrikizumab Without TCSLebrikizumab Dose-Optimization After Ph2a Drove Substantial Improvements in EASI-75 Lebrikizumab Precedent EVO301 matched Lebri's Ph2a efficacy without TCS EVO301 reached 20% with no TCS; Lebri's Ph2a arms reached 5-21%, all with TCS Phase 3 optimization drove a step-change in efficacy Dose, regimen and trial-design refinements increased EASI-75 from 5%-21% in Phase 2a to as high as 43% in pivotal studies © Evommune, Inc. 125mg single dose + TCS 250mg single dose + TCS 125mg Q4W + TCS PBO-Adjusted EASI-75, % 500 mg LD;250 mg Q2W + TCS 500 mg LD;250 mg Q2W 5mg/kg dosesNo TCS dose optimized 500 mg LD;250 mg Q2W Phase 2a (12 wk) Lebrikizumab EVO301 Phase 3 (16 wk) Phase 2b/3 (16 wk) Phase 2a (12 wk) TBD All Ph2a arms + TCS

EVO301 Impacts Biomarkers Th2 and BeyondMatches IL-13 Therapies on Th2, and Impacts Th1 and Th17/22 © Evommune, Inc. 1Th2-high subjects (n=11): TARC ≥ 929 pg/mL, CCL-22 ≥ 2,348 pg/mL; 2Th1-high subjects (n=9): CXCL9 ≥ 56 pg/mL, CXCL10 ≥ 205 pg/mL; 3Th17-high subjects (n=12): S100A12 ≥ 159 pg/mL; 4all EVO301-treated subjects (n=47); 5Week 16, SOLO1/2 trials, TARC ≥ 1,600 pg/mL; 6Week 16, estimated from Ariens et al. 2020; 7Week 16, estimated from ADvocate1/2 and 8ADhere-J trials; 9Week 28, estimated from Dekkers et al. 2024; 10Week 4, Broaden trial, TARC; EVO301 maximum cytokine reduction represents median % change from baseline.

IL-4/13 Co-administration with EVO301 Showed No Additive Benefit in vivo © Evommune, Inc. Chronic oxazolone-induced atopic dermatitis preclinical model Normal Vehicle anti-IL-4Rα mAb (3 mpk)* EVO301 (3 mpk)* anti-IL-4Rα mAb (3 mpk) + EVO301 (3 mpk)* Mean cumulative score (erythema, scaling, thickness); error bars omitted for clarity. *Significant vs. vehicle at day 27 for each treatment arm.

EVO301 Subcutaneous Formulation Exposure Consistent with IVSubcutaneous Formulation Work Complete, Trial Initiation On-Track for Mid-2027 © Evommune, Inc. Comparable Nonclinical Serum Exposure Key PK Parameters Parameters 10mg/kg (N = 3/group) Intravenous (IV) Subcutaneous (SC) Cmax (mg/mL) 343 90 AUC (mghr/mL) ~27,000 ~27,000 Tmax (hr) 0.83 72 T1/2 (hr) 101 168 0.1 1.0 10.0 100.0 1,000.0 Time (weeks) Concentration (mg/mL) IC90 (CD4+ T Cells) SC IV

Planned EVO301 Phase 2b Dose-Ranging Trial in ADTrial Initiation Expected Mid-2027 © Evommune, Inc. 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, CFB = Change from Baseline. 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 Planned Countries Poland, Germany, Czechia, Bulgaria, US, Canada, Australia, New Zealand BL W16 Adults with Moderate-to-Severe Atopic Dermatitis (N ≈ 200) Randomized, Double-Blind, Placebo-Controlled Trial Screening Enrollment (1:1:1:1) End of Trial W10 Follow-On Period 8 Weeks Off Drug Durability Check 500mg Q4W 500mg LD, 250mg Q4W 500mg LD, 250mg Q2W Placebo W2 W6 W4 W8 W12 W14 W24 W20

EVO301 in Inflammatory Bowel Disease Extending IL-18BP into ulcerative colitis (UC), where epithelial barrier failure drives disease © Evommune, Inc.

