2. Stem Cell/Wnt Epigenetics Cell Cycle/DNA Damage Autophagy Anti-infection Neuronal Signaling Apoptosis Metabolic Enzyme/Protease
  3. Organoid HDAC Autophagy Mitophagy HIV Notch Apoptosis Endogenous Metabolite
  4. Valproic acid sodium

Valproic acid sodium  (Synonyms: Sodium Valproate; VPA sodium; 2-Propylpentanoic acid sodium)

製品番号: HY-10585AG
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Valproic acid (Sodium Valproate) sodium is an orally active HDAC inhibitor, with IC50 in the range of 0.5 and 2 mM, also inhibits HDAC1 (IC50, 400 μM), and induces proteasomal degradation of HDAC2. Valproic acid sodium activates Notch1 signaling and inhibits proliferation in small cell lung cancer (SCLC) cells. Valproic acid sodium is used in the treatment of epilepsy, bipolar disorder, metabolic disease, HIV infection and prevention of migraine headaches.

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Valproic acid sodium

Valproic acid sodium 構造式

CAS 番号 : 1069-66-5

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10 mg $1080 在庫あり
50 mg $3240 在庫あり
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Valproic acid sodium 関連抗体

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製品説明

Valproic acid (Sodium Valproate) sodium is an orally active HDAC inhibitor, with IC50 in the range of 0.5 and 2 mM, also inhibits HDAC1 (IC50, 400 μM), and induces proteasomal degradation of HDAC2. Valproic acid sodium activates Notch1 signaling and inhibits proliferation in small cell lung cancer (SCLC) cells. Valproic acid sodium is used in the treatment of epilepsy, bipolar disorder, metabolic disease, HIV infection and prevention of migraine headaches[1][2][3][4][5][6][7].

IC50 & Target

IC50: 400 μM (HDAC1), 0.5-2 mM (HDAC)[5] HDAC2[6]
体外実験

Valproic acid (VPA) (0-15 mM; 24 and 72 h) inhibits Hela cell growth in a dose- and time- dependent manner[1].
Valproic acid (10 mM; 24 h) significantly attenuates the activities of total, cytosol and nuclear HDACs[1].
Valproic acid (0-15 mM; 24 h) induces a G1 phase arrest at 1–3 mM and a G2/M phase arrest at 10 mM, and increases the percentage of sub-G1 cells in HeLa cells. Valproic acid also induces necrosis, apoptosis and lactate dehydrogenase (LDH) release[1].
Valproic acid (0-20 mM; 24 h) activates Tcf/Lef-dependent transcription and synergizes with lithium[2].
Valproic acid (0-5 mM; 0-18 h) increases β-catenin levels in Neuro2A cells[2].
Valproic acid (0-2 mM; 0-24 h) stimulates phosphorylation of AMPK and ACC in hepatocytes[5].
Valproic acid (0-10 mM; 2 days) induces Notch1 signaling and morphologic differentiation, suppresses production of NE tumor markers in SCLC cells[6].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Valproic acid sodium 関連抗体

Cell Viability Assay[1]

Cell Line: HeLa cells
Concentration: 0, 1, 3, 5, 10 and 15 mM
Incubation Time: 24 and 72 h
Result: HeLa cell growth was dose- and time-dependently decreased with an IC50 of ~10 and 4 mM at 24 and 72 h.

Western Blot Analysis[1][2][5]

Cell Line: HeLa cells, Neuro2A cells or primary mouse hepatocytes
Concentration: 10 mM (HeLa); 0, 2, and 5 mM (Neuro2A); 0.2, 0.4, 0.8, 1.2 and 2 mM (hepatocytes)
Incubation Time: 24 h (HeLa); 0-18 h (Neuro2A); 0-24 h (hepatocytes)
Result: Increased the form of acetylated histone 3.
Reduced PARP, induced cleavage PARP, and downregulated Bcl-2.
Increased β-catenin levels.
Increased the phosphorylation of AMPK and ACC.

Cell Cycle Analysis[1]

Cell Line: HeLa cells
Concentration: 0, 1, 3, 5, 10 and 15 mM
Incubation Time: 24 h
Result: Induced a G1 phase arrest at 1–3 mM, significantly induced a G2/M phase arrest at 10 mM, and increased the percentage of sub-G1 cells in HeLa cells in a dose-dependent manner at 24 h.
体内実験

Valproic acid (VPA) (500 mg/kg; i.p.; daily for 12 days) inhibits tumor angiogenesis in mice transplanted with Kasumi-1 cells[3].
Valproic acid (350 mg/kg; i.p.; once) enhances social behavior in rats[4].
Valproic acid (0.26% (w/v); p.o. via drinking water; 14 days) decreases liver mass, hepatic fat accumulation, and serum glucose in obese mice without hepatotoxicity[5].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Female BALB/c nude mice, Kasumi-1 tumor model[3]
Dosage: 500 mg/kg
Administration: Intraperitoneal injection, daily for 12 days
Result: Inhibited tumor growth and tumor angiogenesis.
Inhibited the mRNA and protein expression of VEGF, VEGFR2 and bFGF.
Inhibited HDAC activity and increased acetylation of histone H3.
Enhanced the accumulation of hyperacetylated histone H3 on VEGF promoters.
Animal Model: Timed-pregnant Long Evans rats[4]
Dosage: 350 mg/kg
Administration: Intraperitoneal injection, once
Result: Demonstrated more social investigation and play fighting than control animals.
Animal Model: Obese phenotype of ob/ob mice[5]
Dosage: 0.26% (w/v)
Administration: Oral via drinking water, 14 days
Result: Revealed a marked reduction in the accumulation of fats in the liver as compared with the untreated mice, significantly decreased liver mass to body mass, decreased serum triglyceride concentrations, and did not induce hepatotoxicity.
分子量

166.19

分子式

C8H15NaO2
CAS 番号
Appearance

Solid

Color

White to off-white

SMILES

O=C(O[Na])C(CCC)CCC
輸送条件

Shipping with dry ice.
保管条件

Please store the product under the recommended conditions in the Certificate of Analysis.
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Keywords:

Valproic acid sodium (GMP)1069-66-5Sodium Valproate (GMP) VPA sodium (GMP) 2-Propylpentanoic acid sodium (GMP)OrganoidHDACAutophagyMitophagyHIVNotchApoptosisEndogenous MetaboliteHistone deacetylasesMitochondrial AutophagyHuman immunodeficiency virusHelaproteasomaldegradationNotch1SCLCepilepsybipolar disordermigraineheadachessmall cell lung canceranticanceranticonvulsanthepatic fat accumulationInhibitorinhibitorinhibit

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