Valproic Acid (NSC 93819) sodium salt

Catalog No.S1168 Synonyms: Sodium valproate

For research use only.

Valproic Acid sodium salt (NSC 93819, 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 induces Notch1 signaling in small cell lung cancer (SCLC) cells. Valproic acid is under investigation for treatment of HIV and various cancers. Valproic acid (VPA) induces autophagy and mitophagy by upregulation of BNIP3 and mitochondrial biogenesis by upregulating PGC-1α.

Valproic Acid (NSC 93819) sodium salt Chemical Structure

CAS No. 1069-66-5

Selleck's Valproic Acid (NSC 93819) sodium salt has been cited by 28 publications

Purity & Quality Control

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Biological Activity

Description Valproic Acid sodium salt (NSC 93819, 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 induces Notch1 signaling in small cell lung cancer (SCLC) cells. Valproic acid is under investigation for treatment of HIV and various cancers. Valproic acid (VPA) induces autophagy and mitophagy by upregulation of BNIP3 and mitochondrial biogenesis by upregulating PGC-1α.
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]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
HEK293 MVTGeY5kfGmxbjDhd5NigQ>? NX7yTVNZOSCvTR?= NIfkSoFKdmO{ZXHz[UBqdiCycn;0[YlvKGSrc4Xs[oll\SCrc3;t[ZJie2VibHX2[YwhcW5iSFXLNlk{KGOnbHzzJIF1KDFibV2gZpkhcW2vdX7vZoxwfA>? MnzMQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOTd3Nk[3N|IoRjF5NU[2O|MzRC:jPh?=
HEK293 Mmn6SpVv[3Srb36gZZN{[Xl? MY[xJI1O NHXkWG9KdmO{ZXHz[UBqdiCJUmC3PEBxem:2ZXnuJIxmfmWuIHnuJGhGUzJ7MzDj[YxteyCjdDCxJI1OKGK7IHntcZVvd2Kub4S= MmDrQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOTd3Nk[3N|IoRjF5NU[2O|MzRC:jPh?=
A549 MYjGeY5kfGmxbjDhd5NigQ>? M1;tOlE2OCC3TR?= M1fCe|I1KGi{cx?= MoexTY5pcWKrdHnvckBw\iCqdX3hckBJTEGFIHnuJGE2PDliY3XscJMh[XO|ZYPz[YQh[XNiaX7jdoVie2ViaX6gbIl{fG:wZT3IOEBi[2W2eXzheIlwdiCjdDCxOVAhfU1iYX\0[ZIhOjRiaILzJIJ6KFenc4Tldo4h[myxdB?= M{XRcVxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzF6Mkm0PFQ1Lz5zOEK5OFg1PDxxYU6=
GM15850 NHHvcFhHfW6ldHnvckBie3OjeR?= NV;1UpJSPDByIIXN NWf2VXRWOTJiaILz M4PoeWlvcGmkaYTpc44hd2ZiSFTBR{BqdiCqdX3hckBIVTF3OEWwJINmdGy|IHHzd4V{e2WmIHHzJIlv[3KnYYPlJIlvKHSxdHHsJIFk\XS7bHH0[YQhcGm|dH;u[UBt\X[nbDDheEA1ODBidV2gZYZ1\XJiMUKgbJJ{KGK7IGfld5Rmem5iYnzveEBidmGueYPpdy=> M3;5SVxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzF4OUKxN|Y4Lz5zNkmyNVM3PzxxYU6=
PC12 NF\BfotHfW6ldHnvckBie3OjeR?= M3vMOVEhfU1? MXiyOEBpenN? MX;JcoR2[3Srb36gc4Yh[XW2b4DoZYd6KGmwIILheEB{fGGkbHWgbY5lfWOrYnzlJHBEOTJiY3XscJMh\XiycnXzd4lv\yCDNUPUJIFteGijLYP5cpVkdGWrbjDhd5Nme3OnZDDhd{BCPTOWIHHsdIhiNXO7boXjcIVqdiClbHXhdoFv[2ViYYSgNUB2VSCjZoTldkAzPCCqcoOgZpkh\GWwc3n0c41mfHKrYzDhcoFtgXOrcx?= Mk[wQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOTh|OUG5OFkoRjF6M{mxPVQ6RC:jPh?=
PC12 NUfSOIxnTnWwY4Tpc44h[XO|YYm= NHLnVW8yKHWP MUO5OkBpenN? MXnJcoR2[3Srb36gc4Yh[XW2b4DoZYd6KGmwIILheEB{fGGkbHWgbY5lfWOrYnzlJHBEOTJiY3XscJMh\XiycnXzd4lv\yCHR1\QMWhFWTd2IHHzd4V{e2WmIHHzJJNwdHWkbHWgSWdHWC2KRGG3OEBkdGWjcnHuZ4Uh[XRiMTD1UUBi\nSncjC5OkBpenNiYomg[IVve2m2b33leJJq[yCjbnHsfZNqew>? NX34e3U{RGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMUizPVE6PDlpPkG4N|kyQTR7PD;hQi=>
SK-N-MC M2PBNmZ2dmO2aX;uJIF{e2G7 M{TMc|EhdU1? MmnNOFghcHK| MkLiTY5lfWO2aX;uJI9nKGG3dH;wbIFogSCrbjDoeY1idiCVSz3OMW1EKGOnbHzzJIV5eHKnc4PpcochTUeIUD3ISHE4PCCjc4Pld5Nm\CCjczDy[YR2[3Srb36gbY4hTUeIUD3ISHE4PCCjZ3fy[YdifGmxbjDheEAyKHWPIHHmeIVzKDR6IHjyd{BjgSCmZX7zbZRwdWW2cnnjJIFv[Wy7c3nz NGT6NZU9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9zOEO5NVk1QSd-MUizPVE6PDl:L3G+
HL60 MoroSpVv[3Srb36gZZN{[Xl? MUWxJI1O MnHVNlQhcHK| NV3WUYZNUW6qaXLpeIlwdiCxZjDISGFEKGmwIHj1cYFvKEiONkCgZ4VtdHNiYYPz[ZN{\WRiYYOgbY5kemWjc3WgbY4hcGm|dH;u[UBJOyCjY3X0fYxifGmxbjDheEAyKG2PIHHmeIVzKDJ2IHjyd{BjgSCZZYP0[ZJvKGKub4T0bY5oKG2ndHjv[C=> M3;UeFxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ3M{C0PFk3Lz5{NUOwOFg6PjxxYU6=
Assay
Methods Test Index PMID
Western blot Acetyl Histone H3 ; Active caspase-3 / PARP / Cleaved PARP ; acetyl-H4 28542253 20025549
Growth inhibition assay Cell viability 28498322
In vivo Valproic acid delays growth of the primary tumors in the MT‐450 rat breast cancer model. [2]

