2. Epigenetics Cell Cycle/DNA Damage Autophagy Anti-infection Stem Cell/Wnt Neuronal Signaling Apoptosis Metabolic Enzyme/Protease
  3. HDAC Autophagy Mitophagy HIV Notch Apoptosis Endogenous Metabolite
  4. Valproic acid sodium (2:1)

Valproic acid sodium (2:1)  (Synonyms: Sodium Valproate (2:1); VPA sodium (2:1); 2-Propylpentanoic acid sodium (2:1))

製品番号: HY-10585B
取扱説明書 Technical Support

Valproic acid (VPA) sodium (2:1) 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 (2:1) activates Notch1 signaling and inhibits proliferation in small cell lung cancer (SCLC) cells. Valproic acid sodium (2:1) is used in the treatment of epilepsy, bipolar disorder, metabolic disease, HIV infection and prevention of migraine headaches.

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CAS 番号 : 76584-70-8

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Valproic acid sodium (2:1) 関連抗体

Top Publications Citing Use of Products

顧客検証

Cell Proliferation/Viability Assay
WB
RT-PCR
In Vivo Efficacy Study
Histological Imaging/Staining

    Valproic acid sodium (2:1) purchased from MedChemExpress. Usage Cited in: J Nanobiotechnology. 2025 Oct 14;23(1):670.  [Abstract]

    Cell viability under treatment with different concentrations of VPA (0-40 mM; 24 h).

    Valproic acid sodium (2:1) purchased from MedChemExpress. Usage Cited in: J Nanobiotechnology. 2025 Oct 14;23(1):670.  [Abstract]

    Pregnant females received intraperitoneal injections of 600 mg/kg VPA or saline on gestational day 12.5. Immunohistochemical staining representative images and quantification of Iba1 and GFAP in hippocampal CA1, CA3, and DG regions.

    Valproic acid sodium (2:1) purchased from MedChemExpress. Usage Cited in: Acta Pharmacol Sin. 2024 Nov;45(11):2290-2299.

    Schemes of generating Fsp1-Cre:R26R-loxp-tdTomato mice and drug treatment to induce in situ transdifferentiation. Fsp1-Cre mice were crossed with R26Rloxp-tdTomato mice in which the expression of tdTomato is prevented by a loxP-flanked STOP cassette. The F1 mice would have the red fluorescent protein tdTomato expressed specifically in the fibroblasts. CRFVPTM were given once a week for 6 weeks. Immunofluorescence staining of the cryosections of the hearts from Fsp1-Cre:R26R-loxp-tdTomato mice treated with vehicle (b) or CRFVPTM (c) for 6 weeks. C: CHIR99021, 14 mg/kg; R: RepSox, 8.6 mg/kg; F: Forskolin, 61.6 mg/kg; V: VPA, 250 mg/kg; T: TTNPB, 1 mg/kg and M: Rolipram, 2.5 mg/kg; P: Parnate, 2.7 mg/kg, CRFTM by oral gavage and VP by intraperitoneal injection once a week for 6 weeks in mice at about 8 weeks of age.

    Valproic acid sodium (2:1) purchased from MedChemExpress. Usage Cited in: Acta Pharmacol Sin. 2024 Nov;45(11):2290-2299.

    Whole-heart imaging with light-sheet fluorescence microscopy after tissue clearing of the hearts from Fsp1-Cre:R26R-loxp-tdTomato mice treated with vehicle (a) or CRFVPTM (b). (C: CHIR99021, 14 mg/kg; R: RepSox, 8.6 mg/kg; F: Forskolin, 61.6 mg/kg; V: VPA, 250 mg/kg; T: TTNPB, 1 mg/kg and M: Rolipram, 2.5 mg/kg; P: Parnate, 2.7 mg/kg, CRFTM by oral gavage and VP by intraperitoneal injection once a week for 6 weeks in mice at about 8 weeks of age).

    Valproic acid sodium (2:1) purchased from MedChemExpress. Usage Cited in: Acta Pharmacol Sin. 2024 Nov;45(11):2290-2299.

    a Schemes of obtaining PDGFRα-DreER:R26R-rox-tdTomato mice and drug treatment to induce in situ cardiac reprogramming in PDGFRα-DreER:R26R-roxtdTomato mice. PDGFRα-DreER mice were mated with R26R-rox-tdTomato mice in which the expression of tdTomato is prevented by a roxflanked STOP cassette. The expression of tdTomato in fibroblasts was turned on by tamoxifen treatment. CRFVPTM were given once a week for 6 weeks. b Body weigh change of the mice after chemical treatment. Immunofluorescence staining of the cryosections of the hearts from PDGFRα-DreER:R26R-rox-tdTomato mice treated with vehicle (c) or CRFVPTM (d) for 6 weeks. (C: CHIR99021, 14 mg/kg; R: RepSox, 8.6 mg/kg; F: Forskolin, 61.6 mg/kg; V: VPA, 250 mg/kg; T: TTNPB, 1 mg/kg and M: Rolipram, 2.5 mg/kg; P: Parnate, 2.7 mg/kg, CRFTM by oral gavage and VP by intraperitoneal injection once a week for 6 weeks in mice at about 8 weeks of age).

