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

Valproic acid  (Synonyms: VPA; 2-Propylpentanoic Acid)

Cat. No.: HY-10585 Purity: ≥98.0%
COA Handling Instructions

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

For research use only. We do not sell to patients.

Valproic acid Chemical Structure

Valproic acid Chemical Structure

CAS No. : 99-66-1

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Customer Review

Based on 23 publication(s) in Google Scholar

Other Forms of Valproic acid:

Top Publications Citing Use of Products

    Valproic acid purchased from MCE. Usage Cited in: Acta Pharmacol Sin. 2020 Jun 17.

    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).
    • Biological Activity

    • Purity & Documentation

    • References

    • Customer Review

    Description

    Valproic acid (VPA) 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 activates Notch1 signaling and inhibits proliferation in small cell lung cancer (SCLC) cells. Valproic acid 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[5][6]

    HDAC1

    400 μM (IC50)

    HDAC

    0.5-2 mM (IC50)

    HDAC2

     

    Autophagy

     

    Mitophagy

     

    In Vitro

    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].

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

    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: 10 mM (HeLa); 0, 2, and 5 mM (Neuro2A); 0.2, 0.4, 0.8, 1.2 and 2 Mm (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.
    In Vivo

    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].

    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.
    Molecular Weight

    144.21

    Formula

    C8H16O2

    CAS No.
    SMILES

    CCCC(CCC)C(O)=O

    Shipping

    Room temperature in continental US; may vary elsewhere.

    Storage
    Pure form -20°C 3 years
    4°C 2 years
    In solvent -80°C 6 months
    -20°C 1 month
    Solvent & Solubility
    In Vitro: 

    DMSO : 100 mg/mL (693.43 mM; Need ultrasonic)

    H2O : 1 mg/mL (6.93 mM; Need ultrasonic and warming)

    Preparing
    Stock Solutions
    Concentration Solvent Mass 1 mg 5 mg 10 mg
    1 mM 6.9343 mL 34.6717 mL 69.3433 mL
    5 mM 1.3869 mL 6.9343 mL 13.8687 mL
    10 mM 0.6934 mL 3.4672 mL 6.9343 mL
    *Please refer to the solubility information to select the appropriate solvent.
    In Vivo:
    • 1.

      Add each solvent one by one:  PBS

      Solubility: 100 mg/mL (693.43 mM); Clear solution; Need ultrasonic and warming and heat to 60°C

    • 2.

      Add each solvent one by one:  0.5% CMC/saline water

      Solubility: 20 mg/mL (138.69 mM); Suspended solution; Need ultrasonic

    • 3.

      Add each solvent one by one:  10% DMSO    40% PEG300    5% Tween-80    45% saline

      Solubility: ≥ 2.5 mg/mL (17.34 mM); Clear solution

    • 4.

      Add each solvent one by one:  10% DMSO    90% (20% SBE-β-CD in saline)

      Solubility: ≥ 2.5 mg/mL (17.34 mM); Clear solution

    • 5.

      Add each solvent one by one:  10% DMSO    90% corn oil

      Solubility: ≥ 2.5 mg/mL (17.34 mM); Clear solution

    *All of the co-solvents are available by MCE.
    Purity & Documentation

    Purity: ≥98.0%

    References
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