Press release
Gyre Therapeutics Announces Publication in Journal of Gastroenterology and Hepatology
SAN DIEGO, June 18, 2024 (GLOBE NEWSWIRE) -- Gyre Therapeutics (“Gyre”) (Nasdaq: GYRE), a clinical-stage, self-sustainable biotechnology company developing
About this update from Gyre Therapeutics, Inc.
[{"type":"text","content":"SAN DIEGO, June 18, 2024 (GLOBE NEWSWIRE) -- Gyre Therapeutics (“Gyre”) (Nasdaq: GYRE), a clinical-stage, self-sustainable biotechnology company developing anti-fibrotic therapeutics for a variety of chronic organ diseases, today announced the publication of the manuscript titled “Hydronidone induces apoptosis in activated hepatic stellate cells through endoplasmic reticulum stress-associated mitochondrial apoptotic pathway” in the Journal of Gastroenterology and Hepatology. This publication includes both in vivo and in vitro studies supporting the potential of hydronidone (F351), a novel derivate of pirfenidone, as a promising therapy for the treatment of liver fibrosis. “Preclinical animal studies have shown that treatment with hydronidone attenuated liver fibrosis by inhibiting the activation of hepatic stellate cells (HSCs), although the underlying mechanisms of action are still not fully understood,” said Han Ying, Ph.D., CEO of Gyre. “The findings of these in vivo and in vitro studies demonstrate that hydronidone induces apoptosis in activated HSCs (aHSCs) via the endoplasmic reticulum stress (ERS)-associated mitochondrial apoptotic pathway and suggest that hydronidone may contribute to the improvement of liver fibrosis. These findings further enhance our understanding of hydronidone and underscore its therapeutic potential in treating liver fibrosis.” Liver fibrosis is characterized by the progressive accumulation of extracellular matrix (ECM), which disrupts the normal liver architecture. Research has shown that quiescent HSCs undergo activation and transform into myofibroblast-like cells to produce ECM in chronic liver disease, and therefore that liver fibrosis can be reversed by eliminating aHSCs. This study found that treatment with hydronidone significantly promoted apoptosis in aHSCs in both the CCl4- and DDC-induced liver fibrosis in mice and LX-2 cells. Mechanistic studies revealed that hydronidone triggered ERS and subsequently activated the IRE1α-ASK1-JNK pathway and subsequent dysfunction of the mitochondria, ultimately resulting in the apoptosis of aHSCs. Gyre Pharmaceuticals, Gyre’s majority indirectly owned subsidiary in the People's Republic of China (PRC), is currently evaluating hydronidone in a Phase 3 trial for the treatment of Chronic Hepatitis B (CHB)-associated liver fibrosis in the PRC with topline ...