• Masahiko Tanaka.
• Pharmaceuticals Development Division, Mitsubishi Pharma Corporation, 2-2-6 Nihonbashi-Honcho, Chuo-ku, Tokyo 103-8405, Japan. Tanaka.Masahiko@md.m-pharma.co.jp
• Nippon Yakurigaku Zasshi. 2002 May 1;119(5):301-8.

AbstractThe involvement of oxygen radical species has been implicated in ischemic and post-ischemic brain cell damage. Edaravone (3-methyl-1-phenyl-2-pyrazolin-5-one; M.W. 174.20, MCI-186, Radicut Injection) has an inhibitory effect on lipid peroxidation by scavenging free radicals and prevents vascular endothelial cell injury. In rat brain ischemic models, post-ischemic treatment with edaravone reduces .OH production and infarction of the ischemic penumbral area and suppresses delayed neuronal death. It also improves neurological deficits and diminishes deterioration of brain edema observed after ischemia. We investigated the efficacy and safety of edaravone in acute ischemic stroke patients. Edaravone improved the core neurological deficits, impaired activities of daily living, and disability, without serious safety problems. Edaravone was approved in Japan for the treatment of acute brain infarction within 24 h after onset in April, 2001. We hope that edaravone represents a promising neuroprotective agent that can contribute to the treatment of acute ischemic stroke.

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