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Merck

382111

Histone Acetyltransferase Inhibitor IV, CPTH2

同義詞:

Histone Acetyltransferase Inhibitor IV, CPTH2, HAT Inhibitor IV, Cyclopentylidene-(4-(4ʹ-chlorophenyl)thiazol-2-yl)hydrazone, GCN5 Inhibitor II, N-acetyltransferase 10 Inhibitor I, NAT10 Inhibitor I

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選擇尺寸

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關於此項目

經驗公式(希爾表示法):
C14H14ClN3S
CAS 編號:
分子量::
291.80
MDL號碼:
分類程式碼代碼:
12352200
NACRES:
NA.54

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化驗

≥95% (HPLC)

品質等級

形狀

solid

製造商/商標名

Calbiochem®

儲存條件

OK to freeze
protect from light

顏色

brown

溶解度

DMSO: 50 mg/mL

運輸包裝

ambient

儲存溫度

2-8°C

InChI

1S/C14H14ClN3S/c15-11-7-5-10(6-8-11)13-9-19-14(16-13)18-17-12-3-1-2-4-12/h5-9H,1-4H2,(H,16,18)

InChI 密鑰

YYTHPXHGWSAKIZ-UHFFFAOYSA-N

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本產品
382110540211528111
assay

≥95% (HPLC)

assay

≥97% (HPLC)

assay

≥95% (HPLC)

assay

≥95% (HPLC)

form

solid

form

solid

form

solid

form

solid

Quality Level

100

Quality Level

100

Quality Level

100

Quality Level

100

manufacturer/tradename

Calbiochem®

manufacturer/tradename

Calbiochem®

manufacturer/tradename

Calbiochem®

manufacturer/tradename

Calbiochem®

storage temp.

2-8°C

storage temp.

2-8°C

storage temp.

2-8°C

storage temp.

2-8°C

storage condition

OK to freeze, protect from light

storage condition

OK to freeze, protect from light

storage condition

OK to freeze, protect from light

storage condition

OK to freeze, desiccated (hygroscopic), protect from light

一般說明

A cell-permeable thiazolyl-hydrazone compound that inhibits the acetylation of histone H3 by recombinant human Gcn5 in a substrate-competive manner, while exhibiting little activity against rhGcn5 autoacetylation. Although functional knockout of Gcn5 in Saccharomyces cerevisiae by genetic deletion or by CPTH2 treatment is not detrimental to the survival of the budding yeast, CPTH2 treatment is shown to inhibit the growth of yeast strain genetically deleted of Gcn5, but not strains deleted of Elp3 or Sas2.

包裝

Packaged under inert gas

準備報告

Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 6 months at -20°C.

其他說明

Larrieu, D., et al. 2014. Science, 344, 527.
Chimenti, F., et al. 2009. J. Med. Chem.52, 530.

法律資訊

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

免責聲明

Toxicity: Standard Handling (A)

儲存類別代碼

11 - Combustible Solids

水污染物質分類(WGK)

nwg

閃點(°F)

Not applicable

閃點(°C)

Not applicable


分析證明 (COA)

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存取文件庫

Joshy George et al.
Cancer research communications, 2(6), 402-416 (2023-01-24)
The emergence of treatment resistance significantly reduces the clinical utility of many effective targeted therapies. Although both genetic and epigenetic mechanisms of drug resistance have been reported, whether these mechanisms are stochastically selected in individual tumors or governed by a

相關內容

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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