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  3. Valproic acid (sodium)(2:1)

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

目录号: HY-10585B
产品使用指南

Valproic acid (VPA) sodium (2:1) 是一种具有口服活性的 HDAC 抑制剂,IC50 值为 0.5-2 mM,抑制 HDAC1 的活性,(IC50,400 μM),同时可诱导 HDAC2 的降解。Valproic acid sodium (2:1) 激活 Notch1 信号并抑制小细胞肺癌 (SCLC) 细胞的增殖。Valproic acid sodium (2:1) 可用于癫痫、双相情感障碍、代谢疾病、HIV 感染和偏头痛等的研究。

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Valproic acid (sodium)(2:1) Chemical Structure

Valproic acid (sodium)(2:1) Chemical Structure

CAS No. : 76584-70-8

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Valproic acid (sodium)(2:1) 的其他形式现货产品:

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MCE 顾客使用本产品发表的 33 篇科研文献

WB

    Valproic acid (sodium)(2:1) purchased from MCE. Usage Cited in: Acta Pharmacol Sin. 2020 Jun 17.  [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).
    • 生物活性

    • 纯度 & 产品资料

    • 参考文献

    生物活性

    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

     

    体外研究
    (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: 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.
    体内研究
    (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.
    Clinical Trial
    分子量

    154.71

    Formula

    C8H15O2.1/2Na

    CAS 号
    结构分类
    初始来源
    运输条件

    Room temperature in continental US; may vary elsewhere.

    储存方式

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

    纯度 & 产品资料
    参考文献
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    • Do most proteins show cross-species activity?

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