3-(trimethylammonioamino)propionate

3-(trimethylammonioamino)propionate - Names and Identifiers

Name	MILDRONATE
Synonyms	MET88 Kvaterin Quateri MILDRONATE Mildonate Meldomiun 3-(trimethylammonioamino)propanoate 3-(trimethylammonioamino)propionate 3-(trimethylazaniumylamino)propanoate 3-(2,2,2-trimethylhydrazine)propionate 3-(2,2,2-trimethylhydrazine)propionate 3-(2,2,2-Trimethylhydrazinium)propionate 3-(2,2,2-triMethylhydraziniuM)propionate dehydrate Mildronate 3-(2,2,2-Trimethylhydrazine)propionate 3-(2,2,2-trimethyldiazan-2-iumyl)propanoate dihydrate 2-(2-Carboxyethyl)-1,1,1-trimethyl Hydrazinium Inner Salt 2-(2-carboxyethyl)-1,1,1-trimethylhydrazinium hydroxide inner salt 2-(2-carboxyethyl)-1,1,1-trimethylhydrazinium hydroxide inner salt
CAS	76144-81-5
EINECS	682-135-0
InChI	InChI=1/C8H17NO5/c10-2-1-9-3-6(12)8(14)7(13)5(9)4-11/h5-8,10-14H,1-4H2/t5?,6-,7-,8?/m1/s1

3-(trimethylammonioamino)propionate - 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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