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ZX-29 Sale

目录号 : GC64013

ZX-29 is a potent and selective ALK inhibitor with an IC50s of 2.1, 1.3 and 3.9 nM for ALK, ALK L1196M and ALK G1202R mutations, respectively.

ZX-29 Chemical Structure

Cas No.:2254805-62-2

规格 价格 库存 购买数量
5 mg
¥2,700.00
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10 mg
¥4,320.00
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25 mg
¥8,550.00
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50 mg
¥13,050.00
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Sample solution is provided at 25 µL, 10mM.

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产品描述

ZX-29 is a potent and selective ALK inhibitor with an IC50s of 2.1, 1.3 and 3.9 nM for ALK, ALK L1196M and ALK G1202R mutations, respectively.

[1] Gou W, et al. Biochim Biophys Acta Mol Cell Res. 2020 Jul;1867(7):118712.

Chemical Properties

Cas No. 2254805-62-2 SDF Download SDF
分子式 C23H28ClN7O3S 分子量 518.03
溶解度 DMSO : 50 mg/mL (96.52 mM; ultrasonic and warming and heat to 60°C) 储存条件 4°C, protect from light
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1 mg 5 mg 10 mg
1 mM 1.9304 mL 9.652 mL 19.3039 mL
5 mM 0.3861 mL 1.9304 mL 3.8608 mL
10 mM 0.193 mL 0.9652 mL 1.9304 mL
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Research Update

ZX-29, a novel ALK inhibitor, induces apoptosis via ER stress in ALK rearrangement NSCLC cells and overcomes cell resistance caused by an ALK mutation

Biochim Biophys Acta Mol Cell Res 2020 Jul;1867(7):118712.PMID:32224191DOI:10.1016/j.bbamcr.2020.118712.

Although anaplastic lymphoma kinase (ALK) inhibitors have good clinical efficacy, the inevitable development of drug resistance is the most common obstacle to their clinical application. There is an urgent need to develop more effective and selective ALK inhibitors to overcome the problem of drug resistance. Here, we screened a series of ALK inhibitors and found that ZX-29 displayed potent cytotoxic activity against ALK rearrangement non-small cell lung cancer (NSCLC) NCI-H2228 cells. Then, we investigated the antitumor effects of ZX-29. We demonstrated that ZX-29 time- and dose-dependently inhibited the viability of NCI-H2228 cells, induced cell cycle arrest in the G1 phase, and then they subsequently progressed into cell death. The type of cell death induced by ZX-29 was apoptosis through endoplasmic reticulum (ER) stress. Interestingly, ZX-29 induced protective autophagy, and inhibiting autophagy could enhance the antitumor effect of ZX-29. Furthermore, ZX-29 suppressed tumor growth in a mouse xenograft model. More importantly, ZX-29 could overcome the drug resistance caused by the ALK G1202R mutation. In conclusion, we demonstrated that ZX-29 showed excellent anti-ALK rearrangement NSCLC activity in vitro and in vivo and overcame the drug resistance caused by an ALK mutation. Therefore, ZX-29 is a promising antitumor drug targeting ALK rearrangement or ALK G1202R mutation NSCLC.

The novel ALK inhibitor ZX-29 induces apoptosis through inhibiting ALK and inducing ROS-mediated endoplasmic reticulum stress in Karpas299 cells

J Biochem Mol Toxicol 2021 Mar;35(3):e22666.PMID:33140567DOI:10.1002/jbt.22666.

It is a well-known fact that 60%-85% of anaplastic large cell lymphoma (ALCL) is mainly driven by the anaplastic lymphoma kinase (ALK) fusion protein. Although ALK-positive ALCL patients respond significantly to ALK inhibitors, the development of resistance is inevitable, which requires the development of new therapeutic strategies for ALK-positive ALCL. Here, we investigated the anticancer activities of N-(2((5-chloro-2-((2-methoxy-6-(4-methylpiperazin-1-yl)pyridin-3yl)amino)pyrimidin-4-yl)amino)phenyl)methanesulfonamide (ZX-29), a newly synthesized ALK inhibitor, against nucleophosmin-ALK-positive cell line Karpas299. We demonstrated that ZX-29 decreased Karpas299 cells growth and had better cytotoxicity than ceritinib, which was mediated through downregulating the expression of ALK and related proteins, inducing cell cycle arrest, and promoting cell apoptosis. Moreover, ZX-29-induced cell apoptosis by inducing endoplasmic reticulum stress (ERS). In addition, ZX-29 increased the generation of reactive oxygen species (ROS), and cells pretreatment with N-acetyl- l-cysteine could attenuate ZX-29-induced cell apoptosis and ERS. Taken together, ZX-29 inhibited Karpas299 cell proliferation and induced apoptosis through inhibiting ALK and its downstream protein expression and inducing ROS-mediated ERS. Therefore, our results provide evidence for a novel antitumor candidate for the further investigation.