Coya Therapeutics, Inc. · NASDAQ:COYA

Coya Therapeutics — Investor Presentation (January 2026)

43 slides from Coya Therapeutics's investor presentation, January 2026

  1. Slide 1: Addressing Neuro-Inflammation through Therapeutic Intervention

    Addressing Neuro-Inflammation through Therapeutic Intervention Investor Overview January 2026

  2. Slide 2: Cautionary Note of Forward-Looking Statements and Disclaimers

    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-lo

  3. Slide 3: A Large and Global Problem

    A Large and Global Problem Neurodegeneration is affecting millions of people without clear therapeutic pathways. 1 in 3 people will be affected by neurological conditions in their lifetime. 3-5 50 Million+ $9 Trillion People Impacted Global Cost of Years Worldwide Dementia by 2050 Life Expectancy Af

  4. Slide 4: Coya Therapeutics: Investment Highlights

    Coya Therapeutics: Investment Highlights Novel Therapies, High Unmet Need ○ Differentiated approach targeting Treg dysfunction through combination therapies ○ Targeting high unmet diseases ALS, FTD, Alzheimer's Disease ○ De-Risked approach targeting diseases (ALS, FTD) with regulatory flexibility ○

  5. Slide 5: Our Pipeline is > $10Bn Opportunity

    Our Pipeline is > $10Bn Opportunity Coya is prioritizing therapies for ALS, FTD, AD, and PD Alzheimer’s as key initial neurodegenerative diseases Disease Parkinson’s Disease ALS and Frontotemporal Dementia ALS and FTD both have high unmet need, are designated as orphan indications, and have flexible

  6. Slide 6: The Coya Solution

    The Coya Solution We will address neurodegeneration at its source by Alzheimer’s developing innovative therapies to meet the needs of Disease Parkinson’s patients with these diseases. Disease Combining Therapeutic Approaches Neurodegenerative disorders impact people in a variety of ways. There are c

  7. Slide 7: Intro to TRegs

    Intro to TRegs Healthy Treg cells Inflammation occurs when Treg block inflammation cells become dysfunctional What are Tregs? How do Tregs influence disease? How to treat disease by targeting Tregs? Tregs are cells within the body When Tregs do not function that keep the immune system properly, auto

  8. Slide 8: Inflammation - A Critical Role in Neurodegeneration

    Inflammation - A Critical Role in Neurodegeneration Regulatory T cells (Tregs) are Dysfunctional; COYA aims to repair these cells Neurodegeneration: Inflammation in the Loss of Selective Population of Neurons Nervous System Healthy Neuron Sick Neuron Dead Neuron Regulatory T Cells (Tregs) play a cen

  9. Slide 9: Key Catalysts and Milestones

    Key Catalysts and Milestones Additional Clinical ➢ 1Q 2025: Phase 2 LD IL-2 investigator initiated trial in patients with AD additional clinical data release: Data Release: Publication and release of additional and comprehensive systemic immune panel and inflammatory Phase 2 IIT AD Trial cerebrospin

  10. Slide 10: COYA 302

    LEAD PRODUCT COYA 302 Proprietary, Recombinant Human Low Dose Interleukin-2 (LD rhIL-2) and CTLA4-Ig

  11. Slide 11: COYA 302: Phase 2 Study in Patients with ALS

    COYA 302: Phase 2 Study in Patients with ALS Initiated a Phase 2 multicenter, double-blind, placebo-controlled clinical study to evaluate the efficacy and safety of COYA 302 in patients with ALS Trial Initiation NEALS-affiliated Study First Patient Dosed: NEALS, the world's largest The COYA 302 stud

  12. Slide 12: The Future of Neurodegenerative Disease Therapy

    The Future of Neurodegenerative Disease Therapy COYA 302 (proprietary LD rhIL-2 + CTLA4-Ig Combination Immunotherapy Dysfunctional Tregs Pro-inflammatory Adaptive and Innate Macrophages Immune-Mediated Neuroinflammation CD80 CD80 LD IL-2 + CTLA4-Ig LD IL-2 CTLA4-Ig FoxP3 FoxP3 FoxP3 FoxP3 Tregs Incr

  13. Slide 13: Current Therapies for ALS aim to slow disease progression

    Current Therapies for ALS aim to slow disease progression Average rate of patient decline is 1.02 points/month in ALSFRS-R score1 Many companies have garnered significant value by demonstrating a limited benefit of slowing the rate of ALS progression Weeks 1. The PRO-ACT database is the largest ALS

  14. Slide 14: LD IL-2 + CTLA4-Ig Investigator Initiated Clinical Trial

    LD IL-2 + CTLA4-Ig Investigator Initiated Clinical Trial Open-Label, Single-Arm PoC Clinical Study in ALS Patients (N=4) Screening Treatment Period Follow-Up 20 weeks LD IL-2 + CTLA4-Ig was administered via 8 weeks subcutaneous injection over 48 weeks Screening Assessments Treatment Period Assessmen

