product name Sodium valproate
Description: Valproate (VPA), also known valproic acid, sodium valproate, and divalproex sodium, is a medication primarily used to treat epilepsy and bipolar disorder and to prevent migraine headaches. It is useful for the prevention of seizures in those with absence seizures, partial seizures, and generalized seizures. It can be given intravenously or by mouth. Long acting formulations exist. Valproic acid dissociates to the valproate ion in the gastrointestinal tract. The mechanisms by which valproate exerts its antiepileptic effects have not been established. It has been suggested that its activity in epilepsy is related to increased brain concentrations of gamma-aminobutyric acid (GABA).
References: J Biol Chem. 2001 Sep 28;276(39):36734-41; EMBO J. 2001 Dec 17;20(24):6969-78.
166.19
Formula
C8H15NaO2
CAS No.
1069-66-5
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 33 mg/mL (198.6 mM)
Water: 33 mg/mL (198.6 mM)
Ethanol: 33 mg/mL (198.6 mM)
Solubility (In vivo)
Synonyms
Valproic acid sodium salt
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19397213
| In Vitro |
In vitro activity: Valproic acid acts through a distinct pathway that involves direct inhibition of histone deacetylase (IC(50) for HDAC1 = 0.4 mM). Valproic acid mimics the histone deacetylase inhibitor trichostatin A, causing hyperacetylation of histones in cultured cells. Valproic acid, like trichostatin A, also activates transcription from diverse exogenous and endogenous promoters. Valproic acid and trichostatin A have remarkably similar teratogenic effects in vertebrate embryos, while non-teratogenic analogues of valproic acid do not inhibit histone deacetylase and do not activate transcription. Valproic acid induces proliferation of peroxisomes in the rodent liver. Valproic acid at a concentration of 1 mM induces relief of this repression by Gal4 fusions of N‐CoR, TR or PPARδ in a cell line expressing the ligand‐binding domain of PPARδ fused to the DNA‐binding domain of the glucocorticoid receptor (GR) together with a GR‐controlled reporter gene. Valproic acid induces accumulation of hyperacetylated histone and inhibits HDAC activity. Valproic acid induces a specific type of differentiation characterized by reduced proliferation, morphological alterations, marker gene expression and particularly the accumulation of the AP-2 transcription factor as a potential marker of neuronal or neural crest cell-like differentiation in F9 teratocarcinoma cells. Valproic acid impairs cell proliferation or survival as indicated by decreased incorporation of [3H]thymidine in F9 and P19 teratocarcinoma cells. Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | Valproic acid delays growth of the primary tumors in the MT‐450 rat breast cancer model. |
| Animal model | |
| Formulation & Dosage | |
| References | J Biol Chem. 2001 Sep 28;276(39):36734-41; EMBO J. 2001 Dec 17;20(24):6969-78. |
Related Posts
product name Sodium valproate
Description: Valproate (VPA), also known valproic acid, sodium valproate, and divalproex sodium, is a medication primarily used to treat epilepsy and bipolar disorder and to prevent migraine headaches. It is useful for the prevention of seizures in those with absence seizures, partial seizures, and generalized seizures. It can be given intravenously or by mouth. Long acting formulations exist. Valproic acid dissociates to the valproate ion in the gastrointestinal tract. The mechanisms by which valproate exerts its antiepileptic effects have not been established. It has been suggested that its activity in epilepsy is related to increased brain concentrations of gamma-aminobutyric acid (GABA).
References: J Biol Chem. 2001 Sep 28;276(39):36734-41; EMBO J. 2001 Dec 17;20(24):6969-78.
166.19
Formula
C8H15NaO2
CAS No.
1069-66-5
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 33 mg/mL (198.6 mM)
Water: 33 mg/mL (198.6 mM)
Ethanol: 33 mg/mL (198.6 mM)
Solubility (In vivo)
Synonyms
Valproic acid sodium salt
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19397213
| In Vitro |
In vitro activity: Valproic acid acts through a distinct pathway that involves direct inhibition of histone deacetylase (IC(50) for HDAC1 = 0.4 mM). Valproic acid mimics the histone deacetylase inhibitor trichostatin A, causing hyperacetylation of histones in cultured cells. Valproic acid, like trichostatin A, also activates transcription from diverse exogenous and endogenous promoters. Valproic acid and trichostatin A have remarkably similar teratogenic effects in vertebrate embryos, while non-teratogenic analogues of valproic acid do not inhibit histone deacetylase and do not activate transcription. Valproic acid induces proliferation of peroxisomes in the rodent liver. Valproic acid at a concentration of 1 mM induces relief of this repression by Gal4 fusions of N‐CoR, TR or PPARδ in a cell line expressing the ligand‐binding domain of PPARδ fused to the DNA‐binding domain of the glucocorticoid receptor (GR) together with a GR‐controlled reporter gene. Valproic acid induces accumulation of hyperacetylated histone and inhibits HDAC activity. Valproic acid induces a specific type of differentiation characterized by reduced proliferation, morphological alterations, marker gene expression and particularly the accumulation of the AP-2 transcription factor as a potential marker of neuronal or neural crest cell-like differentiation in F9 teratocarcinoma cells. Valproic acid impairs cell proliferation or survival as indicated by decreased incorporation of [3H]thymidine in F9 and P19 teratocarcinoma cells. Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | Valproic acid delays growth of the primary tumors in the MT‐450 rat breast cancer model. |
| Animal model | |
| Formulation & Dosage | |
| References | J Biol Chem. 2001 Sep 28;276(39):36734-41; EMBO J. 2001 Dec 17;20(24):6969-78. |