Odyssey Therapeutics, Inc. · NASDAQ:ODTX

Odyssey Therapeutics — Investor Presentation (October 2026)

45 slides from Odyssey Therapeutics's investor presentation, Oct 20, 2026

1. Slide 1: Corporate Presentation October 2026

   Corporate Presentation October 2026

2. Slide 2: Forward-looking statements and third-party information

   Forward-looking statements and third-party information This presentation contains forward-looking statements within the meaning of the “safe harbor” provisions of the Private Securities Litigation Reform Act of 1995. All statements other than statements of historical facts are forward-looking statem

3. Slide 3: Few Patients With Autoimmune Disease Have Durable Remission

   Few Patients With Autoimmune Disease Have Durable Remission Patients need: Increased remissions and more treatable diseases Deep and durable disease-modifying responses Better safety and tolerability with reduced infection risk Anti-Inflammatory 1970s Steroid-Sparing 1990s Anti-TNFs 2000s Additional

4. Slide 4: Targeting Upstream Signaling Has Potential to Unlock Durable Remissions

   Targeting Upstream Signaling Has Potential to Unlock Durable Remissions Defined pathogenic triggers underlie inflammatory disease… …by converging on disease-specific signaling nodes… …initiating a broad immune response… …causing tissue damage and disease Cytokines & chemokines Inflammatory cell recr

5. Slide 5: Experienced Team and Organization to Maximize Success

   BOARD OF DIRECTORS Experienced Team and Organization to Maximize Success Gary Glick, Ph.D. Founder, CEO, and Director Tony Opipari, M.D., Ph.D. Chief Medical Officer Joe McDonald, Ph.D. Chief Data Officer Jason Haas Chief Financial Officer Valerie Odegard, Ph.D. Tim Walbert Nia Tatsis, Ph.D. Jeff M.

6. Slide 6: Pioneering Next-Generation I&I Therapies to Redefine Standard of Care

   Pioneering Next-Generation I&I Therapies to Redefine Standard of Care Current market: $100B INFLAMMATORY BOWEL DISEASE B CELL-MEDIATED DISEASES INFLAMMATORY AND AUTOIMMUNE DISEASES Differentiated first-in-class oral monotherapy with positive safety profile Potential first-in-class oral therapy to bl

7. Slide 7: Broad Therapeutic Pipeline for Diseases With Unmet Need

   Broad Therapeutic Pipeline for Diseases With Unmet Need Notes: UC = ulcerative colitis; CD = Crohn’s disease; CLE = cutaneous lupus erythematosus; AD = atopic dermatitis; SLE = systemic lupus erythematosus; COPD = chronic obstructive pulmonary disease Target Modality Indications Discovery IND-enabli

8. Slide 8: Oral RIPK2 Scaffolding Inhibitor: OD-001

   Oral RIPK2 Scaffolding Inhibitor: OD-001 Addressing a Root Cause of Inflammation in IBD Using a Novel Mechanism of Action Proof-of-Concept Achieved in Ulcerative Colitis Program Inception to Phase 2 Proof-of-Concept: 4.5 Years

9. Slide 9: Innate Immune Responses to Gut Microbes Are the Root Cause of IBD

   Innate Immune Responses to Gut Microbes Are the Root Cause of IBD STEP 1: Loss of epithelial integrity; microbes breach gut barrier STEP 2: Innate immune cell activation (e.g., monocytes, neutrophils, and macrophages) STEP 3: Recruitment and activation of adaptive immune cells (e.g., T cells) Innate

10. Slide 10: Even With Advanced Therapies, Durable Remission Rates for IBD Remain Low

    miR-124 Even With Advanced Therapies, Durable Remission Rates for IBD Remain Low Sources: (1) Clin Gastroenterol Hepatol 2015;13(3):531; (2) World J Clin Cases 2024;12(10):1718; FDA drug labels; clinicaltrials.gov; EMERALD-2, UEG 2025; ANTHEM-UC, UEG 2025; RELIEVE UCCD, ECCO 2025; ABTECT-1 and ABTEC

11. Slide 11: RIPK2 Is a Validated Target to Treat IBD

    RIPK2 Is a Validated Target to Treat IBD Animal data Human data RIPK2 knockout mice are developmentally normal Pharmacologic validation of RIPK2: Clinical efficacy with OD-001 provides target validation in UC RIPK2 knockout reduces inflammatory cytokines and improves intestinal histology in animal m

