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I N V E S T O R O V E R V I E W I S E P T E M B E R 2 0 2 6 Combating Neurodegeneration Via Treg-Directed Combination Therapy
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Cautionary Note of Forward-Looking Statements and Disclaimers in this Presentation This presentation and the accompanying oral presentation contain “forward-looking” statements that are based on our management’s beliefs and assumptions and on information currently available to management. Forward- looking statements include all statements other than statements of historical fact contained in this presentation, including, without limitation, information concerning our current and future financial performance, business plans and objectives, current and future clinical and preclinical development activities, timing and success of our ongoing and planned clinical trials and related data, the timing of announcements, updates and results of our clinical trials and related data, our ability to obtain and maintain regulatory approval, the potential therapeutic benefits and economic value of our product candidates, competitive position, industry environment and potential market opportunities, and our financial position, including cash runway. The words “believe,” “may,” “will,” “estimate,” “continue,” “anticipate,” “intend,” “expect,” and similar expressions are intended to identify forward- looking statements, though not all forward-looking statements necessarily contain these identifying words. Forward-looking statements are subject to known and unknown risks, uncertainties, assumptions and other factors including, but not limited to, those related to risks associated with the success, cost and timing of our product candidate development activities and ongoing and planned clinical trials; our plans to develop and commercialize targeted therapeutics; the progress of patient enrollment and dosing in our preclinical or clinical trials does not proceed on estimated timelines; the ability of our product candidates to achieve applicable endpoints in the clinical trials; the safety profile of our product candidates; the potential for data from our clinical trials to support a marketing application, as well as the timing of these events; our ability to obtain funding for our operations; development and commercialization of our product candidates; the timing of and our ability to obtain and maintain regulatory approvals; the rate and degree of market acceptance and clinical utility of our product candidates; the size and growth potential of the markets for our product candidates, and our ability to serve those markets; our commercialization, marketing and manufacturing capabilities and strategy; future agreements with third parties in connection with the commercialization of our product candidates; our expectations regarding our ability to obtain and maintain intellectual property protection; our dependence on third party manufacturers; the success of competing therapies or products that are or may become available; our ability to attract and retain key scientific or management personnel; our ability to identify additional product candidates with significant commercial potential consistent with our commercial objectives; and our estimates regarding expenses, future revenue, capital requirements and needs for additional financing. We have based these forward-looking statements largely on our current expectations and projections about future events and trends that we believe may affect our financial condition, results of operations, business strategy, short-term and long-term business operations and objectives, and financial needs. Moreover, we operate in a very competitive and rapidly changing environment, and new risks may emerge from time to time. It is not possible for our management to predict all risks, nor can we assess the impact of all factors on our business or the extent to which any factor, or combination of factors, may cause actual results to differ materially from those contained in any forward-looking statements we may make. In light of these risks, uncertainties and assumptions, the forward-looking events and circumstances discussed herein may not occur and actual results could differ materially and adversely from those anticipated or implied in the forward-looking statements. Although our management believes that the expectations reflected in our forward-looking statements are reasonable, we cannot guarantee that the future results, levels of activity, performance or events and circumstances described in the forward-looking statements