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    Mildronate
    Mildronate

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V0934
    CAS #: 76144-81-5 Purity ≥98%

    Description: Mildronate (Meldonium) is a potent inhibitor of biosynthesis of L-carnitine by gamma-butyrobetaine (GBB) hydroxylase and as a competitive inhibitor of renal carnitine reabsorption. Mildronate (40 μM) inhibits the reaction of γ-butyrobetaine hydroxylase with γ-butyrobetaine with Km and Vmax of 36.8 μM and 0.08 nmol/min/mg protein, respectively.

    References: Biochem Pharmacol. 1988 Jan 15;37(2):195-202; Life Sci. 2008 Oct 24;83(17-18):613-9.

    Related CAS: 86426-17-7 (dihydrate)

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    Molecular Weight (MW)147.19
    FormulaC6H14N2O2 
    CAS No.76144-81-5 
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 29 mg/mL (197.0 mM)
    Water: <1 mg/mL
    Ethanol: 29 mg/mL (197.0 mM)
    Solubility (In vivo)Chemical Name: 3-(2,2,2-Trimethylhydrazine)propionate

    InChi Key: PVBQYTCFVWZSJK-UHFFFAOYSA-N

    InChi Code: InChI=1S/C6H14N2O2/c1-8(2,3)7-5-4-6(9)10/h7H,4-5H2,1-3H3

    SMILES Code: O=C([O-])CCN[N+](C)(C)C           

    SynonymsQuaterin; Meldonium; Kvaterin; Mildronate;


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    In Vitro

    In vitro activity: Mildronate (40 μM) inhibits the reaction of γ-butyrobetaine hydroxylase with γ-butyrobetaine with Km and Vmax of 36.8 μM and 0.08 nmol/min/mg protein, respectively.

    In VivoMildronate administered orally to rats for 10 days (150 mg/kg) elicits a reduction in myocardial free camitine and long-chain acyl carnitine content by 63.7 and 74.3%, respectively. Mildronate treatment (100 mg/kg, orally) subsequent administration of isoproterenol results in a reduction in free camitine concentration by 48.7% in comparison with the rats receiving isoproterenol. A prior administration of Mildronate effectively protects the myocardium from isoproterenol-induced variations in the content of ATP and myocardial energy charge, as well as preventing a rise in creatine phosphokinase and lactic dehydrogenase activity. Mildronate (200 mg/kg) long-term treatment significantly increases the rate of insulin-stimulated glucose uptake by 35% and the expression of glucose transporter 4 (1.7-fold increase), hexokinase II (2.1-fold increase), insulin receptor proteins (2.5-fold increase) and carnitine palmitoyltransferases IA (2.2-fold increase) in mouse hearts. Mildronate long-term treatment statistically significantly decreases fed state blood glucose from 6 to 5 mM. Mildronate reduces the azidothymidine-induced alterations in mouse brain tissue. Mildronate (50 mg/kg) normalizes the increase in caspase-3, cellular apoptosis susceptibility protein (CAS) and iNOS expression. Mildronate also normalizes the changes in cytochromec oxidase (COX) expression, reduces the expression of glial fibrillary acidic protein (GFAP) and cellular infiltration. Mildronate displays protective effects in experimental model of type 2 diabetes in Goto-Kakizaki rats. Mildronate (200 mg/kg) treatment decreases both the fed- and fasted-state blood glucose. Mildronate strongly inhibits fructosamine accumulation and loss of pain sensitivity (by 75%) and also ameliorates the enhanced contractile responsiveness of Goto-Kakizaki rat aortic rings to phenylephrine. In addition, in Mildronate-treated hearts, the necrosis zone following coronary occlusion is significantly decreased by 30%.
    Animal modelRats
    Formulation & Dosage150 mg/kg; oral
    References

    Biochem Pharmacol. 1988 Jan 15;37(2):195-202; Life Sci. 2008 Oct 24;83(17-18):613-9.


    These protocols are for reference only. InvivoChem does not independently validate these methods.

    Mildronate

    Life Sci. 2008 Oct 24;83(17-18):613-9.
     

    Mildronate

    Life Sci. 2008 Oct 24;83(17-18):613-9.


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