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Sodium orthovanadate ATPase inhibitor

Cat.No.S2000

Sodium orthovanadate is an alkaline phosphatase and (Na,K)-ATPase inhibitor with IC50 of 10 μM.
Sodium orthovanadate ATPase inhibitor Chemical Structure

Chemical Structure

Molecular Weight: 183.91

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Quality Control

Batch: Purity: 99.88%
99.88

Solubility

In vitro
Batch:

Water : 10 mg/mL

DMSO : Insoluble
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Ethanol : Insoluble

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In vivo
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Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O, mix and clarify.

Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

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Chemical Information, Storage & Stability

Molecular Weight 183.91 Formula

Na3O4V

 Storage (From the date of receipt)
CAS No. 13721-39-6 Download SDF Storage of Stock Solutions

Synonyms N/A Smiles [O-][V](=O)([O-])[O-].[Na+].[Na+].[Na+]

Mechanism of Action

Targets/IC50/Ki
(Na,K)-ATPase
40 nM
In vitro
In transient forebrain ischemia, Sodium orthovanadate rescues cells from delayed neuronal death in the hippocampal CA1 region. The neuroprotective effects of this compound 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. This chemical treatment also prevents the decrease in phosphorylation of mitogen-activated protein kinase (MAPK). It inhibits ASK1 through the PI3-K/Akt-dependent pathway. This compound 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 vivo
In a rat model of myocardial ischemic infarction, sodium orthovanadate rescues cells from ischemia/reperfusion injuries. Post-treatment with this compound reduces infarct size in a dose-dependent manner. This chemical treatment also ameliorates contractile dysfunction of the left ventricle 72 hours after reperfusion. The cytoprotective action of this treatment is closely associated with inhibition of fodrin breakdown. It inhibits caspase-3 activation induced by ischemia.
References
  • [4] https://pubmed.ncbi.nlm.nih.gov/16762504/
  • [5] https://pubmed.ncbi.nlm.nih.gov/16006742/
  • [6] https://pubmed.ncbi.nlm.nih.gov/15292457/

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