Mitiglinide Calcium - CAS 145525-41-3
Catalog number:
Not Intended for Therapeutic Use. For research use only.
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Molecular Weight:
Potassium Channel
Mitiglinide Calcium is a blood glucose-lowering drugs, stimulating insulin secretion by closing the ATP-sensitive K+ channels in pancreatic beta-cells.
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1.Mitiglinide: KAD 1229, S 21403.
Drugs R D. 2004;5(2):98-101.
Mitiglinide [KAD 1229, S 21403], a derivative of benzylsuccinic acid, is a potassium channel antagonist undergoing development with Kissei for the treatment of type 2 diabetes mellitus. It has potent oral hypoglycaemic activity and is structurally different from the sulphonylureas, although it stimulates calcium influx by binding to the suphonylurea receptor on pancreatic beta-cells and closing K+ATP channels. Mitiglinide belongs to a family of meglitinide analogues that also includes repaglinide and nateglinide. Mitiglinide is licensed to Servier for Europe, where it is undergoing phase III development, and for Russia, the Commonwealth of Independent States, the Baltic Republics, the Middle East, Oceania, China (including Hong Kong) and Taiwan. Kissei exclusively licensed mitiglinide to Choongwae Pharma for South Korea in March 2003. In August 2002, Kissei and Takeda entered into a co-marketing agreement for mitiglinide in Japan. The companies will co-market the agent under a single brand name.
2.[Pharmacological and clinical profile of mitiglinide calcium hydrate (Glufast), a new insulinotropic agent with rapid onset].
Ojima K1, Kiyono Y, Kojima M. Nihon Yakurigaku Zasshi. 2004 Oct;124(4):245-55.
Mitiglinide calcium hydrate (mitiglinide, Glufast) is a new insulinotropic agent of the glinide class with rapid onset. Mitiglinide is thought to stimulate insulin secretion by closing the ATP-sensitive K(+) (K(ATP)) channels in pancreatic beta-cells, and its early insulin release and short duration of action would be effective in improving postprandial hyperglycemia. In studies of various cloned K(ATP) channels, mitiglinide shows a higher selectivity for the beta-cell type of SUR1/Kir6.2 than the cardiac and smooth muscle types of K(ATP) channels in comparison with glibenclamide and glimepiride. In vitro and in vivo studies demonstrated the insulinotropic effect of mitiglinide is more potent than that of nateglinide, and mitiglinide surpassed in controlling postprandial hyperglycemia in normal and diabetic animals. In clinical trials, treatment with mitiglinide provided lasting improvement of postprandial hyperglycemia in Type 2 diabetic patients and decreased the fasting plasma glucose levels and HbA(1C) values.
3.Nateglinide and mitiglinide, but not sulfonylureas, induce insulin secretion through a mechanism mediated by calcium release from endoplasmic reticulum.
Shigeto M1, Katsura M, Matsuda M, Ohkuma S, Kaku K. J Pharmacol Exp Ther. 2007 Jul;322(1):1-7. Epub 2007 Apr 4.
Nateglinide and mitiglinide (glinides) are characterized as rapid-onset and short-acting insulinotropic agents. Although both compounds do not have a sulfonylurea structure, it has been postulated that insulin secretion is preceded by their binding to Kir6.2/SUR1 complex, and a mechanism of insulin secretion of glinides has been accounted for by this pathway. However, we hypothesized the involvement of additional mechanisms of insulin secretion enhanced by glinides, and we analyzed the pattern of time course of insulin secretion from MIN6 cells with the existence of agents that have specific pharmacologic actions. Dose-dependent effects of tolbutamide, glibenclamide, nateglinide, and mitiglinide were observed. Insulin secretion induced by 3 microM tolbutamide and 1 nM glibenclamide was completely inhibited by 10 microM diazoxide and 3 microM verapamil, although the latter half-component of insulin secretion profile induced by 3 microM nateglinide or 30 nM mitiglinide remained with the existence of those agents.
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