MILDRONATE
MILDRONATE
CAS: 76144-81-5
Molecular Formula: C6H14N2O2
MILDRONATE - Names and Identifiers
MILDRONATE - Physico-chemical Properties
| Molecular Formula | C6H14N2O2 |
| Molar Mass | 146.19 |
| Melting Point | 85-900C |
| Solubility | Methanol (Slightly), Water (Slightly) |
| Appearance | Solid |
| Color | White to Off-White |
| Storage Condition | Refrigerator |
| Stability | Hygroscopic |
| Refractive Index | 1.598 |
| Physical and Chemical Properties | Properties: This product is colorless, transparent cubic crystal or white crystalline powder; Slightly odorous, with strong hygroscopicity. |
| In vitro study | Mildronate (40 μm) inhibits the reaction of γ-butyrylbetaine hydroxylase with γ-butyrylbetaine, K m and V max were 36.8 μm and 0.08 nmol/min/mg protein, respectively. |
| In vivo study | Oral administration of Mildronate to rats for 10 days (150 mg/kg) reduced myocardial free carnitine and long-chain acylcarnitine contents by 63.7 and 74.3%, respectively. Isoproterenol administered after Mildronate treatment (100 mg/kg, P. O.) led to a 48.7% reduction in free carnitine concentration compared with rats given isoproterenol alone. Preferential administration of Mildronate can effectively protect the myocardium from isoproterenol-induced changes in ATP content and myocardial energy charge, and also prevent the increase of creatine phosphokinase and lactate dehydrogenase activity. In mouse hearts, chronic treatment with Mildronate (200 mg/kg) significantly increased insulin-stimulated glucose uptake by 35% and increased glucose transporter 4(1.7-fold increase), expression of hexokinase II (2.1-fold increase), insulin receptor protein (2.5-fold increase), and carnitine palmitoyltransferase IA (2.2-fold increase). Long-term treatment with Mildronate, a statistically significant reduction in blood glucose in the supply state, from 6 mM to 5 mM. Mildronate reduces azidothymidine-induced changes in mouse brain tissue. Mildronate (50 mg/kg) normalized the increased expression of caspase-3, apoptosis susceptibility protein (CAS), and iNOS. Mildronate also normalizes changes in the expression of cytochrome C oxidase (COX) and reduces the expression of glial fibrillary acidic protein (GFAP) and cell infiltrates. Mildronate exhibits a protective effect in a Goto-Kakizaki rat experimental model of type 2 diabetes. Mildronate (200 mg/kg) treatment simultaneously reduced blood glucose given food and in the fasted state. Mildronate strongly inhibited fructosamine accumulation and loss of pain sensitivity (75% reduction) and also improved the enhanced contractile response to phenylephrine in Goto-Kakizaki rat aortic rings. In addition, the necrotic area of myocardial infarction was significantly reduced by 30% in Mildronate-treated hearts. |
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MILDRONATE
丁苯氧酸
4'-甲基乙酰苯胺
2,4,6,8-Tetraoxa-5-phosphanonanedioic acid, 5-[[2-(6-amino-9H-purin-9-yl)-1-methylethoxy]methyl]-, bis(2,2-dimethylpropyl) ester, 5-oxide, (R)-
丁苯氧酸
4'-甲基乙酰苯胺
2,4,6,8-Tetraoxa-5-phosphanonanedioic acid, 5-[[2-(6-amino-9H-purin-9-yl)-1-methylethoxy]methyl]-, bis(2,2-dimethylpropyl) ester, 5-oxide, (R)-