Tvardi Therapeutics, Inc. · NASDAQ:TVRD
Tvardi Therapeutics — Investor Presentation (July 2026)
63 slides from Tvardi Therapeutics's investor presentation, Jul 30, 2026
Slide 1: Tvardi Therapeutics Overview July 2026
tvardi. THERAPEUTICS Overview July 2026
Slide 2: Forward-looking statements
This presentation contains forward - looking statements that involve substantial risks and uncertainties. All statements, other th an statements of historical facts, contained in this presentation, including statements about our expectations regarding the potential benefits, activity, effec tiv enes
Slide 3: STAT3: Highly Validated Convergent Node
STAT3: Highly Validated Convergent Node Translational Proof - of - Concept STAT3: central mediator in inflammatory and proliferative disease Our STAT3 Inhibitors are Designed to Address the Unmet Need in Inflammatory and Proliferative Diseases IL6 IL17 I L23 TTI - 109 Validation in P1 Healthy Volunt
Slide 4: Targeting STAT3: a Convergence Point of Inflammatory and Proliferative Disease
4 Targeting STAT3: a Convergence Point of Inflammatory and Proliferative Disease IL - 23 IL - 1 β IL - 6 IL - 21 IL - 17A/F IL - 12 TNF - α direct STAT3 activation indirect STAT3 activation TGF - β HGF Immune dysregulation Inflammation Proliferation Extracellular Cytosol Nucleus P Current Therapies
Slide 5: Diverse Disease Signaling Pathways Converge on STAT3
5 Targeting STAT3: a Convergence Point of Inflammatory and Proliferative Disease Diverse Disease Signaling Pathways Converge on STAT3 IL - 23 IL - 1 β IL - 6 IL - 21 IL - 17A/F IL - 12 TNF - α direct STAT3 activation indirect STAT3 activation TGF - β HGF Immune dysregulation Inflammation Proliferati
Slide 6: STAT3's Multi-modal Mechanism of Action
6 STAT3’s Multi - modal Mechanism of Action in Inflammatory and Proliferative Diseases Restores Humoral & Cellular Immunity Immune Homeostasis Regression Tvardi’s Approach Tvardi’s Impact Down - regulates Inflammation & Proliferation CELLULAR IMMUNE Immune Dysregulation Pro - proliferative cells Act
Slide 7: Seasoned Leadership: Deep R&D and Operational Expertise
7 Seasoned Leadership: Deep R&D and Operational Expertise Sujal Shah Chairman Michael Wyzga Director Cynthia Smith Director Susan Shiff, PhD Director Wallace Hall Director Dan Conn, JD, MBA CFO John Kauh, MD CMO Imran Alibhai, PhD CEO & Director David Tweardy, MD Founder & Advisor Ron DePinho, MD Fo
Slide 8: TTI-109
tvardi. THERAPEUTICS TTI-109
Slide 9: Clinical Foundation for Development of TTI-109
1. Tsimberidou et al. Clin Cancer Res. 2025 ;; 2. Tvardi Press Release: January 8, 2026 ; 3. Kasembeli et al. Biochem Pharmacol. 2021 ; 4. FDA requires warnings about increased risk of serious heart - related events, cancer, blood clots, and death for JAK inhibitors that treat certain chronic inflam
Slide 10: TTI-109 Designed as a Prodrug
TTI - 109 Designed as a Prodrug to Enhance Delivery of STAT3 Inhibitor and Establish Favorable Target Product Profile 10 TTI - 109 Design Objectives • Preserve mechanism of action and observed clinical activity of TTI - 101 • Improve drug delivery • Diminish GI exposure Mean (SD) TTI - 101 and TTI -
Slide 11: Phase 1 Clinical Program Validated TTI-109 as Oral Prodrug
TTI - 101 recommended phase 2 dose of TTI - 101 (400mg BID) determined in oncology studies; PK: pharmacokinetics; BID: twice daily 11 Phase 1 Clinical Program Validated TTI - 109 as the Oral Prodrug of TTI - 101 Part B: Bioequivalence Crossover Study Randomized sequence of treatment of n=6 into each
Slide 12: TTI-109 Rapidly Converted to Active Moiety
