Tvardi Therapeutics, Inc. · NASDAQ:TVRD
Tvardi Therapeutics — Investor Presentation (September 2026)
63 slides from Tvardi Therapeutics's investor presentation, September 2026
Slide 1: Overview September 2026
Overview September 2026
Slide 2: Disclaimer and Forward-Looking Statements
Disclaimer and Forward-Looking Statements This presentation contains forward-looking statements that involve substantial risks and uncertainties. All statements, other than statements of historical facts, contained in this presentation, including statements about our expectations regarding the poten
Slide 3: STAT3 Inhibitors Designed to Address Unmet Need in Inflammatory and Proliferative Diseases
Our STAT3 Inhibitors are Designed to Address the Unmet Need in Inflammatory and Proliferative Diseases STAT3: Highly Validated Translational TTI-109 Validation in P1 TTI-109 Convergent Node Proof-of-Concept Healthy Volunteers Lead Indication IL17 IL6 IL23 Preclinical ↓ pY-STAT3 ↓ immune dysregulatio
Slide 4: Targeting STAT3: a Convergence Point of Inflammatory and Proliferative Disease
Targeting STAT3: a Convergence Point of Inflammatory and Proliferative Disease Diverse Disease Signaling Pathways Converge on STAT3 HGF IL-23 IL-6 IL-21 IL-1β TNF-α IL-17A/F IL-12 TGF-β Extracellular P direct STAT3 activation indirect STAT3 activation Cytosol Nucleus Immune dysregulation Inflammatio
Slide 5: Current Therapies Target Individual Pathways
Targeting STAT3: a Convergence Point of Inflammatory and Proliferative Disease Current Therapies Target Individual Pathways HGF IL-23 IL-6 IL-21 IL-1β TNF-α IL-17A/F IL-12 TGF-β Extracellular P direct STAT3 activation indirect STAT3 activation Cytosol Nucleus Immune dysregulation Inflammation Prolif
Slide 6: Selective Inhibition of STAT3 Nuclear Function
Targeting STAT3: a Convergence Point of Inflammatory and Proliferative Disease Diverse Disease Signaling Pathways Converge on STAT3 HGF IL-23 IL-6 IL-21 IL-1β TNF-α IL-17A/F IL-12 TGF-β Extracellular direct STAT3 activation Tvardi’s oral small …With no impact on indirect STAT3 activation molecules i
Slide 7: Seasoned Leadership: Deep R&D and Operational Expertise
Seasoned Leadership: Deep R&D and Operational Expertise Management Team Imran Alibhai, PhD CEO & Director Dan Conn, JD, MBA CFO John Kauh, MD CMO Scientific Advisory Board Board of Directors David Tweardy, MD Founder & Advisor Sujal Shah Chairman Ron DePinho, MD Founder & Advisor Michael Wyzga Direc
Slide 8: TTI-109
TTI-109
Slide 9: TTI-101 Clinical Foundation for Development of TTI-109
TTI-101 Clinical Foundation for Development of TTI-109 pY-STAT3 Target Engagement IL-6 & Fibrosis Reduction Overall TTI-101 Safety Oncology Phase 11 REVERT IPF Phase 22 Decline in pY-STAT3 Decline in IL-6 0 In over 300 subjects 0% -0.25 treated with TTI-101: pY-STAT3 H-score Change from Baseline -0.