Current Therapies Stall at 20-30% Remission © Evommune, Inc. 1.25M Americans living with UC1 20-30% Remission rates in induction trials of advanced therapies2 1 in 5 Patients hospitalized within five years of diagnosis3 $6.4B Skyrizi IBD sales in 2025, more than double 20244 1. Lewis JD et al., Gastroenterology 2023;165:1197-1205 (claims data extrapolated to 2020 US Census). 2. Alsoud D et al., Lancet Gastroenterol Hepatol 2021;6:589-595. 3. Frontiers in Gastroenterology, 2026 (~20% hospitalized, 7% colectomy within five years). 4. AbbVie 4Q25 earnings, Feb 2026 (Skyrizi total 2025 net revenues $17.6B). 5. Inflamm Bowel Dis 2024 (doi:10.1093/ibd/izad292); Evommune analysis of ClinicalTrials.gov, November 2026. IBD, inflammatory bowel disease; IL-18BP, IL-18 binding protein; UC, ulcerative colitis. No approved therapy targets IL-18: EVO301 is the only IL-18BP program in IBD development5

UC is a Large and Expanding Market Where Innovation Can Win>$21B by 2033, with Durable Remission Still Out of Reach for Most Patients © Evommune, Inc. >$21B UC therapy sales in 20331 +$10.4B (~92%) market growth expected 3.3M Patients in 7MM2 Multiple Mechanisms Expected to Exceed $1B (2033 projections)1 Recent launches suggest differentiated entrants can expand the category, not just redistribute the share ~10-30% of patients do not respond to initial anti-TNF therapy3 ~23-46% of patients lose response over time3 Meaningful Clinical Gaps Durable remission, efficacy in bio-experienced patients, convenience, and prevention of fibrosis Anti-integrin IL-23 inhibitors JAK inhibitors Aminosalicylates IL-12/23 S1P modulators TNF-α inhibitors UC is a $21B+ market with room for multiple winners and headroom for better outcomes Market Scale and Momentum Clinical Opportunity 1. Clarivate, UC Disease Landscape & Forecast (G7: US, EU5, Japan), Oct 2025; Datamonitor, UC Disease Landscape & Forecast. 2. DelveInsight, UC Market Insight, Epidemiology and Market Forecast, 2026 (diagnosed prevalent cases, 2025). 3. Peyrin-Biroulet L, et al. Ther Adv Gastroenterol 2021;14:17562848211059954. Other sources: pivotal trials (GEMINI 1, UNIFI, LUCENT, INSPIRE, QUASAR, ELEVATE, U-ACHIEVE/ACCOMPLISH, ACT 1); CGH 2023. 7MM, seven major markets; TNF, tumor necrosis factor; UC, ulcerative colitis.

© Evommune, Inc. EVO301 Targets Epithelial Barrier Failure, the First Trigger in IBD Translates to Potential Barrier Repair 29 IL-18 blocks goblet cell and mucus barrier repair2 IL18R1-IL18RAP variants raise IBD risk1 IL-18 elevated in inflamed IBD mucosa1 Preclinical Validation Human Genetics Barrier Function Loss of IL-18BP drives severe colitis in mice2 Patient Data 1 Zhernakova et al., Am J Hum Genet, 2008; Harrison et al., Mucosal Immunol, 2015. 2 Nowarski et al., Cell, 2015 (PMID 26638073). 3 EVO301 Phase 2a AD trial biomarker data, EADV 2026. AD Clinical Data EVO301 modulated Th22 (IL-22) biomarkers in the Phase 2a AD trial3 Barrier failure is the first trigger in IBD; IL-18 blocks its repair Mucus Layer Loss Permeability Goblet Cell Loss Key role for IL-18 signaling in IBD Immune Activation Immune CellRecruitment Chemokines and Cytokines Inflammatory Cycle IL-18 Epithelial cell Goblet cell Bacteria Activated macrophage α4β7+ CD4+ T cell B cell Effector T cell Innate immune cells Safety Long-term IL-18 inhibition tolerated; supports potential use in combination

