product name Sodium orthovanadate
Description: Sodium orthovanadate is a commonly used general inhibitor for protein tyrosine phosphatases (PTPs), alkaline phosphatase (ALP), and ATPase. Sodium orthovanadate acts as a competitive inhibitor and is completely reversible upon the addition of EDTA or by dilution.
References: J Cereb Blood Flow Metab. 2001 Nov;21(11):1268-80; J Pharmacol Sci. 2005 Jul;98(3):205-11.
183.91
Formula
Na3O4V
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
Synonyms
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19399671
| 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. Kinase Assay: Cell Assay: |
|---|---|
| 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. |
| Animal model | |
| Formulation & Dosage | |
| References | J Cereb Blood Flow Metab. 2001 Nov;21(11):1268-80; J Pharmacol Sci. 2005 Jul;98(3):205-11. |
Related Posts
product name Sodium orthovanadate
Description: Sodium orthovanadate is a commonly used general inhibitor for protein tyrosine phosphatases (PTPs), alkaline phosphatase (ALP), and ATPase. Sodium orthovanadate acts as a competitive inhibitor and is completely reversible upon the addition of EDTA or by dilution.
References: J Cereb Blood Flow Metab. 2001 Nov;21(11):1268-80; J Pharmacol Sci. 2005 Jul;98(3):205-11.
183.91
Formula
Na3O4V
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
Synonyms
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19399671
| 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. Kinase Assay: Cell Assay: |
|---|---|
| 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. |
| Animal model | |
| Formulation & Dosage | |
| References | J Cereb Blood Flow Metab. 2001 Nov;21(11):1268-80; J Pharmacol Sci. 2005 Jul;98(3):205-11. |