BUSINESS WIRE<\/a>)–
\nTvardi Therapeutics, Inc. (\u201cTvardi\u201d) (NASDAQ: TVRD), a clinical-stage biopharmaceutical company focused on the development of novel, oral, small molecule therapies targeting STAT3 to treat fibrosis-driven diseases, today announced that an abstract will be presented at the American Thoracic Society 2025 Annual Conference, which is being held May 16-21 in San Francisco.\n<\/p>\n\nThe abstract highlights the role of STAT3 as a master regulator of idiopathic pulmonary fibrosis (IPF). In preclinical studies, TTI-101, Tvardi\u2019s STAT3 inhibitor, suppressed fibrotic markers which are not addressed with currently approved therapies (nintedanib and pirfenidone).\n<\/p>\n
\nUsing single-cell RNA sequencing on lung samples from untreated IPF patients and those treated with current approved therapies, McKenna et al. mapped the transcriptional landscape across 40 pulmonary cell types. They found ~60% of IPF-associated dysregulated genes are not addressed by either approved drug, which they termed the \u201cIPF therapeutic gap.\u201d They further identified STAT3 as a dominant regulatory transcription factor both in untreated IPF samples and in the \u201cIPF therapeutic gap.\u201d\n<\/p>\n
\nIn addition, ex vivo<\/i> analysis of human lung slices treated with TTI-101, nintedanib or pirfenidone resulted in greater repression of genes within alveolar fibroblast (key effector cells in fibrosis) with TTI-101 vs current approved therapies. Notably, TTI-101 downregulated genes involved in extracellular matrix production, including collagen genes, which were largely unaffected by nintedanib or pirfenidone.\n<\/p>\n
\nDetails of the presentation are as follows:\n<\/p>\n