EVO301 Reversed Established Fibrosis in vivoA Differentiating Effect Not Observed with Current IBD Therapies © Evommune, Inc. MASH: metabolic dysfunction-associated steatohepatitis. 1 Rieder et al., Gut, 2024;73:854-866. AprilBio 2025, PMID: 40239621, PMID: 27720839 Note: EVO301 vs resmetirom: not significantly different (p = 0.07). Hydroxyproline and Pro-C3 showed the same pattern. Treatment started at week 19; efficacy readout at week 27. Fibrosis Remains a Major Unmet Need in IBD EVO301 Reduced Fibrosis Below Baseline, Matching Resmetirom in a Mouse MASH Model EVO301 matched resmetirom’s antifibrotic effect, with fibrosis falling below pretreatment levels - consistent with true regression rather than prevention alone ~50% of patients with Crohn’s disease develop stricturing or penetrating complications within 10 years Fibrotic complications are a major driver of surgery and irreversible bowel damage Anti-TNF, IL-23, JAK and S1P agents treat inflammation. No approved IBD therapy is antifibrotic Threshold for Obstructive Symptoms Fibrosis Burden Inflammation (flares) Disease course. Flares come and go; fibrosis progresses over time Level at Treatment Start Histological Fibrosis (Sirius red, % positive area)

Planned EVO301 Ulcerative Colitis Proof-of-Concept Phase 2a Trial © Evommune, Inc. UC: ulcerative colitis; mMCS: modified Mayo Clinical Score; PRO: patient reported outcomes; Fcal: fecal calprotectin, hsCRP: high sensitivity C-reactive protein; LRG: Leucine-rich α2-glycoprotein; NGAL: Neutrophil Gelatinase-Associated Lipocalin; MoA: mechanism of action. Primary Endpoint Safety and tolerability Secondary Endpoints (Weeks 2, 4, 8, 12) ΔmMCS vs placebo Endoscopic improvement (Week 8) Fecal calprotectin (Weeks 8 and 12) PROs rectal bleeding and stool frequency Partial and complete remission (weeks 8 and 12) Pharmacokinetics and ADA Exploratory Biomarkers Serum IL-18 and drug-bound IL-18 target engagement Serum and stool: Fcal, Lactoferrin, hsCRP, LRG, NGAL, immune cytokines Biopsy bulk RNA-seq: tissue engagement and MoA BL 10mg/kg IV Adults with Moderate-to-Severe Ulcerative Colitis (N ~ 84) Randomized, Double-Blind, Placebo-Controlled Trial IV treatment at Baseline, Week 2, Week 4 Screening Randomization (2:1) End of Trial W2 5mg/kg IV W4 5mg/kg IV W8 Eval/Endoscopy EVO301: 10mg/kg IV, then 5mg/kg IV Placebo W12

EVO756: Oral MRGPRX2 Antagonist Potential First- and Best-in-Class Dual Mechanism Modulates Both Peripheral Sensory Neurons and Mast Cells © Evommune, Inc.

EVO756: Targeting Major Unmet Need in Migraine Prevention © Evommune, Inc. 1. US/EU5/JP 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). Patients Eligible for Preventive Therapy1 EVO756 - Defining the Next Wave of Preventives Oral Dosing 1 Novel Dual Mechanism 2 First-Line Potential 3 30 M ~

Advanced Treatments Class Route of Admin. MMDs on drug Annual US Sales CGRP Oral QD 12.3 $1.5B Oral EOD * $2B IV 7.9 $1.3B SC 14.6 $0.3B SC *11.2 $0.4B SC 11.3 $0.6B Neuro-toxin IM *11.5 $2B Innovation in Migraine Prevention Has Been Largely Limited to CGRPs © Evommune, Inc. MMD = Monthly Migraine Days. All MMDs are from chronic migraine trials across 12 weeks. *Nurtec ODT does not have trials in chronic patients. *Aimovig is across weeks 9-12. * Botox is across weeks 1-24. Sources: Qulipta - Prescribing Information, Vyepti 300mg - NCT02974153, Emgality - Prescribing Information, Aimovig 140mg - NCT02066415, Ajovy 675mg - NCT02621931, Botox - NCT00156910 Migraine Burden Persists Despite Oral CGRP Therapy Monthly Migraine Days (On Treatment) Placebo Qulipta Preventive Innovation Has Clustered Around a Single Target (CGRP) Efficacy, Not Just Innovation Best therapies beat placebo by only ~1-1.5 monthly migraine days 1.5 MMD