Slide 10: TTI-109 Designed as a Prodrug to Enhance Delivery of STAT3 Inhibitor
TTI-109 Designed as a Prodrug to Enhance Delivery of STAT3 Inhibitor and Establish Favorable Target Product Profile TTI-109 Design Objectives IND-Enabling GLP Results • Preserve mechanism of action and observed clinical • No toxicology findings with TTI-109, mirroring TTI-101 activity of TTI-101 • A
Slide 11: Phase 1 Clinical Program Validated TTI-109 as Oral Prodrug of TTI-101
Phase 1 Clinical Program Validated TTI-109 as the Oral Prodrug of TTI-101 Part A: Single Ascending Dose Part B: Bioequivalence Part C: Multiple Ascending Dose (SAD) Crossover Study (MAD) TTI-101 TTI-109 Wash- out n=8 n=6 n=6 n=6 n=6 n=8 n=8 n=8 n=8 n=8 n=8 250mg 500mg 750mg 1000mg TTI-109 TTI-101 12
Slide 12: TTI-109 Rapidly Converted to Active TTI-101
TTI-109 Rapidly Converted to Active TTI-101: Consistent from Primate to Human SAD Primate Study: Rapid conversion of TTI-109 to Human Study: Rapid conversion of TTI-109 to active moiety TTI-101 active moiety TTI-101 TTI-109 28-Day GLP Primate Study*: Plasma Concentrations of TTI-101 vs TTI-109 (500m
Slide 13: TTI-109 Achieved Equivalent Active Moiety Exposure to TTI-101
TTI-109 Achieved Equivalent Active Moiety Exposure to TTI-101 Bioequivalence Cross-over Study Randomization Plasma Concentrations of TTI-101 vs TTI-109 Dosing (molar equivalent doses) 4000 TTI-101 400mg Fasted 3500 Plasma Concentration (ng/mL) TTI-109 500mg Fasted TTI-109 500mg Washout TTI-101 400mg
Slide 14: TTI-109 Repeat Dosing Delivered Predictable Steady State Parameters
TTI-109 Repeat Dosing Delivered Predictable Steady State Parameters SAD MAD SAD: Plasma Concentrations of TTI-101 After MAD: Plasma Concentrations of TTI-101 After Single Dose of TTI-109 21-Day BID Dosing of TTI-109 6000 6000 Similar PK at Dose 5000 5000 dependent Plasma Concentration (ng/mL) Day 1
Slide 15: TTI-109 Phase 1 TEAE Profile
TTI-109 Phase 1 TEAE Profile TTI-109 500mg ≈ TTI-101 400mg MAD Near molar equivalent dosages TTI-109 TTI-109 TTI-101 Adverse Event Preferred Placebo Doses 1-4 500mg 400mg Term (N=8) (N=32) (N=8) (N=8) No. of participants reporting at 5 (63%) 19 (59%) 6 (75%) 6 (75%) least one TEAE AEs leading to dru
Slide 16: Differential Diarrhea Pattern: TTI-109 vs. TTI-101
Differential Diarrhea Pattern: TTI-109 vs. TTI-101 TTI-109 500mg ≈ TTI-101 400mg MAD Near molar equivalent dosages TTI-109 TTI-109 TTI-101 Placebo Doses 1-4 500mg 400mg Adverse Event Preferred Term (N=8) (N=32) (N=8) (N=8) Grade 1 Grade 2 Grade 1 Grade 2 Grade 1 Grade 2 Grade 1 Grade 2 Diarrhea 2 (2
Slide 17: Preclinical Framework for Exploratory Pharmacodynamic Objectives
Preclinical Framework for Exploratory Pharmacodynamic Objectives pY-STAT3 drives Observed reduction of Th17 in Observed reduction of Th17 in Evaluating cellular and humoral immunity healthy mice with TTI-1012 diseased mice with TTI-1013 pharmacodynamics from HV Th17 in healthy mice Colonic Th17 cell
Slide 18: TTI-109 Selectively Reduced Immune Cell Populations Driven by STAT3
TTI-109 Selectively Reduced Immune Cell Populations Driven by STAT3 in Phase 1 MAD Cohort MAD 80% Th17 At active doses, downregulation of STAT3- T follicular helper cells driven immune populations observed: % Change from baseline normalized to placebo 60% B cells 40% ✓ Effects sustained across activ
