Odyssey Therapeutics, Inc. · NASDAQ:ODTX

Odyssey Therapeutics — Investor Presentation (September 2026)

41 slides from Odyssey Therapeutics's investor presentation, September 2026

Slide 2: Disclaimers
Disclaimers Confidential information, forward-looking statements, and third-party information This presentation (including any discussion that accompanies this presentation) contains highly confidential information regarding Odyssey Therapeutics, Inc. (the “Company,” “Odyssey,” “we,” or “us”) and it
Slide 3: Few Patients With Autoimmune Disease Have Durable Remission
Few Patients With Autoimmune Disease Have Durable Remission Patients need: Additional Cytokines Increased remissions Anti- and and more treatable Biologics Multi- Inflammatory Specifics diseases Steroid- and Targeted Sparing Anti- Orals TNFs Deep and durable disease-modifying responses Better safety
Slide 4: Targeting Upstream Signaling Has Potential to Unlock Durable Remissions
Targeting Upstream Signaling Has Potential to Unlock Durable Remissions Defined pathogenic triggers …by converging on disease- …initiating a broad immune …causing tissue underlie inflammatory disease… specific signaling nodes… response… damage and disease Danger signals Cytokines & chemokines Damage
Slide 5: Experienced Team and Organization to Maximize Success
Experienced Team and Organization to Maximize Success Strategy Portfolio People Execution Capital • First-in-class targets • Targeting large-market • Experienced board and • Lean and agile structure • Efficient capital allocation I&I indications senior management built for speed with disciplined pro
Slide 6: Pioneering Next-Generation I&I Therapies to Redefine Standard of Care
Pioneering Next-Generation I&I Therapies to Redefine Standard of Care INFLAMMATORY BOWEL DISEASE B CELL-MEDIATED DISEASES INFLAMMATORY AND AUTOIMMUNE DISEASES Differentiated Potential Potential first-in-class, oral Potential first-in-class protein agonist to first-in-class, oral paradigm-changing th
Slide 7: Broad Therapeutic Pipeline for Diseases With Unmet Need
Broad Therapeutic Pipeline for Diseases With Unmet Need Target IND- Anticipated upcoming clinical Indications Discovery Phase 1 Phase 2 Phase 3 Modality Enabling milestones RIPK2, Oct 2026: Updated monotherapy data at UEG OD-001 UC, CD H2 2027: Phase 2a combination readout Small molecule H2 2027: Ph
Slide 8: Data to Build a Potential RIPK2 IBD Franchise Expected in 2027 and 2028
Data to Build a Potential RIPK2 IBD Franchise Expected in 2027 and 2028 Break therapeutic ceiling Demonstrate potential of Monotherapy topline Full induction efficacy and through innate-adaptive RIPK2 monotherapy as next induction efficacy exploratory assessments combinations for induction SoC maint
Slide 9: Oral RIPK2 Scaffolding Inhibitor: OD-001
Oral RIPK2 Scaffolding Inhibitor: OD-001 Proof-of-Concept Achieved in Addressing a Root Cause of Ulcerative Colitis Inflammation in IBD Using a Novel Mechanism of Action Program Inception to Phase 2 Proof-of-Concept: 4.5 Years Copyright 2026 | Odyssey Therapeutics | All Rights Reserved In In s ear s
Slide 10: Innate Immune Responses to Gut Microbes is the Root Cause of IBD
Innate Immune Responses to Gut Microbes is the Root Cause of IBD Gut Intestinal lumen lumen RIPK2 transduces NOD1/2 inflammatory Activated NOD1/2 signaling… T cells PGN RIPK2 TNF T cells Bacteria Th1 cells TL1A LTA, flagellin, LPS IL-23 Pathogenic T cell Th17 cells … and RIPK2 activation recruitment
Slide 11: Even With Advanced Therapies, Durable Remission Rates for IBD Remain Low
Even With Advanced Therapies, Durable Remission Rates for IBD Remain Low 30% ~75% of patients fail Ulcerative colitis placebo-adjusted to achieve clinical remission clinical remission rate 20% Efficacy ceiling Remission rates are of non-JAK orals ~50% lower in AT- experienced patients 10% 45% of pat
Slide 12: We Believe RIPK2 Is an Ideal Target for Treating IBD
We Believe RIPK2 Is an Ideal Target for Treating IBD RIPK2 has low homology to other RIPK proteins and a RIPK2 activation leads to scaffolding with XIAP and inflammatory signaling distinct function in inflammatory signaling RIPK2 activity correlates with disease severity PGN NOD1/2 Gene polymorphism
Slide 13: RIPK2 Is Activated in UC and CD and Correlates With Severity
RIPK2 Is Activated in UC and CD and Correlates With Severity Increased levels of activated (ubiquitinated) RIPK2 Increased expression of RIPK2-dependent gene signature in UC and CD patient biopsies in patients with UC and CD *** 12 *** Relative intensity of RIPK2-Ub 10 8 6 4 2 0 Non-IBD UC CD Notes:
Slide 14: OD-001 Achieves Selective Blockade of RIPK2 Scaffolding With XIAP