*The pharmacokinetics of TTI - 109 and TTI - 101 were evaluated in GLP toxicology studies in rats and monkeys. Systemic exposures of TTI - 101 from TTI - 109 administration were predictable in terms of molar equivalent amounts of anticipated TTI - 101. SAD: Single Ascending Dose 12 TTI - 109 Rapidly
Slide 13: TTI-109 Achieved Equivalent Active Moiety Exposure
TTI - 101 plasma concentrations following dosing with TTI - 101 400 mg vs TTI - 109 500 mg (427 mg TTI - 101 molar eq.) in fasted state; Fed and fasted resulted in similar concentrations 13 TTI - 109 Achieved Equivalent Active Moiety Exposure to TTI - 101 Equal molar dosing confirmed equivalent expo
Slide 14: Repeat Dosing Delivered Predictable Steady State Parameters
SAD: Single Ascending Dose; MAD: Multiple Ascending Dose; PK = Pharmacokinetics; STAT3 IC 50 : in a controlled system where proliferation is driven by pY - STAT3, TTI - 101 inhibits cell growth with an IC ₅₀ of approximately 1.5µM (707ng/mL) 14 TTI - 109 Repeat Dosing Delivered Predictable Steady St
Slide 15: TTI-109 Phase 1 TEAE Profile
TTI - 101 400mg (N=8) TTI - 109 500mg (N=8) TTI - 109 Doses 1 - 4 (N=32) Placebo (N=8) Adverse Event Preferred Term 6 (75%) 6 (75%) 19 (59%) 5 (63%) No. of participants reporting at least one TEAE 1 (3%)** - 1 (3%)* - AEs leading to drug withdrawal Grade 2 Grade 1 Grade 2 Grade 1 Grade 2 Grade 1 Gra
Slide 16: Differential Diarrhea Pattern
1.19 1.10 0.47 3.35 0 1 2 3 4 5 Placebo TTI-109 All doses TTI-109 500 mg BID TTI-101 400 mg BID TTI - 101 400mg (N=8) TTI - 109 500mg (N=8) TTI - 109 Doses 1 - 4 (N=32) Placebo (N=8) Adverse Event Preferred Term Grade 2 Grade 1 Grade 2 Grade 1 Grade 2 Grade 1 Grade 2 Grade 1 - 3 (38%) - 2 (25%) 1 (3
Slide 17: Preclinical Framework for Exploratory Pharmacodynamic Objectives
1. Steward - Tharp et al. Immunobiology 2014 ; 2. Tweardy et al. Trans Am Clin Climatol Assoc . 2022 ; 3. Figures digitized from Robinson et al. Cancers 2023 : Dextran sodium sulfate (DSS) model 17 Preclinical Framework for Exploratory Pharmacodynamic Objectives pY - STAT3 drives cellular and humora
Slide 18: TTI-109 Selectively Reduced Immune Cell Populations in MAD Cohort
-80% -60% -40% -20% 0% 20% 40% 60% 80% Adj % Δ D1 Adj % Δ D2 Adj % Δ D3 Adj % Δ D4 Th17 T follicular helper cells B cells TTI - 109 by dose paired % Δ = ( Post−Pre)/Pre; placebo - adjusted (n=8 per dose). Cell population changes assessed by flow cytometry (FACS) on peripheral blood mo nonuclear cell
Slide 19: TTI-109 Reduced Th17 Cells Implicated in UC Pathology
*Placebo - adjusted % change ( %Δ ) = TTI - 109 dose - group mean − pooled placebo mean (per - subject % change). Paired n: D2=8, D3=8, D4=8; pooled placebo n=8. 1. Wen Y, et al. Therap Adv Gastroenterol . 2024 ; 2. Meitei HT, et al. iScience . 2025 ; 3. Sun L, et al. Gastroenterol Res Pract . 2021
Slide 20: TTI-109 Reduced T Follicular Cells Implicated in UC Pathology
* Placebo - adjusted % change ( %Δ ) = TTI - 109 dose - group mean − pooled placebo mean (per - subject % change). Paired n: D2=8, D3=8, D4=8; pooled placebo n=8. 1 . Sun L, et al. Gastroenterol Res Pract . 2021 ; 2. Long Y, et al. Front Immunol . 2020 ; 3. Xue G, et al. Medicine . 2019 20 TTI - 109
Slide 21: TTI-109 Reduced B Cell Populations Implicated in UC
*Placebo - adjusted % change ( %Δ ) = TTI - 109 dose - group mean − pooled placebo mean (per - subject % change). Paired n: D2=8, D3=8, D4=8; pooled placebo n=8. 1 . Uzzan M, et al. Nat Med . 2022 ; 2. Masaki Y, et al. Clin Exp Immunol . 2016 ; 3. Cupi ML, et al. J Immunol . 2014 21 UC Rationale %Δ