12. Slide 12: RIPK2 Is Activated in UC and CD and Correlates With Severity

    Increased expression of RIPK2-responsive gene signature in IBD patient biopsies RIPK2 Is Activated in UC and CD and Correlates With Severity Notes: *** p < 0.001; GSVA = gene set variation analysis; GSVA cutoff for % of UC patients with RIPK2 pathway activity is 0.46. Sources: EMBO J 2018;37(17):e99

13. Slide 13: RIPK2 Drugs Must Block Scaffolding to Fully Inhibit NOD2 Signaling

    RIPK2 Drugs Must Block Scaffolding to Fully Inhibit NOD2 Signaling Mol Cell 2018;69(4):551–565 EMBO J 2018;37(17):e99372

14. Slide 14: Blocking RIPK2 Scaffolding With OD-001 Achieves Maximal Inhibition

    Blocking RIPK2 Scaffolding With OD-001 Achieves Maximal Inhibition Notes: Binding to RIPK2 was measured by competition with a fluorescent ATP-site tracer in cells. XIAP binding to RIPK2 using recombinant protein was measured by HTRF. Cytokine production was assessed after 24 hours by MSD/ELISA in ma

15. Slide 15: Not All RIPK2 Scaffolding Inhibitors Are the Same

    Not All RIPK2 Scaffolding Inhibitors Are the Same OD-001 blocks TL1A production in response to microbial stimulation (PGN) in human macrophages Pharmacology of noncompetitive allosteric inhibitors Inhibitor and XIAP can bind simultaneously to RIPK2 to form a ternary complex Inhibitor binding to RIPK

16. Slide 16: Phase 2a Monotherapy Trial Results

    Phase 2a Monotherapy Trial Results

17. Slide 17: Rationale and Dose Selection for Proof-of-Concept Phase 2a Trial

    Rationale and Dose Selection for Proof-of-Concept Phase 2a Trial OD-001 is the first innate immune-targeted therapy and the first RIPK2 scaffolding inhibitor to enter UC clinical development Trial was designed to assess safety and efficacy of OD-001 and determine whether to advance the program Partn

18. Slide 18: Phase 2a Monotherapy Trial Overview

    Vedolizumab 300 mg Q8W Vedolizumab 300 mg (weeks 12, 14, 18) Day 1 OD-001 start Week 12 OD-001 stop / Vedolizumab start Week 26 Week 52 10 mg BID 20 mg BID Part 1 (n = 16) Part 2 Randomized 1:4 (n = 45) Phase 2a Monotherapy Trial Overview 10 mg BID (2 weeks) then 20 mg BID (10 weeks) Patients with m

19. Slide 19: Participant Characteristics Are Similar to Other Contemporary UC Trials

    Participant Characteristics Are Similar to Other Contemporary UC Trials Notes: (1) Includes both approved advanced therapies and investigational agents; includes golimumab, etrasimod, ustekinumab, rosnilimab, MORF-057, PN-943, infliximab, icotrokinra, TYK2 inhibitor, adalimumab, and etrolizumab. Sou

20. Slide 20: OD-001 Efficacy Across Key Week 12 Outcomes by Dose

    OD-001 Efficacy Across Key Week 12 Outcomes by Dose, With Stronger Activity at 20 mg BID Disclaimer: Data presented are from ongoing studies, which will not be finalized until database lock. Thus, these data are subject to change prior to release of the CSR. Future results may differ from those show

21. Slide 21: OD-001 Is Safe and Well Tolerated at 10 mg BID and 20 mg BID

    OD-001 Is Safe and Well Tolerated at 10 mg BID and 20 mg BID Disclaimer: Data presented are from ongoing studies, which will not be finalized until database lock. Thus, these data are subject to change prior to release of the CSR. Future results may differ from those shown here. Notes: One participa

22. Slide 22: Markers of Systemic and Local Inflammation Are Reduced After OD-001 Treatment

    hsCRP, mg/L Markers of systemic and local inflammation suggest 20 mg BID inhibits colonic and systemic inflammation Markers of Systemic and Local Inflammation Are Reduced After OD-001 Treatment Notes: * p < 0.05; ** p < 0.01; nominal, unadjusted p values from paired Wilcoxon signed-rank tests compar

