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354,00 zł
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Nazwa produktu
Valproic Acid, Sodium Salt, 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
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Ta pozycja | |||
|---|---|---|---|
| assay ≥98% (HPLC) | assay 98% | assay ≥98% (HPLC) | assay ≥98% (TLC) |
| form solid | form powder | form crystalline solid | form solid |
| manufacturer/tradename Calbiochem® | manufacturer/tradename - | manufacturer/tradename Calbiochem® | manufacturer/tradename Calbiochem® |
| Quality Level 100 | Quality Level 200 | Quality Level 100 | Quality Level 100 |
| storage temp. 2-8°C | storage temp. - | storage temp. 2-8°C | storage temp. −20°C |
| storage condition OK to freeze, desiccated (hygroscopic) | storage condition - | storage condition OK to freeze, desiccated (hygroscopic) | storage condition OK to freeze, protect from light |
General description
Biochem/physiol Actions
HDAC1
Packaging
Other Notes
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
Disclaimer
signalword
Warning
hcodes
Hazard Classifications
Acute Tox. 4 Oral - Repr. 2
Klasa składowania
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Certyfikaty analizy (CoA)
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Powiązane treści
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).
Numer pozycji handlu globalnego
| SKU | NUMER GTIN |
|---|---|
| 676380-5GM | 04055977183566 |
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