OD-001 Achieves Selective Blockade of RIPK2 Scaffolding With XIAP OD-001 binds to RIPK2 and holds the protein in a OD-001 blocks cytokine production from OD-001 activity is not reduced by TNF resistance conformation that reduces the affinity for XIAP macrophages stimulated with PGN 100 100 OD-001 80
Slide 15: Only OD-001 Fully Inhibits RIPK2 Scaffolding in Cells
Only OD-001 Fully Inhibits RIPK2 Scaffolding in Cells and Completely Blocks Inflammatory Cytokine Production Binding affinity for XIAP in the presence of drug Inhibition of scaffolding in cells Inhibition of cytokine production 0 200 150 RIPK2:XIAP KD, nM % RIPK2:XIAP binding % TL1A production 500 1
Slide 16: Phase 2a Monotherapy Trial Results
Phase 2a Monotherapy Trial Results Copyright 2026 | Odyssey Therapeutics | All Rights Reserved | Confidential In In s ear c h cof s ear ex ex h of tr aor dinar tr aor y fyorf or dinar patients patients 16
Slide 17: Phase 2a Monotherapy Trial Overview
Phase 2a Monotherapy Trial Overview Trial design (1) Efficacy endpoints and powering • Enrolled patients with moderate-to-severe UC, modified Mayo Clinical score • Primary: 2-point change in 3-component MMCS at week 12 (MMCS) of 5–9; allowed up to three prior advanced therapies - 90% power at the tw
Slide 18: Enrolled Participant Characteristics Are Similar to Contemporary UC Trials
Enrolled Participant Characteristics Are Similar to Contemporary UC Trials Spyre Spyre OD-001 Obefazimod MORF-057 Icotrokinra Tulisokibart Duvakitug Afimkibart (⍺4β7) (TL1A) Phase Phase 2a Phase 2b Phase 3 Phase 2a Phase 2b Phase 2 Phase 2 Phase 2b Phase 2 Phase 2b Phase 2b Age, mean 40 41 42 39 40
Slide 19: OD-001 Was Well Tolerated at 10 mg BID and 20 mg BID
OD-001 Was Well Tolerated at 10 mg BID and 20 mg BID With a Promising Safety Profile Observed Treatment-emergent adverse events Part 1: 10 mg BID, n = 8 Part 2: 20 mg BID, n = 45 (1) Participants with any TEAE (n, %) 2 (25%) 20 (44%) Severe (grade ≥ 3) TEAE 0 0 Drug-related TEAE 0 2 (4%) Liver funct
Slide 20: Trial Met Key Efficacy Endpoints, Including Clinical Remission
Trial Met Key Efficacy Endpoints, Including Clinical Remission Met primary endpoint of change in MMCS from baseline in both parts and on a consolidated basis (-2.6, p < 0.001) Efficacy across endpoints at week 12 (part 1 and 2 combined, n = 49) Median fecal calprotectin by week 12 outcome 70% Regula
Slide 21: Clinical Remission Rates in AT-Experienced vs. AT-Naïve Patients
Clinical Remission Rates in AT-Experienced vs. AT-Naïve Patients Advanced therapy naïve (n = 33) Advanced therapy experienced (n = 16) % of patients in clinical remission 4 clinical remissions and 1 additional endoscopic improvement % of patients in clinical remission △ = 16 △ = 22 Placebo group Tre
Slide 22: Rapid Onset of Action With Deepening of Response, Consistent With MOA
Rapid Onset of Action With Deepening of Response, Consistent With MOA Average rectal bleeding score over treatment 2 Daily bleeding score Average rectal bleeding score 1.5 0 = “No blood seen” 1 = “Stool has streaks of blood” 2 = “Stool has more than just streaks of blood” 3 = “Blood alone passed” 1
Slide 23: Patient Vignette: Clinical Remission With OD-001 but Relapse on Vedolizumab
Patient Vignette: Clinical Remission With OD-001 but Relapse on Vedolizumab • 55-year-old Canadian female with 5-year history of UC - Patient was previously treated with anti-IL-23 and S1P1 Histopathology showed evidence of mucosal healing • MES of 2 and MMCS of 5 at screening • Achieved clinical re
Slide 24: OD-001 Is the First Innate Immune-Targeted Therapy for IBD
OD-001 Is the First Innate Immune-Targeted Therapy for IBD • Efficacy is competitive with leading approved or investigational therapies ‒ Concordant efficacy measures across all endpoints, consistent with the mechanism of action for RIPK2 ‒ Strong efficacy in AT-experienced patients ‒ Innate immune
Slide 25: Multiple Opportunities for OD-001 to Establish a Leading IBD Franchise
Multiple Opportunities for OD-001 to Establish a Leading IBD Franchise Conventional Advanced therapy, including injectable biologics (e.g., TNF) and oral therapies (e.g., JAKi) therapy management Orals Injectables Combinations Current Orals: 5-ASA and methotrexate Tulisokibart $7B+ ~$3B $4B+ Combina
Slide 26: Oral SLC15A4 Inhibitor: OD-002
Oral SLC15A4 Inhibitor: OD-002 CTA Filing in Modulating B Cell Activity H2 2026 and Interferon Signaling AI Platform Drove Program from Inception to GLP Study Initiation in 15 Months Copyright 2026 | Odyssey Therapeutics | All Rights Reserved In In s ear s ear c h cof h of ex ex tr aor tr aor dinar
Slide 27: Pathogenic Signaling Following TLR Activation is Mediated by SLC15A4
