Benzinga | Nov 13, 2020 05:35AM EST

MediciNova Announced Presentation of Positive Findings on MN-001 (tipelukast) in Acute Liver Injury Model at The Liver Meeting Digital Experience 2020

MediciNova, Inc., (NASDAQ:MNOV) announced that Principal Investigators Leila Gobejishvili, PhD and Craig McClain, MD at the University of Louisville School of Medicine presented positive results of the in-vitro and in-vivo studies that evaluated MN-001 (tipelukast, referred to as D46 in the presentation) for its anti-liver fibrotic effect in human hepatic stellate cells (HSCs) and in an acute liver injury model at the Liver Meeting Digital Experience 2020 (TLMdX), the annual meeting of the American Association for the Study of Liver Diseases (AASLD).

The study was a collaborative effort between MediciNova, Inc., and Drs. Craig McClain and Leila Gobejishvili, University of Louisville Alcohol Research Center and Hepatobiology and Toxicology Centers of Biomedical Research Excellence (COBRE) at the University of Louisville in Louisville, Kentucky.

This study, funded by the National Institute of General Medical Sciences (NIGMS), one of the U.S. National Institutes of Health (NIH), sought to examine the pathogenic role of phosphodiesterase 4 (PDE4) in hepatic stellate cell (HSC) activation and TGF1 (transforming growth factor beta 1) signaling. Specifically, the studies evaluated the effect of PDE4 inhibitors on attenuating fibrotic processes with an emphasis on HSC activation.

The highlights of the presentation entitled "Modulation of TGF1 signaling by interaction of cAMP effectors and TGF1 type I receptor in hepatic stellate cells" are as follows:

MN-001 (D46) significantly attenuated

TGF1 induced HSC activationTGF1 mediated increase in HSC motility and contractility by reducing myosin light chain (MLC) phosphorylation and Endothelin-1Fibrogenic signaling in a mouse acute carbon tetrachloride (CCl4) induced liver injury model, specifically,MN-001 (D46) decreased CCl4-induced HSC activation demonstrated by reduced SMAD3 and alpha smooth muscle actin (SMA) levelsMN-001 (D46) decreased CCl4-induced liver SMA, collagen 1a1 and lysyl oxidase 2 mRNA levels

Promoting cAMP signaling by using PDE4 inhibitors could be beneficial in attenuating the development of liver fibrosis.

Yuichi Iwaki, MD, PhD, President and Chief Executive Officer of MediciNova, Inc. commented, "We are very pleased with the positive findings in an acute liver injury model study conducted by Dr. Gobejishvili and Dr. McClain. This is additional scientific evidence to support MN-001's anti-fibrotic effects in the liver. We look forward to advancing to the next step to further investigate the potential of MN-001 in liver fibrosis."

Dr. McClain, Professor of Medicine, Pharmacology and Toxicology, Chief of Research Affairs, Division of Gastroenterology, Hepatology and Nutrition, Director Clinical Trials Unit / Liver Research Program commented, "We are very excited to report positive data from our in-vitro and acute liver injury model study with MN-001 (D46). The attenuation of TGF1 signaling for HSC activation and the anti-fibrogenic effect in an acute liver injury model by MN-001 was very promising. We are looking forward to further collaboration with MediciNova."