Slide 19: TTI-109 Reduced Th17 Cells Implicated in UC Pathology
TTI-109 Reduced Th17 Cells Implicated in UC Pathology MAD Cell Type %Δ UC Rationale Central pathogenic effectors in UC Th17 cells (core) -54% and drive mucosal inflammation.1 CD4 T cells CCR6+ -47% Enriched in active UC biopsies.2 Drive IL-21-mediated B cell activation CD4 T helpers -51% and pathoge
Slide 20: TTI-109 Reduced T Follicular Cells Implicated in UC Pathology
TTI-109 Reduced T Follicular Cells Implicated in UC Pathology MAD Cell Type %Δ UC Rationale Drive UC through humoral autoantibody production and direct T follicular helper cells (Tfh) -34% cellular Bcl6-dependent mucosal inflammation.1,2 Track with UC disease activity and CD4 T cells CXCR5+ -38% pro
Slide 21: TTI-109 Reduced B Cells Implicated in UC Pathology
TTI-109 Reduced B Cells Implicated in UC Pathology MAD Cell Type %Δ UC Rationale Mucosal B-cell and plasma cell expansion is a hallmark of active UC, contributing B cells -20% directly to colonic inflammation and tissue injury.1 Track serum Ig levels and humoral activity in Memory B cells -46% activ
Slide 22: TTI-109 Advances TTI-101's Clinical Profile Across PK, GI Tolerability and Immune Modulation
We Believe TTI-109 Advances TTI-101's Clinical Profile Across PK, GI Tolerability and Immune Modulation TTI-109 is designed to enhance delivery & improve tolerability while preserving P mechanism of action TTI-101 Clinical Observations1,2 TTI-109 Clinical Observations ✓ Target Engagement ✓ PK ↓ pY-S
Slide 23: UC: Large Market Opportunity with High Unmet Medical Need
UC: Large Market Opportunity with High Unmet Medical Need UC Therapy Landscape >1.25M1 $9B2 ~$3B2 Diagnosed US Patients Global Market (2024) US Market (2024) Placebo-adjusted clinical remission (induction) rates by MoA in UC3 >70% of patients do not achieve clinical remission with existing therapies
Slide 24: One Target, Three Mechanisms: pY-STAT3 Drives Shared Biology of UC
One Target, Three Mechanisms: pY-STAT3 Drives the Shared Biology of UC Chronic immune activation and Persistent inflammation, tissue injury and Chronic remodeling, fibrosis and increased perpetuation of intestinal inflammation ulceration dysplasia risk Epithelial Aberrant Crypt Epithelial Injury Reg
Slide 25: pY-STAT3 Reduction Demonstrated in Preclinical Models and Clinical Biopsies
pY-STAT3 Reduction Demonstrated in Preclinical Models Activated STAT3 and Clinical Biopsies pY-STAT3 is associated with pY-STAT3 levels restored to baseline Clinical PoC: UC clinical activity after TVRD STAT3 inhibitor treatment Reduced pY-STAT3 Tissue pY-STAT3 increases with UC activity1 GI model d
Slide 26: STAT3 Inhibition Normalized Preclinical and Clinical Immune Dysregulation
STAT3 Inhibition Normalized Preclinical and Clinical Immune dysregulation Pathogenic Immune Cell Populations Cellular (Th17) and Humoral (B cell) Th17 restored to homeostatic levels Clinical PoC: dysregulation in UC patients after TVRD STAT3 inhibitor Reduced key immune cell populations Th17 cell fr
