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    Sodium orthovanadate
    Sodium orthovanadate

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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 #: V0182
    CAS #: 13721-39-6Purity ≥98%

    Description: Sodium orthovanadate, an inorganic compound with chemical formula of Na3VO4, is a potent inhibitor for several enzymes such as protein tyrosine phosphatases (PTPs), alkaline phosphatase (ALP), and ATPase. It displayed a variety of biological activities, partly due to its structural mimics of phosphates. The inhibitory effects against the aforementioned enzymes can be reversed by dilution or the addition of Ethylenediaminetetraacetic acid (EDTA).

    References: J Cereb Blood Flow Metab. 2001 Nov;21(11):1268-80; J Pharmacol Sci. 2005 Jul;98(3):205-11.

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    Molecular Weight (MW)183.91
    CAS No.13721-39-6
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO:<1 mg/mL
    Water: 37 mg/mL (201.18 mM)
    Ethanol:<1 mg/mL
    Solubility (In vivo)Saline: 30mg/mL 
    SynonymsSodium orthovanadate

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    In Vitro

    In vitro activity: In transient forebrain ischemia, 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. Akt is moderately activated in the cell bodies and dendrites of pyramidal neurons after orthovanadate treatment. The Sodium orthovanadate treatment also prevents the decrease in phosphorylation of mitogen-activated protein kinase (MAPK). Sodium orthovanadate inhibits ASK1 through the PI3-K/Akt-dependent pathway. Sodium orthovanadate up-regulates Akt activity in the brain and in turn rescue neurons from delayed neuronal death by inhibiting FKHR-dependent or -independent death signals in neurons.

    In VivoIn a rat model of myocardial ischemic infarction, sodium orthovanadate rescues cells from ischemia/reperfusion injuries. Post-treatment with Sodium orthovanadate reduces infarct size in a dose-dependent manner. Sodium orthovanadate treatment also ameliorates contractile dysfunction of the left ventricle 72 hours after reperfusion. The cytoprotective action of Sodium orthovanadate treatment is closely associated with inhibition of fodrin breakdown. Sodium orthovanadate treatment inhibits caspase-3 activation induced by ischemia.
    Animal modelRats
    Formulation & DosageN/A

    J Cereb Blood Flow Metab. 2001 Nov;21(11):1268-80; J Pharmacol Sci. 2005 Jul;98(3):205-11.

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


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