will be achieved or will occur. The actual results may vary from the anticipated results, and the variations may be material. Other factors that may cause the Company’s actual results to differ from current expectations are discussed in the Company’s filings with the U.S. Securities and Exchange Commission, including the section titled “Risk Factors” in the Company’s Annual Report on Form 10-K for the year ended December 31, 2025. You are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date this presentation is given. Except as required by applicable law, we undertake no obligation to publicly update any forward-looking statements, whether written or oral, that may be made from time to time, whether as a result of new information, future developments or otherwise. This presentation discusses product candidates that are under clinical study and have not yet been approved for marketing by the U.S. Food and Drug Administration. No representation is made as to the safety or effectiveness of these product candidates for the use for which such product candidates are being studied. 2
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3 Focused Anti-Neurodegenerative Pipeline COYA 302 (Low Dose IL-2 + CTLA4-Ig): A pipeline in a product across ALS, FTD, AD, Parkinson’s Disease. COYA 303 (Low Dose IL-2 + GLP-1 RA): Alzheimer’s Disease Near-Term COYA-302 ALS Data Readout Q1 2027 ALSTARS Phase 2 enrollment completion expected H2 2026, with topline data expected Q1 2027 Established Clinical Signal in Two IIT Studies of Low Dose IL-2 + CTLA4-Ig Data show ALSFRS-R stabilization over 48 weeks in ALS and cognitive stability at 22 weeks in FTD Nobel-Recognized Scientific Foundation SAB member Dr. Shimon Sakaguchi was among the recipients of the 2025 Nobel Prize in Physiology or Medicine for Treg biology Dr. Reddy's Partnership Provides Strategic Support and Validation Up to ~$700M in potential milestones plus mid-teen royalties for global ALS rights (excluding Japan and LATAM) and a $10M equity investment (closed in January 2026) Cash Runway Through Upcoming Key Milestones ~$43.2M as of June 30, 2026, funding operations into 2H 2027, past expected ALS data readout Coya Therapeutics, Inc. (COYA): Investment Highlights › › › › › ›
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LD IL-2 Combination Therapy: 3 Pillars For Success The neurodegeneration field increasingly recognizes combination-based therapeutic strategies such as Coya's as a viable path forward for diseases driven by complex, multifactorial biology 4 Validated Science Differentiated Combination-based Therapeutic Approach Early Clinical Validation Nobel Prize–recognized for discovery & role of Treg Biology(1) Well-established association between Treg dysfunction and ALS/FTD(2) Independent scientific support of Coya's approach in ALS(3) Combination therapy potentially increases likelihood of success Endorsed by external thought leaders (KOLs, ADDF, CTAD) Well-established therapeutics (low- dose IL-2 & Abatacept) Low-dose IL-2 used at ~50x lower doses vs standard IL-2 dosing CTLA4-Ig's safety and efficacy established in millions of patients in RA and other inflammatory and autoimmune conditions Combination therapy restores and maintains Treg function Signals of disease stabilization of disease in ALS & FTD Potential for combo therapies to alter disease trajectory ALS IIT: no ALSFR-S decline at 6 months, minimal decline at 1 year (n=4) FTD IIT: cognitive stability at 6 months (n=9) 1. The 2025 Nobel Prize in Physiology or Medicine awarded to Dr. Shimon Sakaguchi, member of Coya SAB 2. Appel et al, ALS patients' regulatory T lymphocytes are dysfunctional, and correlate with disease progression rate and severity, JCI Insight, 2017 3. Sette et al, Autoimmune response to C9orf 72 protein in amyotrophic lateral sclerosis, Nature, November 2025
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COYA Targets T-Regs Role in Inflammation 5 Tregs are specialized immune cells that help maintain a balanced immune system CD80 pro-inflammatory macrophages COYA’s therapeutics synergistically expand dysfunctional Tregs and shift them to an immune suppressive state 1 The result is re-balanced immune homeostasis, which leads to neuro-protection against neuro-degenerative disease T-reg dysfunction leads to immune activation and chronic inflammation 2 Inflammation drives autoimmune pathology and neuro-degenerative disease progression COYA: Low Dose IL-2 + CTLA-4Ig / GLP-1 RA Functional Tregs 3 Low dose IL-2 expands T-reg numbers and enhances their suppressive functionDysfunctional Tregs CTLA-4Ig promotes a shift of myeloid cells toward an anti- inflammatory phenotype 4 Anti-inflammatory macrophages