23. Slide 23: Higher Remission Rate With 20 mg BID Dose in Severe Patients

    10 mg n = 8 25 mg n = 194 50 mg n = 378 Placebo 20 mg n = 19 ABTECT-1 + ABTECT-2 OD-001 trial % Trial participants Obefazimod - n = 189 Similar activity between OD-001 doses in patients with moderate disease (MES = 2) Higher Remission Rate With 20 mg BID Dose in Severe Patients (MES = 3) Disclaimer:

24. Slide 24: Clinical Remission Rate Similar in AT-Naïve and AT-Experienced Patients

    Clinical Remission Rate at 20 mg BID Is Similar in AT-Naïve and AT-Experienced Patients Disclaimer: Cross-trial comparisons are for context only, and no head-to-head study was conducted; differences in study design, patient populations, and other factors should be considered when interpreting result

25. Slide 25: OD-001 Is Competitive With Other Oral Agents on Early Symptomatic Remission

    OD-001 Is Competitive With Other Oral Agents on Early Symptomatic Remission, With Increases Through Week 12 100 mg QD 200 mg QD Placebo 400 mg QD 25 mg QD 50 mg QD Placebo Icotrokinra (IL-23) OD-001 (20 mg BID) Obefazimod (miR-124) n=41 n=33(1) n=41 n=40 Notes: (1) Part 2 patients were randomized 1:

26. Slide 26: Transcriptomic Assessments to Support Clinical and Biomarker Assessments

    Transcriptomic analysis on mucosal biopsies from patients at baseline and after induction therapy to detect differentially expressed genes Transcriptomic Assessments to Support Clinical and Biomarker Assessments ASSESSMENTS SUPPORT OD-001 THERAPEUTIC ACTIVITY Unbiased assessment of ~20,000 genes acr

27. Slide 27: OD-001 Reduces Inflammatory and Fibrotic Gene Expression in IBD

    OD-001 reduces RIPK2 and microbial signatures OD-001 reduces cytokine expression and signaling OD-001 reduces T cell activity OD-001 reduces fibrotic signaling and increases epithelial homeostasis signaling OD-001 Reduces Inflammatory and Fibrotic Gene Expression in IBD Notes: Week 12–baseline chang

28. Slide 28: OD-001 Is the First Innate Immune-Targeted Therapy for IBD

    OD-001 Is the First Innate Immune-Targeted Therapy for IBD Phase 2a trial provides clinical proof of concept for a first-in-class oral therapy targeting RIPK2 with a compelling efficacy and safety profile Efficacy, biomarker, and transcriptomic data support 20 mg BID as projected therapeutic dose Si

29. Slide 29: Multiple Opportunities for OD-001 to Establish a Leading IBD Franchise

    Multiple Opportunities for OD-001 to Establish a Leading IBD Franchise Conventional therapy Phase 2a vedolizumab combination induction results expected in H2 2027 Phase 2b monotherapy induction results expected in H2 2027 and monotherapy maintenance results expected in 2028 Expansion of addressable

30. Slide 30: Oral SLC15A4 Inhibitor: OD-002

    Oral SLC15A4 Inhibitor: OD-002 Modulating B Cell Activity and Interferon Signaling CTA Filing in H2 2026 AI Platform Drove Program From Inception to GLP Study Initiation in 15 Months

31. Slide 31: Pathogenic Signaling Following TLR Activation Is Mediated by SLC15A4

    Pathogenic Signaling Following TLR Activation Is Mediated by SLC15A4 Extracellular RNA and DNA signal via TLR7/8/9… …through SLC15A4 to activate IRF5… …inducing pathogenic B cells and inflammatory cytokines… …causing disease Myeloid cells produce type I interferon and cytokines Age-associated B cell

32. Slide 32: SLC15A4 Is an Ideal Target in a Validated Pathway

    Type I IFN Pathogenic B cells Cytokines / Chemokines TASL We Believe SLC15A4 Is an Ideal Target in a Validated Pathway to Treat Diseases Driven by B Cells or Pathogenic RNA and DNA Sources: Immunity 2006;25:429; Nat Immunol 2022;23:1457; PLoS One 2021;16:e0244439; Proc Natl Acad Sci U S A 2013;110:2

33. Slide 33: OD-002 Is a High-Quality SLC15A4 Development Candidate

    OD-002 is potent and selective with favorable druglike properties OD-002 Is a High-Quality SLC15A4 Development Candidate Potency in vitro IC50 in human primary cells (e.g., TNF, IFN) Projected once-daily human dose Dose to maintain IC90 Preclinical safety and tolerability Selectivity TLR3, STING, an

