所有图片(1)
别名:
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
经验公式（希尔记法）:
C14H14ClN3S
推荐产品
检测方案
≥95% (HPLC)
质量水平
形式
solid
制造商/商品名称
Calbiochem®
储存条件
OK to freeze
protect from light
颜色
brown
溶解性
DMSO: 50 mg/mL
运输
ambient
储存温度
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 key
YYTHPXHGWSAKIZ-UHFFFAOYSA-N
一般描述
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.
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.
包装
Packaged under inert gas
警告
Toxicity: Standard Handling (A)
重悬
Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 6 months at -20°C.
其他说明
Larrieu, D., et al. 2014. Science, 344, 527.
Chimenti, F., et al. 2009. J. Med. Chem.52, 530.
Chimenti, F., et al. 2009. J. Med. Chem.52, 530.
法律信息
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
WGK
nwg
闪点(°F)
Not applicable
闪点(°C)
Not applicable
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
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