In a preclinical chronic colitis model, Tvardi’s oral small molecule accumulated in the colon at approximately 8-fold higher concentrations than in plasma, at pharmacologically relevant levels, and modulated STAT3-driven disease biology 

Collective findings now span multiple preclinical models of UC, further supporting the scientific rationale for advancing TTI-109, Tvardi’s next-generation STAT3 inhibitor, in UC

HOUSTON, Sept. 24, 2026 (GLOBE NEWSWIRE) -- Tvardi Therapeutics, Inc. ("Tvardi" or the "Company") (NASDAQ:TVRD), a clinical-stage biopharmaceutical company focused on the development of novel, oral small molecule therapies targeting STAT3 to treat inflammatory and proliferative diseases, today announced the publication of preclinical data evaluating Tvardi’s STAT3 inhibitor in the International Journal of Molecular Sciences. The publication provides additional evidence supporting further investigation of STAT3 inhibition as a potential therapeutic approach to treating inflammatory bowel diseases, including ulcerative colitis (UC).

The publication, titled "Colitis-Associated Colorectal Cancer—STAT3 Inhibition as a Preventive Strategy," evaluated Tvardi’s first-generation oral STAT3 inhibitor, TTI-101, in an azoxymethane (AOM)-dextran sodium sulfate (DSS) mouse model, designed to replicate the human progression from chronic colitis to colorectal cancer (CRC). Patients with UC are estimated to have a 20- to 30-fold higher risk of CRC than the general population. In this model, the orally administered STAT3 inhibitor reached pharmacologically relevant concentrations in the colon, normalized STAT3-regulated colonic gene expression and modulated proliferative programs associated with colitis-driven disease progression, preventing the development of colon polyps and adenocarcinomas. The chronic AOM-DSS prevention model is the fourth preclinical model of colitis in which Tvardi’s STAT3 inhibitors have shown biological activity. Previously, Tvardi’s oral small molecules normalized the UC hallmarks of immune dysregulation, inflammation and proliferation across three acute models representing distinct immune axes: DSS (innate/Th17), trinitrobenzene sulfonic acid (TNBS; adaptive Th1) and oxazolone (OXA; adaptive Th2/NKT).