MediciNova Receives Notice of Intention to Grant for New Patent Covering MN-001 for the Treatment of Idiopathic Pulmonary Fibrosis in Europe

LA JOLLA, Calif., Jan. 27, 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 Intention to Grant from the European Patent Office for a pending patent application which covers MN-001 (tipelukast) for the treatment of idiopathic pulmonary fibrosis (IPF).

Once issued, the patent maturing from this allowed patent application is expected to expire no earlier than May 2035. The allowed claims cover the use of MN-001 for treating a patient diagnosed with idiopathic pulmonary fibrosis. The allowed claims also cover the inhibition of pulmonary scarring, the reduction or inhibition of elevated lung hydroxyproline levels, the reduction of elevated lung density, and the reduction of elevated total cell count in bronchoalveolar lavage fluid using MN-001. 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, "Previously, we were granted patents covering IPF in Japan and China, and now we are very pleased to receive notice that this new patent will be granted in Europe. We believe it could substantially increase the potential value of MN-001 as we now have patent or marketing exclusivity coverage for IPF in every major pharmaceutical market in the world. Previously, the U.S. FDA granted orphan-drug designation, which will provide MediciNova with seven years of marketing exclusivity, and fast-track designation to MN-001 for the treatment of IPF. We currently have a Phase 2 clinical trial ongoing that is evaluating the safety and tolerability and clinical effect of MN-001 in IPF.”

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.