Slide 22: TTI-109 Advances Clinical Profile Across PK, GI Tolerability and Immune Modulation
1. Tsimberidou et al. Clin Cancer Res. 2025 ; SD: Stable Disease; 2. Tvardi Press Release: January 8, 2026 ; pY - STAT3: activated STAT3 induced by phosphorylation of tyrosine residue 705; STAT3 IC 50 : in a controlled system where proliferation is driven by pY - STAT3, TTI - 101 inhibits cell growt
Slide 23: UC: Large Market Opportunity with High Unmet Medical Need
~$3B 2 US Market (2024) $9B 2 Global Market (2024) >1.25M 1 Diagnosed US Patients 1. Lewis Gastroenterology. 2023 ; 2. S&S Insider . Estimate includes patients identified with indeterminate IBD. 3. Clinical remission rates from product labels; UC: ulcerati ve colitis; MoA: mechanism of action; IV: i
Slide 24: One Target, Three Mechanisms: pY-STAT3 Drives Shared Biology of UC
Chronic immune activation and perpetuation of intestinal inflammation Persistent inflammation, tissue injury and ulceration 24 One Target, Three Mechanisms: pY - STAT3 Drives the Shared Biology of UC Immune Dysregulation Inflammation APC IL - 17A IL - 17F IL - 21 Autoantibodies Endothelial Activatio
Slide 25: pY-STAT3 Reduction Demonstrated in Preclinical Models and Clinical Biopsies
1. Li et al. Gut 2010 2. Figures digitized from Robinson et al. Cancers 2023 : dextran sodium sulfate (DSS) model; 3. Tvardi data generated with CRO: WuXi oxazolone (OXA) model; n=8 per group statistica l c omparison using exact Mann - Whitney + Kruskal - Wallis; 4. Tsimberidou et al. Clin Cancer Re
Slide 26: STAT3 Inhibition Normalized Pathogenic Immune Cell Populations
0 5 10 15 20 25 30 35 40 45 50 Sham TNBS + vehicle TNBS + TTI-101 IL - 17+ (Th17) cells per field 1. Zhang el al. European Journal of Inflammation . 2023 ; 2. Uo et al. Gut 2013 ; 3. Figures digitized from Robinson et al. J Clin Med 2022 : 2,4,6 - trinitrobenzene sulfonic acid (TNBS) model; 4. Figur
Slide 27: STAT3 Inhibition Reduced IL-6 and Inflammation
0 1 2 3 4 0% DSS + Vehicle 5% DSS + Vehicle 5% DSS + TTI-101 Colonic Inflammatory score -1.5 -1.25 -1 -0.75 -0.5 -0.25 0 0 0.5 1 1.5 2 2.5 3 Sham TNBS + vehicle TNBS + TTI-101 Colonic inflammatory score 1. Fu et al. World J Gastrointest Surg. 2025 ; a P < 0.01; b P < 0.001; 2. Figures digitized from
Slide 28: STAT3 Inhibition Reduced Proliferative Signaling and Fibrosis
0 2 4 6 8 0% DSS (naïve) 5% DSS + Vehicle 5% DSS + TTI-101 Colon Length (cm) 1. Vespa et al. J. Clin Med. 2022 ; 2. Figures digitized from Robinson et al. Cancers 2023 : dextran sodium sulfate (DSS) model; 3. Tvardi Press Release: January 8, 2026 ; *p ⩽ 0.05 TTI - 101 vs vehicle 28 STAT3 Inhibition
Slide 29: Proposed Clinical Trial Designed to Address Key Challenges in UC
QD: once daily dosing; BID: twice daily dosing; SNP: single nucleotide polymorphisms; Subject to IND submission and the avail abi lity of additional funding Proposed Clinical Trial Designed to Address Key Challenges in UC Dose 4 (BID) Dose 3 (BID) Placebo Dose 2 (QD) Dose 1 (QD) R Treatment Period (
Slide 30: Overcoming Persistent Disease Biology
Preserved colon integrity 2 ↓ Colonic inflammatory score 1,2,3 ↓ Pathogenic Th17 1,2 UC Murine Models with TTI - 101/109 ↓ Fibrosis score 4 ↓ Inflammatory cytokine IL - 6 4 ↓ Key immune cell populations Human Data with TTI - 101/109 30 Overcoming Persistent Disease Biology IL - 23 IL - 1 β IL - 6 IL
Slide 31: A Differentiated Oral Therapy with Targeted Exposure
1. FDA requires warnings about increased risk of serious heart - related events, cancer, blood clots, and death for JAK inhibitors th at treat certain chronic inflammatory conditions; 2. Ozanimod Prescribing Information ; 3. Etrasimod Prescribing Information ; 4. Robinson et al. Int. J. Mol. Sci 202