  15. Slide 15: LD IL-2 + CTLA4-Ig Investigator Initiated Clinical Trial

    LD IL-2 + CTLA4-Ig Investigator Initiated Clinical Trial Baseline Characteristics ALS Progression Age Respiratory Respiratory Sex Type Onset Prior to Baseline (years) Status Support (ALSFRS-R score) No Respiratory Patient 1 47 Female Familial Limb -1.6 points / month None Insufficiency Respiratory N

  16. Slide 16: LD IL-2 + CTLA4-Ig Investigator Initiated Clinical Trial

    LD IL-2 + CTLA4-Ig Investigator Initiated Clinical Trial ALSFRS-R Individual Scores remained mostly stable or improved Participant 1: +4 points Participant 2: +3 points Participant 3: Stable Participant 4: -6 points* * Declined at month 1 and remained stable thereafter Thonhoff JR, Beers DR, Zhao W,

  17. Slide 17: LD IL-2 + CTLA4-Ig Investigator Initiated Clinical Trial

    LD IL-2 + CTLA4-Ig Investigator Initiated Clinical Trial Appears to Ameliorate ALS Progression Over 48 Weeks LD IL-2 + CTLA4-Ig was well tolerated over 48 weeks; the most common AE was mild injection site reaction. All patients completed the study; no deaths or serious AEs (SAEs) occurred over the c

  18. Slide 18: LD IL-2 + CTLA4-Ig Investigator Initiated Clinical Trial

    LD IL-2 + CTLA4-Ig Investigator Initiated Clinical Trial Lowered Oxidative Stress Markers Key Takeaways * ** ** * * * ✔ LD IL-2 + CTLA4-Ig significantly expanded Treg suppressive function as early as 4 weeks after initiation of treatment and maintained a ** significantly increased Treg function. ✔ L

  19. Slide 19: Overview of Phase 2 Study Design in ALS

    Overview of Phase 2 Study Design in ALS Trial is active and currently enrolling participants Key Inclusion Criteria Randomized, Double-Blind, Placebo-Controlled • Diagnosis of sporadic or familial Phase 2 Study with Blinded Active Extension Primary Endpoint ALS Change in disease • Time since onset o

  20. Slide 20: Accelerating Research to Commercial

    Accelerating Research to Commercial Commercial Growth enabled by Strategic Partnerships With an already solidified partnership with Dr. Reddy’s for Coya 302 for ALS, partnerships will be catalysts for business growth, regulatory approvals and clinical adoption Research agreements in place Leveraging

  21. Slide 21: COYA 302 in FTD

    COYA 302 in FTD Proprietary, Low Dose Recombinant Human Interleukin-2 (LD rhIL-2) and CTLA4-Ig

  22. Slide 22: Investment by ADDF

    Investment by ADDF “Inflammation has emerged as a promising novel pathway for chronic neurological diseases like FTD. A combination drug, like COYA 302, is an innovative approach being developed to suppress neuroinflammation by targeting multiple inflammatory pathways. Combination therapy will be in

  23. Slide 23: Partnership with Alzheimer's Drug Discovery Foundation

    Partnership with Alzheimer’s Drug Discovery Foundation $5M Investment to accelerate Phase 2 trial in FTD Frontotemporal Disorder (FTD) is a Rare Disease and is one of Alzheimer's Drug Discovery Foundation Most Common Dementias in Younger People. Frontotemporal disorder progresses to death faster tha

  24. Slide 24: Exacerbated Systemic and Central Inflammatory Responses

    Exacerbated Systemic and Central Inflammatory Responses FTD is a devastating disease that unfortunately has no effective treatment Core Inflammation

  25. Slide 25: Targeting Inflammation in FTD to Slow Disease Progression

    Targeting Inflammation in FTD to Slow Disease Progression Periphery BBB CNS CTLA4-IgG Homeostatic glial Treg expansion and restoration TH1 Dysfunctional FTD Tregs X IL-2 CTLA4-IgG Inflammatory glia X pro-inflammatory monocytes Inflammation

  26. Slide 26: COYA 302 FTD Phase 2a Study

    COYA 302 FTD Phase 2a Study Houston Methodist Center is a CoE in ALLFTD - a single infrastructure clinical data platform in FTD with collaborative decision making among 5 leading centers around the USA Group 1 COYA 302 SC Administration 48 Patients 2:1 Randomized Group 2 Placebo SC Administration El

  27. Slide 27: COYA 301

    PIPELINE PRODUCT COYA 301 Proprietary Low Dose Recombinant Human IL-2

  28. Slide 28: Improved Treg Function Improved Cognition

    Phase 1 Proof of Concept Open-Label Trial with LD IL-2 in AD Enhanced Treg Function and halted Cognitive decline Improved Treg Function Improved Cognition Core Translational Neurodegeneration volume 12, Article number: 54 (2023)

  29. Slide 29: Case Study of Brain Imaging of AD Patient Before and After LD IL-2 Treatment

    Case Study of Brain Imaging of AD Patient Before and After LD IL-2 Treatment Neuroinflammation (TSPO) 70-Year-Old Male (11C) ER-176 PET Scan at baseline and Baseline MMSE: 12 after 4-monthly cycles of low dose IL- Positive PIB PET Scan 2. Positive Neurodegeneration MRI The second PET scan was done 2