    Valproic acid sodium (2:1) purchased from MedChemExpress. Usage Cited in: Acta Pharmacol Sin. 2024 Nov;45(11):2290-2299.

    Immunofluorescence staining of α-actinin in cryosections of hearts from Fsp1-Cre:R26R-loxp-tdTomato mice treated with 7 C cocktail (CRFVPTM) or cocktails by removing 1 compound from 7 C (7C-X) for 6 weeks in vivo with Fsp1-Cre:R26R-loxp-tdTomato mice. (C: CHIR99021, 14 mg/kg; R: RepSox, 8.6 mg/kg; F: Forskolin, 61.6 mg/kg; V: VPA, 250 mg/kg; T: TTNPB, 1 mg/kg and M: Rolipram, 2.5 mg/kg; P: Parnate, 2.7 mg/kg, CRFTM by oral gavage and VP by intraperitoneal injection once a week for 6 weeks in mice at about 8 weeks of age).

    Valproic acid sodium (2:1) purchased from MedChemExpress. Usage Cited in: Cell Death Differ. 2023 Jul;30(7):1811-1828.  [Abstract]

    Western blot analysis using indicated antibodies was performed. Lysates were prepared from control (DMSO) cells or cells treated with Trichostatin A (TSA, 5 μM), Valproic acid (VPA, 0.5 mM), or RGFP966 (10 μM) for 24 h. GAPDH served as a loading control.

    Valproic acid sodium (2:1) purchased from MedChemExpress. Usage Cited in: Mil Med Res. 2020 Nov 1;7(1):52.  [Abstract]

    Valproic acid (0.1 mmol/L; 0–14 days) was used. Representative microscopy images depicting the morphological changes after chemical induction were shown. Scale bars = 100 μm.

    Valproic acid sodium (2:1) purchased from MedChemExpress. Usage Cited in: Mil Med Res. 2020 Nov 1;7(1):52.  [Abstract]

    Valproic acid (0.1 mmol/L; 0–7 days) was used. RT-qPCR analysis of mRNA expression levels of neuron-associated genes TUJ1 and MAP2, and DA neuron-associated genes TH and NURR1 was performed during the chemical induction.

    Valproic acid sodium (2:1) purchased from MedChemExpress. Usage Cited in: Acta Pharmacol Sin. 2021 Mar;42(3):470-481.  [Abstract]

    Effects of Butyrate (But, 1 mM), Vpa (5 mM) and SAHA (Vor, 1 μM) on the expression of P-gp and BCRP, NF-кB p65 and phosphorylated p65 (p-p65), and IкBα and phosphorylated IкBα (p-IкBα).

    HDAC アイソフォーム固有の製品をすべて表示:

    すべてのアイソフォームを表示
    HDAC HDAC1 HDAC2 HDAC3 HDAC4 HDAC5 HDAC6 HDAC7 HDAC8 HDAC9 HDAC10 HDAC11 HD1 HD2

    HIV アイソフォーム固有の製品をすべて表示:

    すべてのアイソフォームを表示
    HIV HIV-1 HIV-2

    Endogenous Metabolite アイソフォーム固有の製品をすべて表示:

    すべてのアイソフォームを表示
    Human Endogenous Metabolite Microbial Metabolite

    • 生物活性

    • 純度とドキュメンテーション

    • 参考文献

    • カスタマーレビュー

    製品説明

    Valproic acid (VPA) sodium (2:1) 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 (2:1) activates Notch1 signaling and inhibits proliferation in small cell lung cancer (SCLC) cells. Valproic acid sodium (2:1) 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

    HDAC1

    400 μM (IC50)

    HDAC

    0.5-2 mM (IC50)

    HDAC2

     

    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 (2:1) 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

    154.71

    分子式

    C8H15O2.1/2Na
    CAS 番号
    SMILES

    CCCC(CCC)C([O-])=O.[0.5 Na+]
    Structure Classification
    Initial Source
    輸送条件

    Room temperature in continental US; may vary elsewhere.
    保管条件

    Please store the product under the recommended conditions in the Certificate of Analysis.
    純度とドキュメンテーション
    参考文献
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    Keywords:

    Valproic acid sodium (2:1)76584-70-8Sodium Valproate (2:1) VPA sodium (2:1) 2-Propylpentanoic acid sodium (2:1)HDACAutophagyMitophagyHIVNotchApoptosisEndogenous MetaboliteHistone deacetylasesMitochondrial AutophagyHuman immunodeficiency virusproteasomaldegradationNotch1SCLCepilepsybipolar disordermigraineheadachessmall cell lung canceranticanceranticonvulsanthepatic fat accumulationInhibitorinhibitorinhibit

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