34. Slide 34: OD-002 Blocks IFN Signaling From Both RNA and DNA

    OD-002 Blocks IFN Signaling From Both RNA and DNA SLC15A4 or TLR7/8 inhibitors block cytokines initiated by extracellular RNA TLR7/8 antagonists cannot block both arms of the nucleic acid response driving disease, with pathogenic signaling through TLR9 remaining active TLR7/8 stimulation induced by

35. Slide 35: OD-002 Selectively Blocks Human B Cell Proliferation From Pathogenic Stimuli

    OD-002 Selectively Blocks Human B Cell Proliferation From Pathogenic Stimuli Notes: Isolated memory B cells from healthy donors were pretreated with indicated compound for 24 hours prior to stimuli and % Ki67+ was measured after three days; ** p < 0.01; *** p < 0.001; **** p < 0.0001. SLC15A4 inhibi

36. Slide 36: Blocking Signaling From Both RNA and DNA Is Necessary to Modulate Pathogenic B Cells

    Anti-dsDNA antibodies … while sparing B cells in healthy mice OD-002 reduced pathogenic B cells and autoantibody production in lupus-prone mice… Blocking Signaling From Both RNA and DNA Is Necessary to Modulate Pathogenic B Cells and Autoantibody Production In Vivo Notes: * p < 0.05; **** p < 0.0001

37. Slide 37: Phase 1/2a Trial Initiation Expected in H1 2027

    Phase 1/2a Trial Initiation Expected in H1 2027 With Efficacy Readouts Expected in H2 2028 Small patient cohorts in CLE and 1–2 additional indications SAD: ~6 dose levels MAD: ~4 dose levels Food effect: ~1 dose level H1 2027 H2 2027 H2 2028 Phase 2a: Patient groups Phase 1: Randomized, double-blind

38. Slide 38: Phase 1 Ex Vivo Stimulation Assays Correlate With Activity in Lupus Patients

    Doses advanced into phase 2 trials achieved > 60% IFNα inhibition Enpatoran phase 1 ex vivo stimulation assay Efficacy across enpatoran doses in phase 2 Sponsor, program Status Completed ex vivo stim assay? Activity in SLE or CLE patients? Enpatoran Ph3 initiated March/April 2026 Afimetoran Ph2 comp

39. Slide 39: TNFR2 Agonist: OD-003

    TNFR2 Agonist: OD-003 Modulating Treg to Treat Autoimmune and Inflammatory Disease IND-Enabling Studies Ongoing

40. Slide 40: Treg Therapy Has Broad Therapeutic Potential in Large I&I Diseases

    Treg Therapy Has Broad Therapeutic Potential in Large I&I Diseases Correcting Treg dysregulation or increasing the number of Treg has the potential to be used across many inflammatory and autoimmune diseases Atopic dermatitis SLE Alopecia areata Multiple sclerosis Rheumatoid arthritis Asthma EFFECT

41. Slide 41: TNFR2 Agonism Is the Next Evolution of Treg-Targeted Therapy

    TNFR2 agonism clinical PoC upcoming to unlock next stage of Treg therapy development Expanding Treg number observed to be effective in multiple diseases TNFR2 agonism can potentially address the shortcomings of IL-2 TNFR2 Agonism Is the Next Evolution of Treg-Targeted Therapy Note: *** p < 0.001. So

42. Slide 42: Treg Therapy Has Potential to Transform Some of the Largest I&I Indications

    CLINICAL SIGNAL Rezpeg-treated AD patients with self-reported asthma history showed improvement in asthma control questionnaire (ACQ-5) scores ~$25B Respiratory Asthma MECHANISTIC EVIDENCE Treg maintain intestinal immune tolerance and mucosal integrity; Treg dysregulation contributes to chronic infl

43. Slide 43: Final Words

    Final Words —Yy 2 Q (CA Copyright 2026 | Odyssey Therapeutics | All Rights Reserved In search of extraordinary for patients 43

44. Slide 44: Upcoming Milestones for Lead Programs Through 2028

    Upcoming Milestones for Lead Programs Through 2028 Topline induction results from phase 2b monotherapy and phase 2a combination trials are expected in H2 2027 Phase 2b monotherapy trial is randomized, double-blind, and placebo-controlled Phase 2a combination trial is randomized, double-blind, and ac

45. Slide 45: Odyssey Therapeutics

    ODYSSEY THERAPEUTICS

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