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MediciNova Announces Presentation of Positive Findings on MN-001 (tipelukast) in Acute Liver Injury Model at The Liver Meeting Digital Experience™ 2020
LA JOLLA, Calif., Nov. 12, 2020 (GLOBE NEWSWIRE) -- MediciNova, Inc., a biopharmaceutical company traded on the NASDAQ Global Market (NASDAQ:MNOV) and the
About this update from Medicinova, Inc.
[{"type":"text","content":"LA JOLLA, Calif., Nov. 12, 2020 (GLOBE NEWSWIRE) -- MediciNova, Inc., a biopharmaceutical company traded on the NASDAQ Global Market (NASDAQ:MNOV) and the JASDAQ Market of the Tokyo Stock Exchange (Code Number: 4875), today 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).\n 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 TGFβ1 (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 TGFβ1 signaling by interaction of cAMP effectors and TGFβ1 type I receptor in hepatic stellate cells\" are as follows: MN-001 (D46) significantly attenuated TGFβ1 induced HSC activationTGFβ1 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 (αSMA) levelsMN-001 (D46) decreased CCl4-induced liver αSMA, 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...