Pathogenic Signaling Following TLR Activation is Mediated by SLC15A4 • Inflammatory responses to RNA or DNA are a root cause of many autoimmune diseases and a driver of pathogenic B cell expansion and autoantibody production Extracellular RNA and DNA …through SLC15A4 to …inducing pathogenic B …causi
Slide 28: We Believe SLC15A4 Is an Ideal Target in a Validated Pathway
We Believe SLC15A4 Is an Ideal Target in a Validated Pathway to Treat Diseases Driven by B Cells or Pathogenic RNA and DNA Commercial and clinical validation for targeting SLC15A4:TASL is the optimal node to maximize efficacy and tolerability upstream or downstream components of the pathway TLR7/8 a
Slide 29: OD-002 Is a High-Quality SLC15A4 Development Candidate
OD-002 Is a High-Quality SLC15A4 Development Candidate OD-002 fully inhibits TLR7/8-dependent IRF5 phosphorylation and type I IFN OD-002 is potent and selective with favorable druglike properties production Potency in vitro ≤ 10 nM 100 100 IC50 in human primary cells (e.g., TNF, IFN) % Inhibition, I
Slide 30: OD-002 Blocks IFN Signaling From Both RNA and DNA
OD-002 Blocks IFN Signaling From Both RNA and DNA • TLR7/8 antagonists cannot block both arms of the nucleic acid response driving disease; with pathogenic signaling through TLR9 remaining active SLC15A4 or TLR7/8 inhibitors block cytokines initiated by extracellular RNA SLC15A4 inhibition also bloc
Slide 31: OD-002 Selectively Blocks Human B Cell Proliferation From Pathogenic Stimuli
OD-002 Selectively Blocks Human B Cell Proliferation From Pathogenic Stimuli SLC15A4 inhibition also blocks B cell proliferation SLC15A4 inhibition does not alter normal B cell SLC15A4 inhibition blocks B cell proliferation induced by CpG, a TLR9 agonist that mimics proliferation by activation with
Slide 32: Blocking Signaling From Both RNA and DNA Is Necessary to Modulate Pathogenic B Cells
Blocking Signaling From Both RNA and DNA Is Necessary to Modulate Pathogenic B Cells and Autoantibody Production In Vivo OD-002 reduced pathogenic B cells and autoantibody production in lupus-prone mice… …while sparing B cells in healthy mice ABC cells Anti-dsDNA antibodies Proliferating B cells 6 5
Slide 33: 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 Trial overview Endpoints • Phase 1: Randomized, double-blind, placebo-controlled SAD, MAD, • Phase 1: Healthy participants and food effect cohorts in ~100 healthy participants - Safety, tolerability, and pharm
Slide 34: Phase 1 Ex Vivo Stimulation Assays Correlate With Activity in Lupus Patients
Phase 1 Ex Vivo Stimulation Assays Correlate With Activity in Lupus Patients TLR7/8 antagonists have validated ex vivo assays Enpatoran phase 1 ex vivo stimulation assay Efficacy across enpatoran doses in phase 2 for predicting activity in lupus patients Completed Activity in • Doses advanced into p
Slide 35: TNFR2 Agonist: OD-003
TNFR2 Agonist: OD-003 IND-Enabling Modulating Treg to Treat Autoimmune Studies Ongoing and Inflammatory Disease Copyright 2026 | Odyssey Therapeutics | All Rights Reserved In In s ear s ear c h cof h of ex ex tr aor tr aor dinar dinar y fyorf or patients patients 35
Slide 36: Treg Therapy Has Broad Therapeutic Potential in Large I&I Diseases
Treg Therapy Has Broad Therapeutic Potential in Large I&I Diseases Atopic dermatitis SLE Alopecia areata Vitiligo Multiple sclerosis Rheumatoid arthritis Asthma Correcting Treg dysregulation or increasing the number of Treg has the potential to be used across many inflammatory and autoimmune disease
Slide 37: TNFR2 Agonism Is Next Evolution of Treg-Targeted Therapy
TNFR2 Agonism Is Next Evolution of Treg-Targeted Therapy Expanding Treg number observed to be effective in TNFR2 agonism can potentially address the TNFR2 agonism clinical PoC upcoming to unlock multiple diseases shortcomings of IL-2 next stage of Treg therapy development • Efficacy observed in atop
Slide 38: Treg Therapy Has Potential to Transform Some of the Largest I&I Indications
Treg Therapy Has Potential to Transform Some of the Largest I&I Indications » » » validation CLINICAL PoC CLINICAL SIGNAL TRANSLATIONAL EVIDENCE MECHANISTIC EVIDENCE Stage of $30B+ ~$25B $20B+ ~$25B Dermatology Neurology Respiratory IBD AD, alopecia Multiple Asthma UC and CD areata, vitiligo scleros
Slide 40: Significant Clinical Milestones Expected Through 2028
Significant Clinical Milestones Expected Through 2028 2026 2027 2028 • October: Oral presentation of full • H1: Initiate OD-002 healthy • H2: OD-002 phase 2a readouts in OD-001 Phase 2a induction data participant dosing in Ph1/2 trial multiple indications • H2: Initiation of OD-001 phase 2b • H2: Co

