Mildronate 86426-17-7

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Molecular Weight:

147.19 Mildronate is an inhibitor of biosynthesis of L-carnitine by gamma-butyrobetaine (GBB) hydroxylase and as a competitive inhibitor of renal carnitine reabsorption.






Biological 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.


Mildronate 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%.

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