ZX-29
CAS No. 2254805-62-2
ZX-29 ( —— )
产品货号. M26525 CAS No. 2254805-62-2
ZX-29 is a potent and selective inhibitor of ALK, and also induces protective autophagy and has antitumor effect.
纯度: >98% (HPLC)
COA
Datasheet
HNMR
HPLC
MSDS
Handing Instructions
规格 | 价格/人民币 | 库存 | 数量 |
5MG | ¥2001 | 有现货 |
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10MG | ¥3216 | 有现货 |
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25MG | ¥5370 | 有现货 |
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50MG | ¥7655 | 有现货 |
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100MG | ¥10368 | 有现货 |
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200MG | 获取报价 | 有现货 |
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500MG | 获取报价 | 有现货 |
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1G | 获取报价 | 有现货 |
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生物学信息
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产品名称ZX-29
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注意事项本公司产品仅用于科研实验,不得用于人体或动物的临床与诊断
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产品简述ZX-29 is a potent and selective inhibitor of ALK, and also induces protective autophagy and has antitumor effect.
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产品描述ZX-29 is a potent and selective inhibitor of ALK(IC50 of 2.1 nM, 1.3 nM and 3.9 nM for ALK, ALK L1196M and ALK G1202R mutations, respectively), and also induces protective autophagy and has antitumor effect.(In Vitro):ZX-29 dose-dependently inhibits colony formation of NCI-H2228 cells. With an increase in ZX-29 concentration, the cell density decreased gradually, and the cells lost their normal morphology and become sharp and slender. In NCI-H2228 cells, ZX-29 (10 nM; 0-48 hours) inhibits the proliferation of and arrests the cells in G1 phase. ZX-29 (0-81 nM; 24-72 hours) treatment resulted in a decrease in the viability with time and dose. ZX-29 (10 nM; 24 hours) treatment causes typical signs of autophagy and the formation of autophagosomes and enhances the expression level of LC3 and Beclin1. ZX-29 (20 nM; 0-48 hours) treatment significantly increases the mRNA level of CHOP. (In Vivo):In a mouse xenograft model, ZX-29 treatment suppresses tumor growth.
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同义词——
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通路Angiogenesis
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靶点ALK
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受体Dnm1 GTPase
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研究领域——
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适应症——
化学信息
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CAS Number2254805-62-2
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分子量518.0
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分子式C23H28ClN7O3S
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纯度>98% (HPLC)
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溶解度——
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SMILESCOc1cc(ccc1Nc1ncc(Cl)c(Nc2ccccc2NS(C)(=O)=O)n1)N1CCN(C)CC1
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化学全称——
运输与储存
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储存条件(-20℃)
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运输条件With Ice Pack
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稳定性≥ 2 years
参考文献
1.N. Gorski, et al. Mixtures of Nonionic and Ionic Surfactants. The Effect of Counterion Binding in Mixtures of Tetradecyldimethylamine Oxide and Tetradecyltrimethylammonium Bromide. Langmuir 1994, 10, 8, 2594-2603.
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