Slide 27: STAT3 Inhibition Reduced IL-6 and Inflammation Preclinically and in Patients
STAT3 Inhibition Reduced IL-6 and Inflammation Preclinically Inflammation and in Patients Inflammatory cytokine IL-6 correlates Colonic inflammation significantly Clinical PoC: with UC severity attenuated with TVRD STAT3 inhibitor Reduced IL-6 Increases in serum levels of inflammatory GI model drive
Slide 28: STAT3 Inhibition Reduced Proliferative Signaling and Fibrosis
STAT3 Inhibition Reduced Proliferative Signaling and Fibrosis Proliferation Preclinically and in Patients Proliferation and fibrosis correlate Preserved tissue integrity and colon Clinical PoC: with UC severity length with TVRD STAT3 inhibitor Reduced fibrosis Disease severity indices integrate hist
Slide 29: Proposed Clinical Trial Designed to Address Key Challenges in UC
Proposed Clinical Trial Designed to Address Key Challenges in UC Study Design Key inclusion Treatment Period Maintenance Period Endpoints criteria: (Induction 12 weeks) (12 weeks) • Primary: Safety • Moderate to Dose 1 (QD) • Secondary: Efficacy severe UC Dose 2 (QD) • Clinical remission at 12 weeks
Slide 30: Overcoming Persistent Disease Biology
Overcoming Persistent Disease Biology HGF IL-23 IL-6 IL-21 IL-1β TNF-α IL-17A/F IL-12 TGF-β Single-pathway inhibition fails direct STAT3 activation indirect STAT3 activation to suppress STAT3 due to redundant signaling cascades Immune dysregulation Inflammation Proliferation UC Murine Models ↓ Patho
Slide 31: A Differentiated Oral Therapy with Targeted Exposure
A Differentiated Oral Therapy with Targeted Exposure Differentiated safety Tissue-targeted Rapid and durable Safety concerns biologic effect profile exposure • Class-related safety risks with JAK inhibitors1 and S1P2,3 modulators: • MACE, venous thromboembolism, 83% malignancy, ~400 objective respon
Slide 32: Enabling Precision Medicine
Enabling Precision Medicine pY-STAT3 associated with STAT3-associated genetic & Limited Molecular Insight clinical activity1,2 immune signatures Elevated UC risk3,4 • Broad, unselected patient Reduced Clinical populations pY-STAT3 response STAT3 polymorphisms pY-STAT3 rs744166 | rs2293152 • Unpredic
Slide 33: STAT3 Inhibitors Designed to Address Unmet Need in Inflammatory and Proliferative Diseases
Our STAT3 Inhibitors are Designed to Address the Unmet Need in Inflammatory and Proliferative Diseases STAT3: Highly Validated Translational TTI-109 Validation in P1 TTI-109 Convergent Node Proof-of-Concept Healthy Volunteers Lead Indication IL17 IL6 IL23 Preclinical ↓ pY-STAT3 ↓ immune dysregulatio
Slide 34: Our Pipeline
Our Pipeline Program Indication Preclinical Phase 1 Phase 2 Phase 3 Anticipated Milestones Ulcerative Colitis TTI-109 IND submission expected 2027* • Study initiation expected 2027* (UC) Hepatocellular • Phase 1b/2 topline data TTI-101 Carcinoma Phase 1b/2 2H:2026 (HCC) *Tvardi’s ability to initiate
Slide 35: TTI-101 in HCC
TTI-101 in HCC
Slide 36: TTI-101 Reversed Multiple Pathogenic Steps of Liver Cancer in NASH-induced HCC Model
TTI-101 Reversed Multiple Pathogenic Steps of Liver Cancer in a NASH-induced HCC Model Inflammation Fibrosis/Cirrhosis HCC STAT3-mediated pathogenesis Microsteatosis Fibrosis Tumor volume After formation TTI-101 STAT3-inhibition of tumors at in NASH-induced HCC TTI-101 11 months, we observed treatme