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ALS and FTD Market Opportunity Two orphan diseases with short life expectancy from diagnosis and significant loss of quality of life Amyotrophic Lateral Sclerosis Patient Population & Unmet Need ~33,000 patients in U.S. (NIH) Partner & Deal Terms Dr. Reddy’s Laboratories: global rights globally, excluding Japan and LatAm Up to ~$700M in R&D, regulatory, and sales milestones; mid- teen royalties $10M strategic investment (Jan. 2026) Clinical & Regulatory Status Fast Track Designation granted to COYA 302 in ALS Phase 2 ALSTARS study ongoing, topline expected Q1’27 Frontotemporal Dementia 50,000–60,000 patients in U.S. (Alzheimer's Association) Third-Party Support Alzheimer's Drug Discovery Foundation (ADDF): $5M investment (May 2024) to support Phase 2 trial in FTD Clinical & Regulatory Status IND accepted Q1 2026 Study initiation expected H2 2026 Development and Commercial Rights COYA retains 100% development and commercialization rights to COYA 302 in FTD and all other indications, excluding ALS 6 ALS FTD Patient Population & Unmet Need
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COYA 302 in ALS
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ALS: An Urgent Need for New Treatment Options ALS is a progressive disease that attacks the motor neurons in the brain and spinal cord that control voluntary muscles — including those needed to speak, swallow, and breathe1 8 20–30% die within two years of diagnosis, despite approved therapies2 90% develop “sporadic” ALS with no family history3 and therefore no known cause 1 https://www.als.org/understanding-als/stages; 2 Brown RH, Al-Chalabi A. Amyotrophic lateral sclerosis. The Lancet Neurology (2 017); 3 Masrori P, Van Damme P. Amyotrophic lateral sclerosis: a clinical review. Eur J Neurol. 2020;27(10):1918–1929. doi:10.1111/ene.14393
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Approved Therapies Show Only a Modest Treatment Effect 9 3 1. The PRO-ACT database is the largest ALS data repository (Atassi et al, 2014) 2. Relyvrio US Prescribing Information (9/2022) 3. Radicava US Prescribing Information (5/2022) 4 8 12 16 20 24 PRO-ACT ALS Database Mean (SD) Documented Decline (ALSFRS-R) Weeks Baseline RELYVRIO and RADICAVA Mean Change vs. Placebo on ALSFRS-R at Week 24 In the natural history of ALS, patients average a ~1 point/month rate of decline in ALSFRS-R score1 2 Both approved therapies slowed, but did not stop, disease progression and functional decline. RELYVRIO withdrawn from US market in April 2024 following failure of the Phase 3 PHOENIX trial COYA-302 has not been evaluated head–to-head against either molecule
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LD IL-2 + CTLA-4 Ig ameliorates progression in a 48-week IST in ALS Patients Participant 1: +4 points Participant 2: +3 points Participant 3: Stable Participant 4: -6 points (declined at month 1 and remained stable thereafter ) LD IL-2 + CTLA4-Ig IIT: Compelling Signal in Mild-to-Moderate ALS1 10 33.5 33.75 32 30 0 4 8 12 16 20 24 28 32 36 40 44 48 B 4 8 12 16 20 24 28 32 36 40 44 48 52 56 ALSFRS-R Score Mean (±SD) ALSFRS-R Score (N=4) 48-Week Treatment Follow-Up • 4 mild-to-moderate ALS patients • Low-dose IL-2 + CTLA4 Ig led to stable or improved ALSFRS-R Scores • Well tolerated over 48 weeks (the most common AE mild was ISR) • All patients completed the study • No deaths or serious AEs (SAEs) ALSFRS-R improved or stabilized over 6 months 1 Thonhoff et al. A Phase 1 Proof-of-Concept Study Evaluating Safety, Tolerability, and Biological Marker Responses with combination therapy of CTLA4-Ig and Interleukin-2 in Amyotrophic Lateral Sclerosis. Frontiers in Neurology, 2024. In press.
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COYA 302: ALSTARS Phase 2 Study in ALS Ongoing 11 • Diagnosis of sporadic or familial ALS • ALSFR-R score ≥ 35 at Screening • Slow vital capacity (SVC) ≥ 70% of predicted capacity for age, height, and gender at Screening • Documented disease progression between -0.5 and -1.5 points per month on ALSFR-R total score Key Inclusion Criteria Trial is active and enrolling patients I Complete enrollment: expected 2H 2026 I Topline data: expected 1Q 2027 I Fast Track Designation granted to COYA 302 in ALS Primary Endpoint: Change in disease severity over time measured by ALSFRS-R total score from baseline to Week 24 vs. placebo Study Objectives: 1.Efficacy 2. Safety and Tolerability 3. Biological Activity 4. Biomarker levels Randomized, Double-Blind, Placebo-Controlled Phase 2 Study with Blinded Active Extension 4 wk. Screening 24 wk. Double Blind Treatment Phase COYA 302 Regimen 1 (N=40) COYA 302 Regimen 2 (N=40) Placebo Group B (N=40) 24 wk. Blinded Active Extension Phase COYA 302 Regimen 1 (N=60) COYA 302 Regimen 2 (N=60)
