メルドニウム

説明Mildronate is a cardiac and neuroprotective drug. It is a compound with a new structure first developed by Latvia Institute of Organic Synthesis. It was first developed by Grindeks in the former Soviet Union in 1989. On the market, the drug is a structural analog of carnitine, which can compete with carnitine for γ-trimethylaminobutyrate hydroxylase, reduce the concentration of free carnitine and long-chain acetylcarnitine in cells, so it can inhibit Carnitine-dependent fatty acid oxidation. Meldonium was added to the WADA list of banned substances on January 1, 2016 because of "evidence of its use by athletes with the intention of enhancing performance."

使用Mildronate is a drug used to treat angina, myocardial infarction, and chronic heart failure. It is a novel pharmaceutical composition based on a reverse transcriptase inhibitor and meldonium.This compound generally contains a significant amount of water.

一般的な説明Mildronate (3-(2,2,2-trimethylhydrazinium)propionate; MET-88; meldonium, quaterine) is an antiischemic drug developed at the Latvian Institute of Organic Synthesis. Mildronate was designed to inhibit carnitine biosynthesis in order to prevent accumulation of cytotoxic intermediate products of fatty acida-oxidation in ischemic tissues and to block this highly oxygen-consuming process. Mildronate is efficient in the treatment of heart is chemia and its consequences. Extensive evaluation of pharmacological activities of mildronate revealed its beneficial effect on cerebral circulation disorders and central nervous system (CNS) functions. The drug is used in neurological clinics for the treatment of brain circulation disorders. It appears to improve patients’ mood; they become more active, their motor dysfunction decreases, and asthenia, dizziness and nausea become less pronounced. Since the brain does not utilize fatty acids as fuel other mechanisms of action of mildronate in CNS should be considered. Several reports indicate the possible existence of an alternative, non-carnitine dependent mechanism of action of mildronate. Our recent findings suggest that CNS effects of mildronate could be mediated by stimulation of the nitric oxide production in the vascular endothelium by modification of the butyrobetaine and its esters pools. It is hypothesized that mildronate may increase the formation of the -butyrobetaine esters. The latter are potent cholinomimetics and may activate eNOS via acetylcholine receptors or specific-butyrobetaine ester receptors.