[CAS NO. 13721-39-6] Sodium orthovanadate
Please click "REQUEST A QUOTE" button if you need other sizes or custom synthesis
request a quote
If there is no stock, or you need other sizes or custom synthesis, please:
PRODUCTS SPECIFICATIONS [13721-39-6]
Store
Catalog
SLK-S2000
Brand
Selleck
CAS
13721-39-6
DESCRIPTION [13721-39-6]
Overview
| MDL | MFCD00003511 |
|---|---|
| Molecular Weight | 183.91 |
| Molecular Formula | Na3O4V |
| SMILES | [Na].[V].[O] |
For research use only.
Storage
3 years,-20°C,powder
1 years,-80°C,in solvent
1 years,-80°C,in solvent
Shipping
Room temperature shipping(Stability testing shows this product can be shipped without any cooling measures.)
Preparing Stock Solutions
| 1 mg | 5 mg | 10 mg | |
| 1 mM | 5.4374 mL | 27.1872 mL | 54.3744 mL |
| 5 mM | 1.0875 mL | 5.4374 mL | 10.8749 mL |
| 10 mM | 0.5437 mL | 2.7187 mL | 5.4374 mL |
| 50 mM | 0.1087 mL | 0.5437 mL | 1.0875 mL |
Description
Sodium orthovanadate is an alkaline phosphatase and inhibitor with of 10 μM.
Targets
| (Na,K)-ATPase [2] |
| 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 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 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. 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.
References
[1] Wu Y, et al. Acta Pharmacol Sin, 2005, 26(3), 345-352.
[2] Cantley LC Jr, et al. J Biol Chem, 1977, 252(21), 7421-7423.
[3] Kawano T, et al. J Cereb Blood Flow Metab, 2001, 21(11), 1268-1280.
[4] Wu DN, et al. Neurosci Lett, 2006, 404(1-2), 98-102.
[5] Fukunaga K, et al. J Pharmacol Sci, 2005, 98(3), 205-211.
[6] Takada Y, et al. J Pharmacol Exp Ther, 2004, 311(3), 1249-1255.
[2] Cantley LC Jr, et al. J Biol Chem, 1977, 252(21), 7421-7423.
[3] Kawano T, et al. J Cereb Blood Flow Metab, 2001, 21(11), 1268-1280.
[4] Wu DN, et al. Neurosci Lett, 2006, 404(1-2), 98-102.
[5] Fukunaga K, et al. J Pharmacol Sci, 2005, 98(3), 205-211.
[6] Takada Y, et al. J Pharmacol Exp Ther, 2004, 311(3), 1249-1255.
Synonyms
Sodium vanadium oxide (Na3VO4)
Vanadic acid (H3VO4), trisodium salt
Sodium vanadate(V) (Na3VO4)
Trisodium orthovanadate
Sodium orthovanadate (Na3VO4)
Sodium orthovanadate
Sodium vanadate
Sodium vanadate (Na3VO4)
Vanadate (VO43-), trisodium, (T-4)-
Trisodium vanadate
Sodium tetraoxovanadate(3-)
Sodium o-vanadate
NSC 79534
Powered by Arctom Copyright © 2026 Arctom. All rights
reserved.