English 
MediciNova, Inc., a biopharmaceutical company traded on the NASDAQ Global Market and the Standard Market of the Tokyo Stock Exchange, provides an update on the enrollment of two key ongoing clinical trials for the Company’s developmental compounds MN-166 (ibudilast) and MN-001 (tipelukast), each of which is poised to complete randomization.
Specifically, the Company is now down to single digit required randomization in its ongoing Phase 2/3 COMBAT-ALS trial. Concurrently, the Company is seeking the final two randomized subjects for its Phase 2 trial in patients with dyslipidemia and fatty liver disease due to type 2 diabetes.
About MN-166 (ibudilast)
MN-166 (ibudilast) is an orally available small molecule compound that inhibits phosphodiesterase type-4 (PDE4) and inflammatory cytokines, including macrophage migration inhibitory factor (MIF). It is in late-stage clinical development for the treatment of neurodegenerative diseases such as ALS (amyotrophic lateral sclerosis), progressive MS (multiple sclerosis), and DCM (degenerative cervical myelopathy); and is also in development for glioblastoma, Long COVID, CIPN (chemotherapy-induced peripheral neuropathy), and substance use disorder. In addition, MN-166 was evaluated in patients that are at risk for developing acute respiratory distress syndrome (ARDS). MediciNova holds Orphan Drug Designation for MN-166 in ALS by U.S. FDA and EU EMA. MN-166 has received Fast Track Designation by FDA for treatment of ALS. In addition, MN-166 holds Orphan Disease Designation for the treatment of Glioblastoma.
こちらもお読みください： Curadh, Alpha Fusion Advance Astatine-211 Collaboration
About MN-001 (tipelukast)
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 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, MN-001 was found to inhibit triglyceride synthesis in hepatocytes by inhibiting arachidonic acid uptake.
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