High Demand for Preventive Migraine Therapy © Evommune, Inc. 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). 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. AHS Consensus Statement Prevention Drives ~50% of $25B Migraine Market 0 10 20 30 7MM Sales ($B) 10.2 9.3 2026 13.0 12.7 2030 $19.5 $25.7 Acute Prophylaxis >75M People Living with Migraine in 7 Major Markets ~30M Patients Eligible for Preventive Therapy in 7 Major Markets Most Patients Remain on Legacy Preventives - Targeted Therapies Drive Sales % Patients 5% 13% 20% 36% 9% 30% 113% >$8B in 2026 NSAIDs/Analgesics Calcium Channel Blockers Tricyclic Antidepressants Beta Blockers Antiepileptics Neurotoxin CGRPs Limited Therapeutic Diversity Only CGRP inhibitors and neurotoxin Inadequate Efficacy ~45% of episodic and chronic patients do not achieve 50% improvement and have ≥8 monthly migraine days Tolerability Challenges Remain CGRPs associated with constipation, hypertension, Raynaud’s, nausea, allergic and injection site reactions

Strong Scientific Rationale for EVO756 in Migraine © Evommune, Inc. MRGPRX2 is expressed in human trigeminal neurons and meningeal mast cells Disease-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 benefit in-line with CGRPs Clinical Validation

MRGPRX2: Positioned to Address Neuronal and Mast Cell Drivers of Migraine © Evommune, Inc. 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

PACAP Inhibition Achieves CGRP-Like Efficacy in Migraine Prophylaxis © Evommune, Inc. Note: Lundbeck’s bocunebart is a humanized mAb that neutralizes PACAP. Results above from Phase 2a trial in migraine prophylaxis (HOPE; N=237; single IV administration of bocunebart in patients who 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 in Patients Who Had Failed 2-4 Preventive Treatments Second Neuropeptide Axis Validated in Migraine Prevention PACAP is a key neuropeptide trigger of migraine attacks Antibody blockade reduced migraine frequency in controlled clinical trial Effect size exceeds the ~1-1.5 MMD benefit of approved CGRP therapies ~2 MMD benefit vs. placebo, above the ~1-1.5 MMD of marketed CGRP inhibitors Mean Change in Monthly Migraine Days Bocunebart (IV) Placebo

PACAP Triggers Migraine via MRGPRX21 © Evommune, Inc. 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 MRGPRX21 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

PACAP Impact in Migraine Is Primarily Through MRGPRX2 © Evommune, Inc. 1. Trigeminal sensory neurons, brainstem pain circuits, hypothalamus, cortex, thalamus. Note: In addition to MRGPRX2, PACAP binds PAC1, VPAC1, VPAC2, but PAC1 inhibition (Amgen’s AMG301: PAC1 blocking mAb) does not show therapeutic benefit in migraine. Sources: PMID: 33231489, PMID: 39085771, PMID: 37706270. 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 Top-line Data Expected 2027 VPAC1 VPAC2 ? X

3 Neuropeptides That Trigger Migraine Signal Through MRGPRX2 © Evommune, Inc. Note that PACAP also binds PAC1, VPAC1, VPAC2, but PAC1 inhibition does not show therapeutic benefit in migraine. PACAP VIP Substance P MRGPRX2

Neuropeptide Preclinical Evidence Induced Headache in Humans Clinical Validation PACAP VIP Substance P Blocking MRGPRX2 Addresses Validated Migraine Triggers © Evommune, Inc. Note that PACAP also binds PAC1, VPAC1, VPAC2, but PAC1 inhibition does not show therapeutic benefit in migraine.

EVO756 Clinical Development Overview © Evommune, Inc. CIndU = Chronic inducible urticaria; CSU = Chronic Spontaneous Urticaria; AD = Atopic dermatitis Trial Phase 1 Proof-of-Concept Phase 2 Phase 2b N 132 30 ~330 Indication Healthy Volunteers CIndU Migraine Key Takeaways Well-tolerated Clear target engagement ~70% human skin penetration PK supports full target coverage as low as 25mg BID Well-tolerated Complete responses as early as week 1 Clear POC achieved with 70% responders Similar activity at 50mg BID and 300mg QD doses Trial Initiated in July 2026, Top-line Data Expected 2027 Safety and Tolerability Established Across All Trials to Date including CSU and AD

Phase 2b Dose-Ranging Trial in Migraine ProphylaxisTop-line Data Expected in 2H 2027 © Evommune, Inc. 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, 25mg BID EVO756, 50mg BID Placebo Randomized, Double-Blind, Placebo-Controlled Trial Primary Endpoint Mean CFB in MMD Key Secondary Endpoints ≥50%, ≥75% reduction in MMD CFB in MHDs CFB in monthly acute migraine medication use Exploratory Endpoints Patient subtyping Changes in biomarkers Change in migraine-specific QoL

EVO570: VAV1 Molecular Glue Degrader JAK-like Oral Degrader with Potential for Improved Safety and a Best-in-Class Profile in Autoimmune Disease © Evommune, Inc.