Odyssey Therapeutics — Investor Presentation (September 2026) on 6ix

Odyssey Therapeutics — Investor Presentation (September 2026)

Slide 1: Corporate Presentation

Slide 2: Disclaimers

Slide 3: Few Patients With Autoimmune Disease Have Durable Remission

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

Slide 5: Experienced Team and Organization to Maximize Success

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

Slide 7: Broad Therapeutic Pipeline for Diseases With Unmet Need

Slide 8: Data to Build a Potential RIPK2 IBD Franchise Expected in 2027 and 2028

Slide 9: Oral RIPK2 Scaffolding Inhibitor: OD-001

Slide 10: Innate Immune Responses to Gut Microbes is the Root Cause of IBD

Slide 11: Even With Advanced Therapies, Durable Remission Rates for IBD Remain Low

Slide 12: We Believe RIPK2 Is an Ideal Target for Treating IBD

Slide 13: RIPK2 Is Activated in UC and CD and Correlates With Severity

Slide 14: OD-001 Achieves Selective Blockade of RIPK2 Scaffolding With XIAP

Slide 15: Only OD-001 Fully Inhibits RIPK2 Scaffolding in Cells

Slide 16: Phase 2a Monotherapy Trial Results

Slide 17: Phase 2a Monotherapy Trial Overview

Slide 18: Enrolled Participant Characteristics Are Similar to Contemporary UC Trials

Slide 19: OD-001 Was Well Tolerated at 10 mg BID and 20 mg BID

Slide 20: Trial Met Key Efficacy Endpoints, Including Clinical Remission

Slide 21: Clinical Remission Rates in AT-Experienced vs. AT-Naïve Patients

Slide 22: Rapid Onset of Action With Deepening of Response, Consistent With MOA

Slide 23: Patient Vignette: Clinical Remission With OD-001 but Relapse on Vedolizumab

Slide 24: OD-001 Is the First Innate Immune-Targeted Therapy for IBD

Slide 25: Multiple Opportunities for OD-001 to Establish a Leading IBD Franchise

Slide 26: Oral SLC15A4 Inhibitor: OD-002

Slide 27: Pathogenic Signaling Following TLR Activation is Mediated by SLC15A4

Slide 28: We Believe SLC15A4 Is an Ideal Target in a Validated Pathway

Slide 29: OD-002 Is a High-Quality SLC15A4 Development Candidate

Slide 30: OD-002 Blocks IFN Signaling From Both RNA and DNA

Slide 31: OD-002 Selectively Blocks Human B Cell Proliferation From Pathogenic Stimuli

Slide 32: Blocking Signaling From Both RNA and DNA Is Necessary to Modulate Pathogenic B Cells

Slide 33: Phase 1/2a Trial Initiation Expected in H1 2027

Slide 34: Phase 1 Ex Vivo Stimulation Assays Correlate With Activity in Lupus Patients

Slide 35: TNFR2 Agonist: OD-003

Slide 36: Treg Therapy Has Broad Therapeutic Potential in Large I&I Diseases

Slide 37: TNFR2 Agonism Is Next Evolution of Treg-Targeted Therapy

Slide 38: Treg Therapy Has Potential to Transform Some of the Largest I&I Indications

Slide 39: Final Words

Slide 40: Significant Clinical Milestones Expected Through 2028

Slide 41: Thank you!