Slide 37: Phase 1 First in Human TTI-101 Monotherapy Study Design
Phase 1 Clinical Trial: First in Human TTI-101 Monotherapy Study Design Dose Escalation Dose Expansion Liver Cancer Liver Cancer RP2D Advanced Solid Tumors Other Solid Tumors Other Solid Tumors RP2D Objectives: • Primary: Maximum tolerated dose, safety, and pharmacokinetics • Secondary: Clinical eff
Slide 38: TTI-101 Monotherapy Led to Durable Partial Responses in Fibrotic Tumors
Phase 1 Clinical Trial: TTI-101 Monotherapy Led to Durable Partial Responses in Fibrotic Tumors Baseline Cycle 3, Day 1 Cycle 5, Day 1 Partial Responder A: HCC Target Lung Met • Failed sorafenib, pembro, nivo, nivo+bev • Best Response: 42% Reduction in Sum of Targets Overall • Sustained PR for 10 mo
Slide 39: Phase 1: TTI-101 Monotherapy Clinical Trial Summary
Phase 1: TTI-101 Monotherapy Clinical Trial Summary PK / PD Tolerability Biological Activity • Exposures in humans • 100% of patients with • Well-tolerated BID oral • Enhanced biological above the level required elevated pY-STAT3 levels dosing activity in fibrotic cancers for efficacy in preclinical
Slide 40: Strong Rationale for TTI-101 and ICI Combination Therapy
Strong Rationale for TTI-101 and ICI Combination Therapy POC Established for Phase 1 Trial Responder Overcame ICI Preclinical Model STAT3 Inhibition + ICI Resistance After TTI-101 Monotherapy TTI-101 additive to 1L SoC Ph 2: Danvatirsen (STAT3 ASO) + Sum of Tumor Responses After ICI Failure, On TTI-
Slide 41: TTI-101 Distinct and Synergistic Mechanism for Unmet Need in HCC
TTI-101 is Designed to Provide a Distinct and Synergistic Mechanism for Unmet Need in HCC HCC Disease Overview • HCC is 3rd leading cause of cancer deaths in the world1 • Annually in the US, >42,000 new cases of HCC and ~32,000 deaths recorded 2 • Incidence has more than tripled since 1980 3 Overvie
Slide 42: REVERT Liver Cancer: Phase 2 Study of TTI-101 in HCC
REVERTLiver Cancer: Phase 2 Study of TTI-101 in HCC Phase 1b Phase 2 Dose Finding Expansion (N=100) A Last Line: no available TTI-101 RP2D therapies that will confer TTI-101 RP2D clinical benefit (N=30) (21 US Sites) • Overall Response Rate Last Line Rationale: Confirmation of P1 PoC TTI-101 monothe
Slide 43: REVERT Liver Cancer: Interim Phase 1b/2 Data
REVERTLiver Cancer: Interim Phase 1b/2 Data Cohort A: Cohort C: TTI-101 Monotherapy at RP2D TTI-101 + Atezo/Bev *One patient on protocol for 6 weeks. Patient discontinued combination due to an unrelated AE. After recovery from AE, 33% 8%* patient continued with atezo/bev and investigator reported co
Slide 44: Key Takeaways: TTI-101 in HCC
Key Takeaways: TTI-101 in HCC STAT3: Well- Differentiated Encouraging Near-Term Clinical Established Biology Approach Clinical Activity Milestone STAT3 long Inhibition of STAT3 Clinically meaningful Topline results from recognized as prime activation to have activity in both ongoing Phase 2 target i
Slide 45: Appendix A. Preclinical Support
Appendix A. Preclinical Support
Slide 46: TVRD STAT3 Inhibition Active Across Multiple Validated IBD Immune Axes