VAV1 Could Be the Next Major I&I Class JAK-like oral convenience with immune-cell selectivity, starting in RA © Evommune, Inc. JAK Inhibitors Today ~$12.5B4 2025 WW JAK class sales Oral, once-daily dosing Approved in 10+ I&I indications Boxed warning limits most use to 2L How VAV1 Differs Immune-cell restricted VAV1 is expressed in immune cells; JAKs signal across most tissues Targeted pathway Acts downstream of T- and B-cell receptors, not broad cytokine signaling Same oral convenience Once-daily oral small molecule, like the JAKs Where VAV1 can go 1 · START ~18M1 RA patients Rheumatoid arthritis Clear development and regulatory path 2 · SUPPLANT JAKS 200M+2 patients in JAK-approved diseases 10+ JAK-approved indications Including Psoriasis · UC · Crohn’s · PsA · AD 3 · GO BEYOND JAKS 6.5M+3 patients in diseases JAKs don’t treat MS · MG · Sjögren’s · lupus Novartis Ph2 underway in Sjögren’s All figures are global prevalence. 1. RA patients worldwide: 17.6M (GBD 2021; Lancet Rheumatol 2023). 2. Patients across JAK-approved I&I diseases, led by AD (2.54% global prevalence; GBD, JAAD Int 2024), plus IBD (UC and Crohn’s), PsA, axSpA and alopecia areata. 3. Lupus 3.41M (Ann Rheum Dis 2023) and MS 3.1M (Atlas of MS 2024); excludes Sjögren’s and MG. AD, atopic dermatitis; axSpA, axial spondyloarthritis; GCA, giant cell arteritis; GVHD, graft-versus-host disease; IBD, inflammatory bowel disease; I&I, immunology and inflammation; MG, myasthenia gravis; MS, multiple sclerosis; Ph2, Phase 2; PsA, psoriatic arthritis; RA, rheumatoid arthritis; UC, ulcerative colitis. 4. Evaluate Pharma, WW JAK class sales 2025 (incl. Rinvoq $8.3B per AbbVie FY2025; includes Jakafi heme indications). Boxed warning per FDA labels (2021 class update after ORAL Surveillance). Expression: Human Protein Atlas.

VAV1 Biology Overlaps with Approved I&I Drug MechanismsSeven drug classes span nine indications; VAV1 has direct evidence in each T-cell mediated T/B-cell mediated Drug class Example drugs Psoriasis UC Crohn’s PsA RA MS MG SLE Sjögren’s Route TNF Humira, Enbrel Inj. IL-17A Taltz, Cosentyx Inj. IL-6 Actemra, Kevzara Inj. FcRn Vyvgart Inj. CD20 Ocrevus, Rituxan Inj. JAK Rinvoq, Xeljanz, Olumiant Oral TYK2 Sotyktu Oral VAV1 Direct evidence Genetics; expression Colitis model Colitis model Ph2a/b posted Arthritis model; genetics EAE model; genetics Genetics Lupus model; patient cells Lupus model; patient cells; Ph2a/b Oral Approved in indication Investigational © Evommune CONFIDENTIAL VAV1 row: direct evidence only (blank = none); Ph2a/b = trial underway / posted, no efficacy data. Source: Evaluate Pharma.

VAV1: JAK-Like with a More Selective Profile © Evommune CONFIDENTIAL VAV1 JAK1 JAK2 JAK3 TYK2 T-cell depletion B-cell depletion (Rituximab) Expression is limited to immune cells Modulates T-cell function Modulates B-cell function Phenotype of KO mouse N/A N/A Modulates cytokine production Immune cell chemotaxis Safety Key Strong yes Yes Somewhat Mostly no No

EVO570 Meets or Exceeds MRT-6160 and Standard of Care Across All Tested Disease Models © Evommune CONFIDENTIAL Multiple Sclerosis (MS) Rheumatoid Arthritis (RA) Inflammatory Bowel Disease (IBD) EVO570 previously known as HC118