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ALS Summary 12 The Disease & Unmet Need Rapidly fatal — ~1- point/month ALSFRS-R decline; 20–30% die within two years of diagnosis ~90% of cases are sporadic, with no family history Approved therapies only modestly effective; RELYVRIO withdrawn in 2024 Early Clinical Signal 48-week investigator- initiated study in mild-to- moderate ALS 3 of 4 patients stable or improved ALSFRS-R (+4, +3, stable) Well tolerated — no deaths or SAEs Market Opportunity Orphan indications with high unmet need Short life expectancy and major loss of quality of life Combination therapy seen as a viable path forward COYA 302: Coya's Approach Low-dose IL-2 + CTLA4-Ig combination therapy Restores regulatory and maintains T-cell (Treg) function to reduce neuroinflammation Built for the complex, multifactorial biology of ALS ＋＋ ＋ ＋
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COYA 302 in FTD
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LD IL-2 & CTLA-4 Ig: Signal in Mild-to-Moderate FTD 14 Encouraging clinical data in FTD in Investigator Sponsored Study (n=9) Treg suppressive function and percentage: (1) Increased after first treatment (2) Remained elevated across 22-week treatment period Expansion of Treg Percentage Increased Treg Suppressive Function *<0.05 **<0.01 ***<0.001 ****<0.0001 (% of CD4+ T cells)
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LD IL-2 & CTLA-4 Ig: Signal in FTD – cont. 15 SC W22 0 2 4 6 8 10 12 14 16 18 20 22 MOCA Score SC W22 0 1 2 3 4 5 6 7 8CDR-FTLD (% of CD4+ T cells) Cognitive Stability in 22-Week Investigator Sponsored Study CDR‐FTLD, MoCA, PASS cognitive tests exhibited no cognitive decline at end of study compared with baseline Moca Scores Remain Unchanged Compared to Baseline CDR-FTLD Scores Remains Unchanged Compared to Baseline
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COYA-302 in FTD: Phase 2 Expected 2H 2026 Start 16 * CDR® Dementia Staging Instrument PLUS National Alzheimer’s Coordinating Center (NACC) Behavior and Language Domains for FTLD - sum of boxes • Non-Fluent Primary Progressive Aphasia Subtype • Global Clinical Dementia Rating - Frontotemporal Lobar Degeneration (CDR® plus NACC FTLD) score of 0.5, 1 or 2 Key Inclusion Criteria Randomized, Double-Blind, Placebo-Controlled Phase 2 Proof-of-Concept Study 4 wk. Screening 52-Week Double Blind Treatment Phase COYA 302 (N=32) Placebo (N=16) Study initiation: expected 2H 2026 Primary Endpoint Safety and tolerability Clinical Efficacy Endpoints CDR+NACC-FTLD-SB* Neuropsychological tests Biomarkers Plasma Glial Fibrillary Acidic Protein (GFAP) Inflammatory cytokines NfL * CDR® Dementia Staging Instrument PLUS National Alzheimer’s Coordinating Center (NACC) Behavior and Language Domains for FTLD - sum of boxes
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＋＋ ＋ ＋ FTD Summary 17 The Disease & Unmet Need Frontotemporal dementia (FTD) — progressive neurodegeneration affecting behavior, language and cognition A leading cause of dementia in people under 60 No approved disease- modifying therapies — high unmet need Early Clinical Signal 22-week investigator- sponsored study in mild-to- moderate FTD (n=9) Treg suppressive function rose after first dose and stayed elevated No cognitive decline vs baseline on CDR-FTLD, MoCA and PASS COYA 302: Coya's Approach Low-dose IL-2 + CTLA4-Ig combination therapy Restores and maintains regulatory T-cell (Treg) function to reduce neuroinflammation Same immune-modulating approach advancing in ALS Market Opportunity Orphan indication with high unmet need Short life expectancy and major loss of quality of life Combination therapy seen as a viable path forward
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COYA 303 in AD
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COYA 303 in Alzheimer's: Compelling Preclinical Signal Encouraging in-vitro data and in LPS mouse model • Lipopolysaccharide (LPS) mouse model is an established murine model of systemic and neuro- inflammation • COYA 303 decreased both peripheral inflammation and in neuro-inflammation • Mechanistic synergy: complementary effects on Treg enhancement and myeloid-driven inflammation Systemic Tregs NeuroinflammationSystemic inflammation Improved Treg function Reduced Inflammation Clinical development of COYA 303 contingent upon securing non-dilutive funding or a partnership COYA-303: Reduced peripheral pro- inflammatory cell expansion Enhanced Treg function Attenuated CNS inflammation Shifted macrophages to an anti-inflammatory phenotype Decreased neuroinflammation
