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 presented the positive results from the interim analysis of the Phase 2 clinical trial of MN-001 (tipelukast) in NASH (non-alcoholic steatohepatitis) and NAFLD (non-alcoholic fatty liver disease) with hypertriglyceridemia at the International Liver Congress 2018, the 53rd annual meeting of the European Association for the Study of the Liver (EASL) in Paris, France.
The data from the 15 subjects who completed 8 weeks of treatment was re-analyzed after excluding one outlier (subject 5019 RM with an extremely high triglyceride level of 1288 mg/dL before treatment which was reduced to 300 mg/dL after treatment).
- After 8 weeks of treatment with MN-001, the serum triglyceride level was reduced in 13 out of 14 subjects.
- Pre-treatment mean serum triglycerides was 260.1 mg/dL and post-treatment mean serum triglycerides was 185.2 mg/dL. MN-001 significantly reduced mean serum triglycerides by 74.9 mg/dL, resulting in a 28.8% reduction (p=0.00006).
MN-001 (tipelukast) significantly reduced mean serum triglycerides, a primary endpoint, during the study. Having achieved the most important endpoint of the study, MediciNova has discontinued enrollment and will stop the study in order to accelerate further development of MN-001. There were no clinically significant safety or tolerability issues during the study.
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.