EVO570 Outperforms MRT-6160 in Preclinical Head-to-Head~20× greater degradation potency with clean selectivity and a potential for low dosing © Evommune, Inc. Property MRT-6160 (Novartis) EVO570 EVO570 Advantage VAV1 DC50 (HiBiT, Jurkat) 7 nM 0.3 nM ~20× more potent Max degradation (Dmax) 97% 99% Deeper knockdown CRBN binding IC50 1.4 µM 0.145 µM ~10× higher affinity Ternary complex EC50 11 nM 2.7 nM ~4× stronger T-cell IL-2 IC50 0.98 nM 0.08 nM ~12× more potent B-cell IL-6 IC50 0.6 nM 0.06 nM ~10× more potent Lymphoma REC-1 / LY10 IC50 18 / 19 nM 3 / 0.6 nM ~6-30× more potent Durability of degradation - >85% at 7 days QW-dosing potential Selectivity / neo-substrates Clean Clean Comparable Safety window ~600-1,000× >1,000× Comparable / better

PART A: SAD Dosing 8 Cohorts: Oral dose of EVO570 or pbo (10 per group, 8:2) Planned China Phase 1 Trial DesignWill support global Phase 2 program © Evommune, Inc. Cohort A1 (0.1mg) Cohort A8 Cohort A4 Cohort A3 Cohort A2 Cohort B1 Cohort B3 Cohort B2 PART B: MAD Dosing 4 Cohorts: Oral doses of EVO570 or pbo (12 per group, 10:2) Phase 1 FIH Randomized, Double-Blind, Pbo-Controlled SAD, MAD, and Food Effect Trial N = 146 Cohort A7 Cohort A5 Cohort A6 Cohort B4 PART C: Food Effect Oral dose of EVO570 in two-way crossover design (18 total, one dose fasted, one dose fed conditions) Endpoints China/US IND submission: Sep/Oct 2026, US opened Nov 2026 Phase 1 start: Jan 2027 Phase 1 data: ~Mid-2027 Phase 1b: exploring an RA patient cohort for early proof-of-concept Projected timeline Primary Safety and tolerability of single and multiple oral doses, and food effect Secondary PK and PD: VAV1 degradation in T and B cells; ex vivo response to TCR and BCR stimulation (CD69, IL-2, IL-17A, IFNγ, IL-6) Adaptive design Safety Review Committee can adjust SAD and MAD doses based on prior cohorts

EVO646: Oral TLR7/8 Antagonist Potential Best-in-Class Dual Mechanism (Type I Interferon and Pathogenic B-Cell / Autoantibody) for Autoimmune Disease © Evommune, Inc.

TLR7/8 Inhibition Suppresses Two Major Drivers of Autoimmune Disease © Evommune, Inc. Type I Interferon Pathway Pathogenic B-Cell Pathway ↓ Type I IFN ↓ Autoantibodies Elevated antibody B cell IL-1β TNFα IL-6 Inflammation IFNα IFNβ pDC Plasma cell Single Target with Complementary Effects on Two Major Drivers of Autoimmune Disease Suppresses pDC-driven type I interferon production Reduces B-cell activation, plasmablast differentiation, and autoantibody production Pathway validated: anifrolumab (anti-IFNAR1), approved in SLE Pathway validated: belimumab (anti-BLyS), approved in SLE

Large Autoimmune Market Opportunity for TLR7/8 © Evommune, Inc. Strong Scientific Rationale for TLR7/8 in Autoimmune Diseases Mechanistic Insights Human Genetics Clinical POC Preclinical Validation Strong causal link of TLR7 to autoimmune disease TLR7-/- mice resistant to autoimmune/inflammatory models Multimodal MoA: limiting type 1 interferons and pathogenic B-cells/auto-antibody production TLR7/8 inhibition demonstrated clinical benefit in CLE and SLE TLR7/8 Potential Indications 6M Patients Initial Targeted Indications1 Type 1 IFN Driven B-Cell / aAb Driven Psoriasis Cutaneous Lupus Erythematosus Systemic Lupus Erythematosus Graves / Thyroid Eye Disease Systemic Sclerosis Myasthenia Gravis Immune Thrombo- Cytopenia Multiple Pemphigoid Indications Autoimmune Hemolytic / Pernicious Anemia Sjögren’s Syndrome Lupus Nephritis 1. Evommune internal estimates based on initial potential indications.

