Sodium orthovanadate is an alkaline phosphatase and (Na,K)-ATPase inhibitor with IC50 of 10 μM. Sodium orthovanadate rescues cells from delayed neuronal death in the hippocampal CA1 region. The neuroprotective effects of Sodium orthovanadate and IGF-1 are associated with preventing decreased Akt-Ser-473 phosphorylation in the CA1 region observed immediately after reperfusion. Sodium orthovanadate inhibits ASK1 through the PI3-K/Akt-dependent pathway. Sodium orthovanadate rescues cells from ischemia/reperfusion injuries in a rat model of myocardial ischemic infarction. Sodium orthovanadate treatment also ameliorates contractile dysfunction of the left ventricle 72 hours after reperfusion.
|Body Surface Area (m2)||0.007||0.025||0.15||0.05||0.02||0.5|
|Animal A (mg/kg) = Animal B (mg/kg) multiplied by||Animal B Km|
|Animal A Km|
For example, to modify the dose of resveratrol used for a mouse (22.4 mg/kg) to a dose based on the BSA for a rat, multiply 22.4 mg/kg by the Km factor for a mouse and then divide by the Km factor for a rat. This calculation results in a rat equivalent dose for resveratrol of 11.2 mg/kg.
|Solubility||Water 35 mg/mL|
Hypoglycemic effect of Astragalus polysaccharide and its effect on PTP1B.
Wu Y, et al. Acta Pharmacol Sin. 2005 Mar;26(3):345-52. PMID: 15715932.
Cytoprotective effect of sodium orthovanadate on ischemia/reperfusion-induced injury in the rat heart involves Akt activation and inhibition of fodrin breakdown and apoptosis.
Takada Y, et al. J Pharmacol Exp Ther. 2004 Dec;311(3):1249-55. PMID: 15292457.
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