Slide 32: Enabling Precision Medicine
1. Schreiber et al Gastroenterology 2021 ; 2. Verstockt et al J. Crohn’s and Colitis 2025 ; 3. Zhang et al Plos One 2014 ; 4. Wang et al Genet Mol Res. 2014 32 Enabling Precision Medicine Exploratory Candidate Biomarkers Limited Molecular Insight • Current available therapies have broad unselected p
Slide 33: STAT3: Highly Validated Convergent Node
STAT3: Highly Validated Convergent Node Translational Proof - of - Concept STAT3: central mediator in inflammatory and proliferative disease Our STAT3 Inhibitors are Designed to Address the Unmet Need in Inflammatory and Proliferative Diseases IL6 IL17 I L23 TTI - 109 Validation in P1 Healthy Volunt
Slide 34: Our Pipeline
*Tvardi’s ability to initiate these programs is subject to clearance of Investigational New Drug (IND) application and the av ail ability of additional funding 34 Our Pipeline Anticipated Milestones Phase 3 Phase 2 Phase 1 Preclinical Indication Program • Study initiation expected 2027* Ulcerative C
Slide 35: TTI-101 in HCC
tvardi. THERAPEUTICS TTI-101 in HCC
Slide 36: Reversed Multiple Pathogenic Steps of Liver Cancer in NASH-induced HCC Model
Jung KH et al. Clin Cancer Res. 2017 . Genetically engineered HepPTEN - murine model that replicates nonalcoholic steatohepatitis (NASH) induced hepatocellular carcin oma (HCC) 36 TTI - 101 Reversed Multiple Pathogenic Steps of Liver Cancer in a NASH - induced HCC Model Inflammation Fibrosis/Cirrhos
Slide 37: Phase 1 First in Human Monotherapy Study Design
Tsimberidou et al. Clin Cancer Res. 2025 37 Phase 1 Clinical Trial: First in Human TTI - 101 Monotherapy Study Design Advanced Solid Tumors Liver Cancer Liver Cancer RP2D Other Solid Tumors Other Solid Tumors RP2D Objectives: • Primary: Maximum tolerated dose, safety, and pharmacokinetics • Secondar
Slide 38: Monotherapy Led to Durable Partial Responses in Fibrotic Tumors
Tsimberidou et al. Clin Cancer Res. 2025 38 Phase 1 Clinical Trial: TTI - 101 Monotherapy Led to Durable Partial Responses in Fibrotic Tumors Baseline Cycle 5, Day 1 Cycle 3, Day 1 Diameter Length in mm (% Change from Baseline) 41mm (0%) 14mm ( - 66%) 21mm ( - 49%) 14mm ( - 70%) 19mm ( - 59%) 46mm (
Slide 39: Phase 1 Monotherapy Clinical Trial Summary
Tsimberidou et al. Clin Cancer Res. 2025 ; *STAT3 IC 50 : in a controlled system where proliferation is driven by WT STAT3, TTI - 101 inhibits cell growth with an IC ₅₀ of approximately 1.5µM; Kasembeli et al. Blood. 2022 . SD: Stable Disease; TRAE: Treatment related adverse events; F1 - 3: Formulat
Slide 40: Strong Rationale for TTI-101 and ICI Combination Therapy
1. Adapted from Zhao, Y et al. Hepatology. 2021 2. Cohen et al. Ann Oncol. 2018 3. Siu et al. JAMA Oncol. 2019 . ICI: Immune Checkpoint Inhibition; Bev: Bevacizumab. Certain data on this slide are based on cross - study comparisons and are not based on any head - to - head clinical trials. C ross -
Slide 41: TTI-101 Designed to Provide Distinct Mechanism for Unmet Need in HCC
1. World Health Organization (WHO) 2. WHO US Statistics 3. American Cancer Society 4. Represents range of ORRs from previous studies (MORPHEUS, Tempest, IMBrave150). 5. 2nd line ORR expected to be <5% as 2nd line therapies inhibit VEGF/angiogenesis as common mechanism with bevacizumab and pembrolizu
Slide 42: REVERT Liver Cancer: Phase 2 Study in HCC
