3-oxo-3-(sodiooxy)-2,4-dioxa-3-vanada-1,5-disodapentane

• ChemBase ID: 72834
• Molecular Formular: Na3O4V
• Molecular Mass: 183.90841
• Monoisotopic Mass: 183.89292582
• SMILES: O([Na])[V](=O)(O[Na])O[Na]
• Canonical SMILES: [Na]O[V](=O)(O[Na])O[Na]
• InChI: InChI=1S/3Na.4O.V
• InChIKey: HQHUIUQMQXUPHI-UHFFFAOYSA-N

NAMES AND DATABASE IDS

Names

• IUPAC name: 3-oxo-3-(sodiooxy)-2,4-dioxa-3-vanada-1,5-disodapentane
• IUPAC Traditional name: 3-oxo-3-(sodiooxy)-2,4-dioxa-3-vanada-1,5-disodapentane
• Synonyms: Sodium orthovanadate

Database IDs

• CAS Number: 13721-39-6
• PubChem SID: 162037755
• PubChem CID: 454045

CALCULATED PROPERTIES

• H Acceptors: 3
• H Donor: 0
• LogD (pH = 5.5): 1.0622
• LogD (pH = 7.4): 1.0622
• Log P: 1.0622
• Molar Refractivity: 5.4935 cm^3
• Polarizability: 12.07504 Å^3
• Polar Surface Area: 44.76 Å^2
• Rotatable Bonds: 3
• Lipinski's Rule of Five: true

PROPERTIES

Safety Information

• Storage Condition: -20°C

Product Information

• Salt Data: Sodium Salt

DETAILS

Selleck Chemicals - S2000

Research Area

• Description: Cancer

Biological Activity

• Description: Sodium orthovanadate is an alkaline phosphatase and (Na,K)-ATPase inhibitor with IC50 of 10 μM.
• Targets: Phosphatase; (Na,K)-ATPase
• IC50: 10 μM ^[1]; 40 nM ^[2]
• In Vitro: 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). ^[3] Sodium orthovanadate inhibits ASK1 through the PI3-K/Akt-dependent pathway. ^[4] 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. ^[4]
• In Vivo: In 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. ^[5] 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. ^[6]

Protocol

• Protocol: Kinase Assay ^[2]
• ATPase assay: The coupled assay linking ADP production to NADH oxidation is used for all ATPase assays. The fraction of active enzyme is determined by measuring enzyme activity after linearity has been achieved by the activity prior to addition of Sodium orthovanadate. Final steady state hydrolysis rates are independent of the order addition of Sodium orthovanadate and enzyme.
• Protocol: Animal Study ^[6]
• Animal Models: Male Sprague-Dawley rats
• Formulation: 0.9% saline
• Doses: 0.005 mL/min/100g of b.wt. over 20 minutes
• Administration: Administered via i.v.

References

• References: [1] Wu Y, et al. Acta Pharmacol Sin, 2005, 26(3), 345-352.
• References: [2] Cantley LC Jr, et al. J Biol Chem, 1977, 252(21), 7421-7423.
• References: [3] Kawano T, et al. J Cereb Blood Flow Metab, 2001, 21(11), 1268-1280.
• References: [4] Wu DN, et al. Neurosci Lett, 2006, 404(1-2), 98-102.
• References: [5] Fukunaga K, et al. J Pharmacol Sci, 2005, 98(3), 205-211.
• References: [6] Takada Y, et al. J Pharmacol Exp Ther, 2004, 311(3), 1249-1255.

REFERENCES

• Wu Y, et al. Acta Pharmacol Sin, 2005, 26(3), 345-352.
• Cantley LC Jr, et al. J Biol Chem, 1977, 252(21), 7421-7423.
• Kawano T, et al. J Cereb Blood Flow Metab, 2001, 21(11), 1268-1280.
• Wu DN, et al. Neurosci Lett, 2006, 404(1-2), 98-102.
• Fukunaga K, et al. J Pharmacol Sci, 2005, 98(3), 205-211.
• Takada Y, et al. J Pharmacol Exp Ther, 2004, 311(3), 1249-1255.