Valproic acid sodium salt (Sodium valproate)
For research use only. Not for use in humans.
Molecular Weight(MW): 166.19
Valproic acid sodium salt (Sodium valproate) is a HDAC inhibitor by selectively inducing proteasomal degradation of HDAC2, used in the treatment of epilepsy, bipolar disorder and prevention of migraine headaches.
Selleck's Valproic acid sodium salt (Sodium valproate) has been cited by 10 publications
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Western blot analysis of Acetylated Histone and Histone. 0-10μM sodium valproate was added.
2011 Dr. Zhang of Tianjin Medical University. Valproic acid sodium salt (Sodium valproate) purchased from Selleck.
(A,B) Wild-type C57BL/6 male mice were treated with vehicle (saline) or 10 mg/kg of paraquat (PQ) for 3 days, and mice received VPA (3.5 mg/kg) or anacardic acid (5 mg/kg) starting 24 and 1 h before PQ injection. IL-6 mRNA expression was determined by real-time PCR.
Front Immunol, 2017, 7:696. Valproic acid sodium salt (Sodium valproate) purchased from Selleck.
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Choose Selective HDAC Inhibitors
|Description||Valproic acid sodium salt (Sodium valproate) is a HDAC inhibitor by selectively inducing proteasomal degradation of HDAC2, used in the treatment of epilepsy, bipolar disorder and prevention of migraine headaches.|
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. 
|In vivo||Valproic acid delays growth of the primary tumors in the MT‐450 rat breast cancer model. |
|In vitro||DMSO||33 mg/mL (198.56 mM)|
|Water||33 mg/mL (198.56 mM)|
|Ethanol||33 mg/mL (198.56 mM)|
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