NCT05440708 ; Dayyani et al. JCO . 2024 ; Data as of April 2025 42 REVERT Liver Cancer : Phase 2 Study of TTI - 101 in HCC • Overall Response Rate (ORR) • Duration of Response (DoR) • Progression - free survival • Liver stiffness (elastogram) • Biomarkers (IL - 6/AFP) • pY - STAT3 in tumor (21 US Si
Slide 43: REVERT Liver Cancer: Interim Phase 1b/2 Data
Preliminary radiographic change from baseline RECIST measurements (best response). Data as of Aug 2024. This interim data set wa s not subject to the standard quality control measures typically associated with final clinical trial results. 1. Tempest press release 23 Apr 2023 of Phase 2 Study. Tempe
Slide 44: Key Takeaways: TTI-101 in HCC
44 Key Takeaways: TTI - 101 in HCC Inhibition of STAT3 activation to have dual therapeutic effect on cancer cells – overcoming tumorigenesis and immune suppression Clinically meaningful activity in both monotherapy and combination therapy in areas of unmet need Topline results from ongoing Phase 2 R
Slide 45: Appendix A. Preclinical Support
Appendix A. Preclinical Support
Slide 46: STAT3 Inhibition Demonstrated Activity Across Multiple Validated IBD Immune Axes
Tvardi data generated with CRO: WuXi ; Comparative targets in the IBD space and select therapies approved or developed for IBD used for demonstrative purposes; DS S: dextran sodium sulfate ulcerative colitis (UC) model; TNBS: 2,4,6 - trinitrobenzene sulfonic acid Crohn’s disease (CD) model; OXA: oxa
Slide 47: TVRD STAT3 Inhibitors in the DSS-UC Model
0.0 0.5 1.0 1.5 2.0 2.5 3.0 3.5 4.0 0% DSS + Vehicle 5% DSS + Vehicle 5% DSS + TTI-101 Diarrheal Score 0.0 0.5 1.0 1.5 2.0 2.5 3.0 3.5 4.0 0% DSS + Vehicle 5% DSS + Vehicle 5% DSS + TTI-101 Colonic Inflammatory Score 0 20 40 60 80 100 120 140 0% DSS + Vehicle 5% DSS + Vehicle 5% DSS + TTI-101 pY - S
Slide 48: TVRD STAT3 Inhibitors in the TNBS-CD Model
0 5 10 15 20 25 30 35 40 45 50 Sham TNBS + vehicle TNBS + TTI-101 IL - 17+ (Th17) cells per field * 0 20 40 60 80 100 120 Sham TNBS + vehicle TNBS + TTI-101 pY - STAT3 (relative units, norm. to total protein) 0 10 20 30 40 50 60 70 80 Sham TNBS + vehicle TNBS + TTI-101 Colon length (mm) 1. Figures d
Slide 49: TVRD STAT3 Inhibitors in the OXA-UC Model
0.0 0.5 1.0 1.5 2.0 2.5 3.0 3.5 4.0 Sham OXA+Vehicle OXA+TTI-109 Disease Activity Index (0 – 4) 0 5 10 15 20 25 30 35 40 Sham OXA+Vehicle OXA+TTI-109 pY - STAT3 H - Score 1. Tvardi data generated with CRO: WuXi; n=8 per group statistical comparison using exact Mann - Whitney + Kruskal - Wallis 49 TV
Slide 50: Attenuated Growth Factor Driven Fibrosis and Dermal Thickening
Figures digitized from Pedroza et al. Rheum. 2017 : SSc: systemic sclerosis; Genetically engineered model (GEM) of Tight skin (Tsk - 1) mice which spontaneously develop fibrosis as a result of a duplication in the fibrillin - 1 gene and BLM (bleomycin - induced SSc) model; Fold Δ = Fold Change 50 TT
Slide 51: Attenuated Inflammation Driven Fibrosis and Dermal Thickening
Figures digitized from Pedroza et al. Rheum. 2017 : SSc: systemic sclerosis; Bleomycin (BLM) treated mice develop fibrosis through an inflammatory mechanism; Fold Δ = Fold Change 51 TTI - 101 Attenuated Inflammation Driven Fibrosis and Dermal Thickening Chemically - induced inflammatory skin model T
Slide 52: Appendix B. TTI-101 in IPF
tvardi. THERAPEUTICS Appendix B. TTI-101 in IPF
Slide 53: Initial Clinical Proof of Mechanism: IPF Well-Established Target
Pulmonary Fibrosis 2,3 Initial Clinical Proof of Mechanism: IPF Well - Established Target 1 . Pedroza et al. Rheum. 2017 : Genetically engineered model of Tight skin (Tsk - 1) mice which spontaneously develop fibrosis as a result of a duplication in the fibrillin - 1 gene; 2. Pedroza et al. FASEB J.
