MediciNova Receives Notice of Allowance for New Patent Covering MN-001 and MN-002 for the Treatment of Advanced NASH in Japan

LA JOLLA, Calif., Feb. 17, 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 it has received a Notice of Allowance from the Japan Patent Office for a pending patent application which covers MN-001 (tipelukast) and MN-002 (a major metabolite of MN-001) for the treatment of advanced nonalcoholic steatohepatitis (NASH).

Once issued, the patent maturing from this allowed patent application is expected to expire no earlier than May 2035. The allowed claims cover MN-001 and MN-002 for use in the treatment of a patient with advanced NASH. The allowed claims also cover advanced NASH patients that exhibit hepatic fibrosis, spider angiomata, ascites, splenomegaly, hard liver border, palmar erythema, asterixis, portal hypertension, hepatic scarring, cirrhosis, or hepatocellular carcinoma (HCC). In addition, the allowed claims cover MN-001 and MN-002 for use in reducing hepatic fibrosis and for use in reducing hepatic scarring in a patient with advanced NASH. The allowed claims cover oral administration, including tablets and capsules, as well as liquid dosage forms.

Yuichi Iwaki, MD, PhD, President and CEO of MediciNova, Inc. commented, "We are very pleased to receive notice that this new patent will be granted as we believe it could substantially increase the potential value of MN-001. We previously reported positive results from a Phase 2 clinical trial of MN-001 that enrolled NAFLD and NASH patients with hypertriglyceridemia. The U.S. FDA has granted Fast Track designation for MN-001 for the treatment of NASH with fibrosis and the U.S. Patent and Trademark Office previously granted a patent which covers MN-001 and MN-002 for advanced NASH with fibrosis.”

About MN-001

MN-001 (tipelukast) is a novel, orally bioavailable small molecule compound thought to exert its effects through several mechanisms to produce its anti-inflammatory and anti-fibrotic activity in preclinical models, including leukotriene (LT) receptor antagonism, inhibition of phosphodiesterases (PDE) (mainly 3 and 4), and inhibition of 5-lipoxygenase (5-LO). The 5-LO/LT pathway has been postulated as a pathogenic factor in fibrosis development, and MN-001's inhibitory effect on 5-LO and the 5-LO/LT pathway is considered to be a novel approach to treat fibrosis. MN-001 has been shown to down-regulate expression of genes that promote fibrosis including LOXL2, Collagen Type 1 and TIMP-1. MN-001 has also been shown to down-regulate expression of genes that promote inflammation including CCR2 and MCP-1. In addition, histopathological data shows that MN-001 reduces fibrosis in multiple animal models.