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Merck
CN

676380

Valproic Acid sodium salt

≥98% (HPLC), solid, HDAC1 inhibitor, Calbiochem®

别名:

丙戊酸钠盐, 2-丙基戊酸钠

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关于此项目

经验公式(希尔记法):
C8H15NaO2
化学文摘社编号:
分子量:
166.19
UNSPSC Code:
12352106
NACRES:
NA.77
MDL number:
Assay:
≥98% (HPLC)
Form:
solid
Quality level:
Storage condition:
OK to freeze, desiccated (hygroscopic)
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产品名称

丙戊酸钠盐, A cell-permeable, short-chained fatty acid that inhibits histone deacetylase (IC50 = 400 µM for HDAC1).

Quality Level

description

Merck USA index - 14, 9913

assay

≥98% (HPLC)

form

solid

potency

400 μM IC50

manufacturer/tradename

Calbiochem®

storage condition

OK to freeze, desiccated (hygroscopic)

color

white

solubility

water: 50 mg/mL

shipped in

ambient

storage temp.

2-8°C

SMILES string

[Na+].[O-]C(=O)C(CCC)CCC

InChI

1S/C8H16O2.Na/c1-3-5-7(6-4-2)8(9)10;/h7H,3-6H2,1-2H3,(H,9,10);/q;+1/p-1

InChI key

AEQFSUDEHCCHBT-UHFFFAOYSA-M

General description

一种细胞可渗透性短链脂肪酸,可抑制组蛋白脱乙酰酶活性(HDAC1的IC50 = 400 µM)。诱导分化并抑制来源于人类恶性胶质瘤的细胞系的增殖。在治疗水平(350 µM-1.04 mM),引起肌醇耗竭,抑制GSK-3α和-3β,激活ERK通路,并产生神经营养效应。已被用作抗癫痫药。也有报告刺激过氧化物酶体增殖物激活受体(PPAR)活性。在人类和啮齿动物模型中显示出强效的致畸活性。

Biochem/physiol Actions

细胞可渗透性:是
主要靶标
HDAC1
产物不与ATP竞争。
可逆:否

Packaging

用惰性气体包装

Other Notes

Gottlicher, M., et al. 2001.EMBO J.20, 6969.
Knupfer, M.M., et al. 2001.Anticancer Res.21, 347.
Phiel, C.J., et al. 2001.J. Biol. Chem.276, 36734.
Vaden, D.L., et al. 2001.J. Biol. Chem.276, 15466.
Yuan, P.X., et al. 2001.J. Biol. Chem.276, 31674.
Chen, G., et al. 1999.J. Neurochem.72, 1327.

Legal Information

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

Disclaimer

毒性:有害 & 致癌/致畸性(E)


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pictograms

Health hazardExclamation mark

signalword

Warning

Hazard Classifications

Acute Tox. 4 Oral - Repr. 2

存储类别

11 - Combustible Solids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable



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Cancer is a complex disease manifestation. At its core, it remains a disease of abnormal cellular proliferation and inappropriate gene expression. In the early days, carcinogenesis was viewed simply as resulting from a collection of genetic mutations that altered the gene expression of key oncogenic genes or tumor suppressor genes leading to uncontrolled growth and disease (Virani, S et al 2012). Today, however, research is showing that carcinogenesis results from the successive accumulation of heritable genetic and epigenetic changes. Moreover, the success in how we predict, treat and overcome cancer will likely involve not only understanding the consequences of direct genetic changes that can cause cancer, but also how the epigenetic and environmental changes cause cancer (Johnson C et al 2015; Waldmann T et al 2013). Epigenetics is the study of heritable gene expression as it relates to changes in DNA structure that are not tied to changes in DNA sequence but, instead, are tied to how the nucleic acid material is read or processed via the myriad of protein-protein, protein-nucleic acid, and nucleic acid-nucleic acid interactions that ultimately manifest themselves into a specific expression phenotype (Ngai SC et al 2012, Johnson C et al 2015). This review will discuss some of the principal aspects of epigenetic research and how they relate to our current understanding of carcinogenesis. Because epigenetics affects phenotype and changes in epigenetics are thought to be key to environmental adaptability and thus may in fact be reversed or manipulated, understanding the integration of experimental and epidemiologic science surrounding cancer and its many manifestations should lead to more effective cancer prognostics as well as treatments (Virani S et al 2012).





全球贸易项目编号

货号GTIN
676380-5GM04055977183566