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Financial Summary and Dr. Reddy’s Collaboration 20 Financial Summary As of June 30, 2026 Cash: $43.2 million Greenlight Capital: 9.9% ownership* Dr. Reddy’s: 9.7% ownership* No debt Cash runway: Into H2 2027, past the ALSTARS Phase 2 ALS data readout (anticipated in Q1 2027) Shares outstanding: ~23.5 million shares of common stock outstanding as of 8/11/2026 *Based on publicly available ownership schedules filed with the Securities and Exchange Commission Dr. Reddy’s Collaboration Announced December 2023 Dr. Reddy’s gets: An exclusive license to commercialize COYA 302 for ALS in the US, Canada, the EU and UK, if approved COYA gets: $7.5m upfront (received December 2023); $4.2m upon IND acceptance (received August 2025); $4.2m upon dosing of the first patient in the P2 study (received December 2025) Up to $40m in potential development and regulatory milestones; Approximately $677m in potential sales-based milestones, and; Low-to-mid teens royalties on net sales COYA responsible for ongoing development of 302 and for obtaining US regulatory approval
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Multi-Layered IP Protection 21 Formulation Granted patent on low- dose IL-2 aqueous formulation — enables at- home administration via prefilled syringe (vs. Proleukin, which is lyophilized and IV-only) Combination Patent on combinations of any IL-2 (including long- acting) with any CTLA-4 Ig Biomarker Biomarker IP for 302 in ALS provides an additional layer of protection Regulatory ALS and FTD are orphan diseases — potential 7 years of market exclusivity if 302 receives Orphan Drug Designation from the FDA Earliest patent expiry: 2042
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COYA 302 in ALS: ALSTARS (Phase 2) Complete enrollment: expected 2H 2026 Topline data: expected 1Q 2027 Management to provide periodic updates COYA 302 in FTD: IND accepted in 1Q 2026 Phase 2 study: expected initiation 2H 2026 Translational Datasets Present further translational and clinical datasets across Coya programs Including biomarker, proteomics, and single-cell data Further elucidate role of Tregs in neuroinflammation and neurodegeneration Provide additional insight into target engagement, pathway modulation, and patient-level biology: COYA 303 in Alzheimer's Continue to evaluate path forward Clinical advancement contingent upon securing non-dilutive funding or a partnership Key Catalysts and Milestones 22
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Management and Board 23 Board of Directors Mark Pavao, M.B.A. Managing Partner Biotech Value Advisors Ann Lee, Ph.D. Chief Technical Officer Prime Medicine Dov Goldstein, M.D., MBA Chief Financial Officer BioAge Labs Wilbur Ross Former U.S. Secretary of Commerce Anabella Villalobos, Ph.D. Former Head of Biotherapeutics and Medicinal Sciences, Biogen Dieter Weinand Former Chairman and CEO Bayer Pharma, AG David Snyder Chief Financial Officer & Chief Operating Officer DisperSol Exicure Cellular Dynamics Roche NimbleGen Fred Grossman, D.O., FAPA President & Chief Medical Officer Johnson-Johnson Sunovion Bristol Myers Squibb Mesoblast Eli Lilly Glenmark Bristol Myers Squibb Actinium Covance Alteogen Lynkogen Arun Swaminathan, Ph.D. Chief Executive Officer
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Scientific Advisors Board 24 Shimon Sakaguchi, M.D., Ph.D. Member of the National Academy of Sciences Nobel Prize for discovery & role of Treg Biology Distinguished Professor at the World Premier International Research Institute - Immunology Frontier Research Center at Osaka University Clive Svendsen, Ph.D. Director, Cedars-Sinai Regenerative Medicine Institute Professor in Residence at UCLA Consulting Professor at Stanford University Renowned expert on stem cell biology and regenerative therapeutic approaches Malcolm Brenner, M.D., Ph.D. Director, Center for Cell and Gene Therapy Professor, Baylor College of Medicine Dedicated career to the field of stem cell transplantation through the therapeutic use of T cell immunologic approaches Stanley Appel, M.D. Co-Director, Houston Methodist Neurological Institute For more than 50 years, Dr. Appel has devoted his life to finding solutions for people living with ALS Pioneered role of Tregs in Neurodegeneration
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I N V E S T O R O V E R V I E W I S E P T E M B E R 2 0 2 6 Thank You