Prometic announced that results from recent studies of its lead candidate PBI-4050 showed that the therapy reduced activation of hepatic stellate cells and decreased liver fibrosis through modulation of the LKB1-AMPK-mTOR pathway, according to a press release.
“In studying the mechanism of action of PBI-4050 in liver diseases, including nonalcoholic steatohepatitis, we have clearly demonstrated that PBI-4050 acts through a major signaling AMPK pathway, thus linking metabolism to fibrosis,” Lyne Gagnon, PhD, vice president of research and development at Prometic, said in the

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