InterMune announces preclinical data for pirfenidone

By Elaine Rigoli

Tampa, Fla., May 8 - InterMune, Inc. announced results from preclinical studies that demonstrate that pirfenidone suppresses fibrogenesis through selective inhibition of the p38-gamma mitogen-activated protein kinase.

Pirfenidone is Intermune's small-molecule drug candidate being developed for the treatment of patients with idiopathic pulmonary fibrosis in the phase 3 Capacity program, according to a news release.

In idiopathic pulmonary fibrosis, fibrosis occurs when wound healing cells deposit collagen, which leads to abnormal scarring of the lung tissues.

InterMune scientists have shown a principal anti-fibrotic mechanism of action of pirfenidone as the inhibition of the p38- gamma kinase.

In support of this, InterMune studies have demonstrated specificity of pirfenidone for the p38-gamma isoforms in biochemical kinase assays as well as the attenuation of TGF-beta induced collagen synthesis following treatment of cells with pirfenidone.

These new studies demonstrate a link between inhibition of p38-gamma and a specific marker of fibrogenesis, according to the release.

Based in Brisbane, Calif., InterMune is a biotechnology company that develops therapies in pulmonology and hepatology.

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