TVRD STAT3 Inhibition Demonstrated Activity Across Multiple Validated IBD Immune Axes Model Systems and Select Therapies Approved or Developed for IBD TVRD Anti- Anti-TNFα Anti-TL1A Anti-IL-6 JAK1i JAK2/3i TyK2i S1P1m STAT3i IL12/23 Model Immune Axis / Key Cytokines DSS • Innate → Th1/Th17 ✓ ✓ ✓ ✓ (
Slide 47: TVRD STAT3 Inhibitors in the DSS-UC Model
TVRD STAT3 Inhibitors in the DSS-UC Model 5% DSS UC Model with TTI-1011 Colon Morphology and Length pY-STAT3 8 Vehicle 7 * 140 Colon Length (cm) pY-STAT3 / total protein 6 120 5 100 4 80 5% DSS 3 60 * 2 40 1 20 5% DSS + TTI-101 0 0 0% DSS (naïve) 5% DSS + Vehicle 5% DSS + TTI-101 0% DSS + Vehicle 5%
Slide 48: TVRD STAT3 Inhibitors in the TNBS-CD Model
TVRD STAT3 Inhibitors in the TNBS-CD Model TNBS CD Model with TTI-1011 Colon Morphology and Length pY-STAT3 80 Sham 70 * 120 pY-STAT3 (relative units, 60 Colon length (mm) norm. to total protein) 100 50 TNBS + vehicle 80 40 60 30 40 TNBS + TTI-101 20 * 10 20 0 0 Sham TNBS + vehicle TNBS + TTI-101 Sh
Slide 49: TVRD STAT3 Inhibitors in the OXA-UC Model
TVRD STAT3 Inhibitors in the OXA-UC Model OXA UC Model with TTI-1091 Colon Morphology and Length 10 Vehicle 9 8 * Colon Length (cm) 7 6 OXA 5 pY-STAT3 4 3 40 2 35 OXA + TTI-109 1 0 30 pY-STAT3 H-Score 2 Sham 3 OXA+Vehicle 4 OXA+TTI-109 25 Colonic inflammation Diarrhea 20 4.0 4 15 10 * 3.5 3.5 Diseas
Slide 50: TTI-101 Attenuated Growth Factor Driven Fibrosis and Dermal Thickening
TTI-101 Attenuated Growth Factor Driven Fibrosis and Dermal Thickening Genetically-induced proliferative skin model Therapeutic treatment with TTI-101 …and significantly reduced key drivers of significantly reduced dermal thickness… inflammation and proliferation 20 15 15 TGF-β Tsk-1 mice + Placebo
Slide 51: TTI-101 Attenuated Inflammation Driven Fibrosis and Dermal Thickening
TTI-101 Attenuated Inflammation Driven Fibrosis and Dermal Thickening Chemically-induced inflammatory skin model Therapeutic treatment with TTI-101 …and significantly reduced key drivers of significantly reduced dermal thickness inflammation and proliferation 5 6 4 TGF-β BLM mice + TTI-101 Fold Δ BL
Slide 52: Appendix B. TTI-101 in IPF
Appendix B. TTI-101 in IPF
Slide 53: STAT3 Inhibitors: Preclinical Activity and Initial Clinical Proof of Mechanism in IPF
Our STAT3 Inhibitors are Designed to Address the Unmet Need in Inflammatory and Proliferative Diseases Preclinical Initial Clinical Proof of Well-Established Target Biological Activity Mechanism: IPF IL6 IL23 Tsk-1 mice + Tsk-1 mice + Placebo TTI-101 Skin Fibrosis1 IL-6 (Fold Change) Placebo TTI-101
Slide 54: REVERT IPF: Preliminary Conclusions Released October 2025
REVERTIPF: Preliminary Conclusions Released October 2025 (28 US Sites, N = 88) • Placebo arm overperformed compared to Treatment Period 12 weeks historical data • FVC change from baseline overlapped between TTI-101 800 mg/day (N=29) treatment arms, with large variability within each Randomization co
Slide 55: Patient Characteristics
Patient Characteristics TTI-101 TTI-101 Placebo Characteristic 400mg/day 800mg/day (n=29) (n=30) (n=29) Age 72.0 (9.3) 72.4 (6.9) 72.8 (7.7) Sex, Male – no. (%) 23 (79.3) 25 (83.3) 21 (72.4) Time since diagnosis of IPF – yrs., mean (SD) 2.4 (2.0) 2.6 (1.7) 2.5 (1.5) Standard of care use, nintedanib