~30-Point SRI-4 Benefit at Every Dose in Phase 2 SLE3,4 TLR7/8 Inhibition Is Clinically Validated in Lupus, with Oral Best-in-Disease Efficacy and Favorable Tolerability in Phase 25 © Evommune, Inc. 1. Enpatoran is an investigational product being developed by EMD Serono. 2. Enpatoran WILLOW Phase 2, Cohort A (ACR 2025). 3. Afimetoran is an investigational product being developed by Beeline Medicines. 4. Afimetoran Phase 2 in Systemic Lupus Erythematosus (Oct 2026). 5. Cross-trial comparison; no head-to-head data. Phase 2 Proof-of-Concept Established in CLE1 Enpatoran Demonstrated Phase 2 Activity in CLE WILLOW Cohort A, Week 162 SRI-4 Response at Week 48 Randomized, placebo-controlled (N=248) 34.4% Placebo 67.8% 2.5mg 64.1% 10mg 66.1% 30mg ~30 pt SRI-4 benefit over placebo at every dose at Week 48 Broad Clinical Efficacy Skin, joints, steroid sparing Rapid IFN-GS Suppression Near-maximal by Week 2 Favorable Tolerability TEAEs: 5.9% vs. 12.9% PBO

EVO646 Targets TLR7/8 and Spares TLR9Genetics, disease models and two Phase 2 trials all point to TLR7/8 as the productive pair © Evommune, Inc. HUMAN GENETICS TLR7 gain of function causes lupus TLR7 variants drive disease in patients and in mice¹ No comparable gain-of-function case for TLR9 EVO646 is designed for >100-fold selectivity over TLR9 DISEASE MODELS TLR9 acts as a brake, not a driver Removing TLR7 protects lupus-prone mice; removing TLR9 worsens nephritis and shortens survival² That worsening disappears when TLR7 is also removed³ CLINICAL EVIDENCE TLR7/8 blockade has already worked Afimetoran: Phase 2 SLE met SRI-4 across all three doses Enpatoran: Phase 2 activity in CLE Both programs block TLR7/8 only - no TLR9 engagement required for benefit EVO646 blocks the two validated receptors and leaves TLR9 intact 1. Brown et al., Nature (2022); TLR7 gain-of-function variant causes human lupus. 2. Christensen et al., Immunity (2006). 3. Nickerson et al., PLoS One (2017). Afimetoran (Beeline Medicines) and enpatoran (EMD Serono) are investigational and not developed by Evommune.

EVO646: Selective Interferon and B-Cell Modulator in a PillBest-in-class potential EVO646 (Evommune) Afimetoran (BMS/Beeline) Enpatoran (Merck Serono) Potency (nM) (HEK293T) 6.70 1.70 11.2 In vivo activity Mouse PD* >80% inhibition @ 1mpk >80% inhibition @ 1mpk >80% inhibition @ 1mpk Dosing QD QD BID Safety >10 µM hERG 1/87 CEREP 9.29 uM hERG 6/87 CEREP >10 µM hERG 2/87 CEREP © Evommune, Inc. *acute R848 model output highlights combined impact of potency, PPB, and bioavailability CEREP hits = >50% inhibition @ 10 µM

Key Milestones Ahead For Evommune © Evommune, Inc. ~$290m Cash and Investments1, Current Runway Into 2H 2029 Championing Innovation for Chronic Inflammation EVO301 IL-18BP Plan to initiate Phase 2b in AD with subcutaneous formulation in mid-2027 Plan to initiate Phase 2a in UC in 1H 2027 EVO756 MRGPRX2 Antagonist Expect top-line data from Phase 2b migraine trial in 2027 EVO570 VAV1 MGD Expect Phase 1 HV biomarker data mid-2027 Plan to initiate Phase 2 program 2H 2027 EVO646 TLR7/8 Antagonist Plan to initiate Phase 1 in 1H 2027 Expect Phase 1 HV biomarker data in 2H 2027 1. Pro Forma: $262.3M cash, cash equivalents and investments as of September 30, 2026, plus net proceeds of approximately $28.0 million from the November PIPE financing.

Thank You! www.evommune.com © Evommune, Inc.

Appendix © Evommune, Inc.

Proven and Experienced Leadership Team Has Delivered Almost 30 NDAs and BLAs © Evommune, Inc. 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 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