Slide 54: REVERT IPF: Preliminary Conclusions Released October 2025
• Placebo arm overperformed compared to historical data • FVC change from baseline overlapped between treatment arms, with large variability within each cohort • Treatment emergent adverse events resulted in early discontinuations leading to a small number of patients available for efficacy analysis
Slide 55: Patient Characteristics
SD: standard deviation; 1 GI comorbidity: gastrointestinal medical history collected at baseline 55 Patient Characteristics TTI - 101 800mg/day (n=29) TTI - 101 400mg/day (n=30) Placebo (n=29) Characteristic 72.8 (7.7) 72.4 (6.9) 72.0 (9.3) Age 21 (72.4) 25 (83.3) 23 (79.3) Sex, Male – no. (%) 2.5 (
Slide 56: Summary of Treatment-Emergent Adverse Events
Treatment - emergent adverse event: any adverse event that emerges after treatment with TTI - 101 or placebo. Safety analysis perfor med on all patients treated with at least one dose of TTI - 101. 1 Occurred during safety follow - up after 12 - week treatment period ended; 2 No instances of drug -
Slide 57: TEAEs Resulting in Discontinuations by Concomitant Nintedanib Use
Treatment emergent adverse event: any adverse event that emerges after treatment with TTI - 101 or placebo. Safety analysis perfor med on all patients treated with at least one dose of TTI - 101. 1 No instances of drug - induced liver injury reported across visits or treatment groups. All increases
Slide 58: Most Common Adverse Events in INPULSIS vs REVERT IPF Trials
Adverse events selected to align with INPULSIS categories; safety analysis performed on all patients treated with at least on e d ose of TTI - 101. Certain data on this slide are based on cross - study comparisons and are not based on any head - to - head clinical trials. Cross - study comparisons a
Slide 59: Preliminary Conclusions and Additional Analyses
Post hoc Analysis Population Assessment of Individual Patient Trajectory on Study 2 EES 1 on Treatment at 12 - weeks 59 Preliminary Conclusions and Additional Analyses 1 The Efficacy Evaluable Set (EES) consists of all patients defined as all randomized patients who received at least one dose o f I
Slide 60: Treated Patients Demonstrated Greater Decline in Fibrosis Score vs Placebo
Analysis performed on post hoc analysis population comparing baseline to 12 weeks. One patient missing fibrosis score; overal l p ercent change from baseline was calculated using baseline - weighted aggregation to account for differences in initial fibrosis severity with bootstrap - based standard e
Slide 61: Treated Patients Demonstrated Greater IL-6 Decline vs Placebo
Analysis performed on post hoc analysis population comparing baseline to 12 weeks. Two patients missing IL - 6 change scores (one placebo, one TTI - 101); Decline assessed using OLS: ordinary least squares regression model and standard errors 61 TTI - 101 - treated Patients Demonstrated Greater IL -
Slide 62: Greater Proportion of Treated Patients Demonstrated Increase in FVC
Analysis performed on post hoc analysis population comparing baseline to 12 weeks; 1 Actual mean FVC change in mL (SD) at 12 weeks 62 A Greater Proportion of TTI - 101 - treated Patients Demonstrated Increase in FVC vs Placebo ↓ in FVC from baseline ↑ in FVC from baseline 63% of patients treated wit
Slide 63: Clinical Proof of Mechanism: Reduced IL-6 and Fibrosis in Humans
Well - Established Target 1 . Pedroza et al. Rheum. 2017 : Genetically engineered model of Tight skin (Tsk - 1) mice which spontaneously develop fibrosis as a result of a duplication in the fibrillin - 1 gene; 2. Pedroza et al. FASEB J. 2016 ; 3. Kauh et al. CHEST . 2024 . P ulmonary fibrosis b leom
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