Prometic fibrosis candidate reduces hepatic stellate cell activation

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 release. “Our data show the potential therapeutic effect of PBI-4050 in liver fibrosis and NASH.”

PBI-4050 is an orally active therapy that previously demonstrated clinical activity in patients with idiopathic pulmonary fibrosis and patients with metabolic syndrome and type 2 diabetes.

In an ongoing phase 2 study, PBI-4050 has demonstrated significant reduction of liver and cardiac fibrosis among patients with Alström syndrome.

According to the release, PBI-4050 will soon be tested in a placebo-controlled phase 3 clinical trail for the treatment of idiopathic pulmonary fibrosis.

“We have seen the benefits of PBI-4050 in reducing liver fibrosis in Alström syndrome patients,” Pierre Laurin, CEO of Prometic, said in the release. “With this further validation that the signaling pathway targeted by PBI-4050 is indeed at the core of the genesis of fibrosis in the liver, we are very confident about its potential to address fibrosis-related conditions such as IPF, Alström syndrome, and NASH.”

Reference: www.prometic.com