  30. Slide 30: A Primer on IL-2 Dosing and Treg Function

    A Primer on IL-2 Dosing and Treg Function Lower IL-2 Dose is Better for Tregs Graphical abstract undfig1 Study Summary Previous studies have shown that lower IL-2 doses selectively enhance and increase Treg function reducing pro-inflammatory T Cells while higher IL-2 doses reduce Treg function and e

  31. Slide 31: COYA 301 in AD

    COYA 301 in AD Phase 2 Low Dose Interleukin-2 (LD IL-2) in Patients with Mild to Moderate Alzheimer’s Disease An Investigator Initiated, Randomized, Double-Blind, Placebo-Controlled Clinical Trial led by Dr. Alireza Faridar at Houston Methodist Hospital

  32. Slide 32: Double-Blind, Placebo-Controlled Study in AD Patients

    Double-Blind, Placebo-Controlled Study in AD Patients Study funded by the Gates Foundation and Alzheimer’s Association The encouraging results of the open-label, proof-of-concept study in AD (N=8) supported conducting the ongoing randomized, double- Low Dose IL-2– Dose Regimen 1 (Lower Dose) blind,

  33. Slide 33: LD IL-2 Meets Primary and Secondary Endpoints for Alzheimer's Disease

    LD IL-2 Meets Primary and Secondary Endpoints for Potential Treatment of Alzheimer’s Disease (AD) ✔ Cognition Stabilization (Exploratory Endpoint) for Lower IL-2 Dose Through Drug Treatment vs. Placebo: • 2 out of 3 scales showed cognitive stabilization (ADAS-Cog14 and ADCS-CGIC)* for the Administer

  34. Slide 34: LD IL-2 in Mild to Moderate Alzheimer's Disease

    LD IL-2 in Mild to Moderate Alzheimer’s Disease The trial was designed to detect significant differences in primary and secondary endpoints, and validated that Lower Dose IL-2 is Better Primary Endpoint: Secondary Endpoint: Exploratory Endpoints: Safety and Tolerability Treg Cell Populations CSF Bio

  35. Slide 35: Key Takeaways of the Trial

    Key Takeaways of the Trial Trial validated that lower dose IL-2 is better Key Takeaways: ○ We believe LD IL-2 study results further validate the hypothesis that restoring the numbers and function of Tregs with systemic LD IL-2 alone targets neuroinflammation ○ We believe LD IL-2 study results indica

  36. Slide 36: COYA 303

    COYA 303 An investigational biologic combination of COYA 301, Coya’s low-dose interleukin 2 (LD IL-2) and a GLP-1 receptor agonist (GLP-1RA), designed to deliver a multi- targeted immunomodulatory therapeutic in autoimmune and neurodegenerative diseases

  37. Slide 37: Evaluation of COYA 303 (COYA 301 and GLP-1RA combination)

    Evaluation of COYA 303 (COYA 301 and GLP-1RA combination) Glucagon-like peptide-1 receptor agonists (GLP-1RA) demonstrate promising immunomodulatory effects in preclinical models and clinical trials. To determine whether there are potential additive beneficial effects of GLP-1RA in combination with

  38. Slide 38: Coya Teams

    Coya Teams ⛉ Leadership Team ⛉ Operational Team ⛉ Scientific Advisory Team ⛉ Board of Directors

  39. Slide 39: Expert Leadership Team

    Expert Leadership Team Arun Swaminathan, Ph.D. Fred Grossman, D.O., FAPA David Snyder Chief Executive Officer President & Chief Chief Financial Officer & Medical Officer Chief Operating Officer <– Prior Experiences –> Bristol Myers Squibb Johnson-Johnson DisperSol Technologies Actinium Sunovion Phar

  40. Slide 40: Experienced Development Team

    Experienced Development Team Michelle Frazier, Ph.D. Karen King, MS Daniel Barvin, M.B.A Senior Vice President of Senior Vice President of Vice President of Operations Regulatory Affairs Program Management & Patient Advocacy and Clinical Operations Revance Therapeutics Recursion End The Legacy: Cyto

  41. Slide 41: World Class Scientific Advisors

    World Class Scientific Advisors Shimon Sakaguchi, M.D., Ph.D. Clive Svendsen, Ph.D. Malcolm Brenner, M.D., Stanley Appel, M.D. Member of the National Director, Cedars-Sinai Ph.D. Co-Director, Houston Methodist Academy of Sciences Regenerative Medicine Institute Director, Center for Cell and Neurolog

  42. Slide 42: Distinguished Board of Directors

    Distinguished Board of Directors Howard Berman, Ph.D. Ann Lee, Ph.D. Dov Goldstein, M.D., MBA Executive Chairman Chief Technical Officer Chief Financial Officer of the Board of Prime Medicine of BioAge Labs Wilbur Ross Anabella Villalobos, Ph.D. Dieter Weinand Former U.S. Secretary of Head of Biothe

  43. Slide 43: Thank You!

    THERAPEUTICS Thank You! ,

Coya Therapeutics — Investor Presentation (January 2026) on 6ix