Protocol (from reference)

Solubility (25°C)

In vitro

DMSO 33 mg/mL
(198.56 mM)
Water 33 mg/mL
(198.56 mM)
Ethanol ''33 mg/mL

Chemical Information

Molecular Weight 166.19
Formula

C8H15NaO2

CAS No. 1069-66-5
Storage 3 years -20°C powder
2 years -80°C in solvent
Smiles CCCC(CCC)C(=O)[O-].[Na+]

In vivo Formulation Calculator (Clear solution)

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Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid concentration mg/mL, Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )

Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O, mix and clarify.

Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

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Molarity Calculator

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Clinical Trial Information

NCT Number Recruitment Interventions Conditions Sponsor/Collaborators Start Date Phases
NCT03919292 Recruiting Drug: Neratinib|Drug: Divalproex Sodium Solid Tumor Adult Virginia Commonwealth University|Puma Biotechnology Inc. May 1 2019 Phase 1|Phase 2
NCT03681158 Completed Drug: sodium valproate Epilepsy Sanofi October 5 2018 Phase 1
NCT03112889 Completed Drug: Sodium Valproate Glycogen Storage Disease Type V|McArdle Disease University College London January 2015 Phase 2
NCT00139074 Terminated Drug: Quetiapine fumarate|Drug: sodium valproate Bipolar Disorder AstraZeneca July 2005 Phase 4

(data from https://clinicaltrials.gov, updated on 2022-01-17)

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

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