Valproic acid sodium salt (Sodium valproate)

Catalog No.S1168

Valproic acid sodium salt (Sodium valproate) Chemical Structure

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.

Size Price Stock Quantity  
In DMSO USD 120 In stock
USD 97 In stock
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2 Customer Reviews

  • (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.

    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.

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Biological Activity

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.
Targets
HDAC [1]
(Cell-free assay)
Autophagy [1]
(Cell-free assay)
GABA receptor [1]
(Cell-free assay)
In vitro

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. [1] 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. [2]

In vivo Valproic acid delays growth of the primary tumors in the MT‐450 rat breast cancer model. [2]

Protocol

Solubility (25°C)

In vitro DMSO 33 mg/mL (198.56 mM)
Water 33 mg/mL (198.56 mM)
Ethanol 33 mg/mL (198.56 mM)

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 166.19
Formula

C8H15NaO2

CAS No. 1069-66-5
Storage powder
in solvent
Synonyms N/A

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT02926976 Not yet recruiting Schizophrenia Shanghai Mental Health Center November 2016 --
NCT02920060 Completed Grand Mal Status Epilepticus Banaras Hindu University|Institute of Medical Sciences of the Banaras Hindu University (BHU),India January 2015 Phase 2
NCT02011750 Active, not recruiting Toxoplasmosis|Schizophrenia University of Pittsburgh|Mansoura University|Stanley Medical Research Institute March 2013 Phase 4
NCT01791868 Recruiting Generalized Convulsive Status Epilepticus|Intensive Care Unit Assistance Publique - Hôpitaux de Paris February 2013 --
NCT01730313 Unknown status Nodding Syndrome Centers for Disease Control and Prevention|Ministry of Health, Uganda February 2013 Phase 2
NCT01619644 Completed Rubinstein-Taybi Syndrome University Hospital, Bordeaux|Fondation Syndrome de Rubinstein-Taybi April 2012 Phase 2

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HDAC Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID