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Merck

676380

Sigma-Aldrich

Valproic Acid sodium salt

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

동의어(들):

Valproic Acid, Sodium Salt, 2-Propylpentanoic Acid, Na

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제품정보 (DICE 배송 시 비용 별도)

실험식(Hill 표기법):
C8H15NaO2
CAS 번호:
Molecular Weight:
166.19
MDL number:
UNSPSC 코드:
12352106
NACRES:
NA.77
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제품 이름

Valproic Acid, Sodium Salt, A cell-permeable, short-chained fatty acid that inhibits histone deacetylase (IC50 = 400 µM for HDAC1).

Quality Level

설명

Merck USA index - 14, 9913

분석

≥98% (HPLC)

양식

solid

효능

400 μM IC50

제조업체/상표

Calbiochem®

저장 조건

OK to freeze
desiccated (hygroscopic)

색상

white

solubility

water: 50 mg/mL

배송 상태

ambient

저장 온도

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

일반 설명

A cell-permeable, short-chained fatty acid that inhibits histone deacetylase activity (IC50 = 400 µM for HDAC1). Induces differentiation and inhibits proliferation of cell lines derived from human malignant gliomas. At therapeutic levels (350 µM-1.04 mM), causes inositol depletion, inhibits both GSK-3α and -3β, activates the ERK pathway, and produces neurotropic effects. Has been used as an anti-epileptic agent. Also reported to stimulate peroxisome proliferator-activated receptor (PPAR) activity. Displays a potent teratogenic activity in humans and rodent models.

생화학적/생리학적 작용

Cell permeable: yes
Primary Target
HDAC1
Product does not compete with ATP.
Reversible: no

포장

Packaged under inert gas

기타 정보

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.

법적 정보

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

면책조항

Toxicity: Harmful & Carcinogenic / Teratogenic (E)

픽토그램

Health hazardExclamation mark

신호어

Warning

유해 및 위험 성명서

Hazard Classifications

Acute Tox. 4 Oral - Repr. 2

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point (°F)

Not applicable

Flash Point (°C)

Not applicable


시험 성적서(COA)

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관련 콘텐츠

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).

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