Slide 56: Summary of Treatment-Emergent Adverse Events
Summary of Treatment-Emergent Adverse Events TTI-101 TTI-101 Placebo Characteristic 400mg/day 800mg/day (n=29) (n=30) (n=29) Any TEAEs 21 (72.4) 30 (100) 26 (89.7) TEAE leading to death 1 (3.4) 1 (3.3)1 1 (3.4) TEAE leading to discontinuation 3 (10.3) 17 (56.7) 18 (62.1) Gastrointestinal disorders 6
Slide 57: TEAEs Resulting in Discontinuations by Concomitant Nintedanib Use
Treatment-Emergent Adverse Events Resulting in Discontinuations by Concomitant Nintedanib Use TTI-101 TTI-101 Placebo Dose 400mg/day 800mg/day (n=29) (n=30) (n=29) TTI-101 + TTI-101 TTI-101 + TTI-101 Reason for discontinuation by Nintedanib Placebo Nintedanib alone Nintedanib alone concomitant ninte
Slide 58: Most Common Adverse Events in INPULSIS vs REVERT IPF Trials
Most Common Adverse Events Reported in INPULSIS vs REVERTIPF Trials INPULSIS-1 and 21 Pooled TTI-101 TTI-101 + Placebo Nintedanib TTI-101 alone Nintedanib (N=423) (N=638) (n=25) (n=34) • TTI-101 treated Any adverse event 379 (89.6) 609 (95.5) 23 (92.0) 33 (97.1) patients reported Diarrhea 78 (18.4)
Slide 59: Preliminary Conclusions and Additional Analyses
Preliminary Conclusions and Additional Analyses EES1 on Treatment at Assessment of Individual Patient Post hoc Analysis 12-weeks Trajectory on Study2 Population Placebo Criteria: duration of treatment, PK data and Placebo n=24 adverse events n=24 5 patients excluded as the following criteria were no
Slide 60: TTI-101 Patients Demonstrated Greater Decline in Fibrosis Score vs Placebo
TTI-101-treated Patients Demonstrated Greater Decline in Fibrosis Score (Baseline to 12 Weeks) vs Placebo Pooled TTI-101 vs Placebo Baseline-Weighted Percent Change in 24 24 Fibrosis Score 5% Baseline-Weighted Overall % Change in 20* 15* 0% -2.4% Greater decrease in fibrosis Fibrosis (SE) -5% score
Slide 61: TTI-101 Patients Demonstrated Greater IL-6 Decline vs Placebo
TTI-101-treated Patients Demonstrated Greater IL-6 Decline vs Placebo TTI-101 vs Placebo Decline in IL-6 0 -0.25 IL-6 is a key pro- -0.5 inflammatory cytokine IL-6 Slope that signals through -0.75 4.5-fold STAT3; inhibition of difference in STAT3 is expected to -1 slope reduce downstream inflammator
Slide 62: Greater Proportion of TTI-101 Patients Demonstrated Increase in FVC vs Placebo
A Greater Proportion of TTI-101-treated Patients Demonstrated Increase in FVC vs Placebo TTI-101 vs Placebo Change in FVC from Baseline 80% ↑ in FVC from -15 mL (177) 1 baseline 60% -22 mL (126) 1 63% of patients treated 40% with TTI-101 63% demonstrated an increase 20% 46% in FVC at 12 weeks, and 0
Slide 63: STAT3 Inhibitors: Preclinical and Clinical Proof of Mechanism in Pulmonary Fibrosis
Our STAT3 Inhibitors are Designed to Address the Unmet Need in Inflammatory and Proliferative Diseases Preclinical Clinical Proof of Well-Established Target Biological Activity Mechanism IL6 Tsk-1 mice + Tsk-1 mice + TTI-101 vs Placebo Decline in IL-6 IL17 IL23 0 Placebo TTI-101 -0.25 Skin Fibrosis1
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