ZX-29
- Product Name
- ZX-29
- CAS No.
- 2254805-62-2
- Chemical Name
- ZX-29
- Synonyms
- ZX-29;ZX-29, 10 mM in DMSO;N-(2-((5-Chloro-2-((2-methoxy-4-(4-methylpiperazin-1-yl)phenyl)amino)pyrimidin-4-yl)amino)phenyl)methanesulfonamide;Methanesulfonamide, N-[2-[[5-chloro-2-[[2-methoxy-4-(4-methyl-1-piperazinyl)phenyl]amino]-4-pyrimidinyl]amino]phenyl]-;N-(2-((5-Chloro-2-((2-methoxy-4-(4-methylpiperazin-1-yl)phenyl)amino)pyrimidin-4-yl)amino)phenyl)methanesulfonamide , ZX-29;arrest,antitumor,Resistance,Anaplastic lymphoma kinase,Bcl-2,ZX-29,Apoptosis,Inhibitor,CD246,p-Akt,caspase-3,endoplasmic,inhibit,CHOP,Anaplastic lymphoma kinase (ALK),ALK tyrosine kinase receptor,ERS,Cluster of differentiation 246,ZX 29,Autophagy,reticulum,ZX29,p-STAT3
- CBNumber
- CB58054583
- Molecular Formula
- C23H28ClN7O3S
- Formula Weight
- 518.03
- MOL File
- 2254805-62-2.mol
ZX-29 Property
- Boiling point:
- 705.5±70.0 °C(Predicted)
- Density
- 1.408±0.06 g/cm3(Predicted)
- storage temp.
- 4°C, protect from light
- solubility
- DMSO : 50 mg/mL (96.52 mM; ultrasonic and warming and heat to 60°C)
- pka
- 8.50±0.10(Predicted)
- form
- Solid
- color
- Light yellow to green yellow
ZX-29 Chemical Properties,Usage,Production
Biological Activity
ZX-29 is a potent and selective ALK inhibitor with an IC50 of 2.1 nM, 1.3 nM and 3.9 nM for ALK, ALK L1196M and ALK G1202R mutations, respectively. ZX-29 is inactive against EGFR. ZX-29 induces apoptosis by inducing endoplasmic reticulum (ER) stress and overcomes cell resistance caused by an ALK mutation. ZX-29 also induces protective autophagy and has antitumor effect[1]. ZX-29 (0-81 nM; 24-72 hours; NCI-H2228 cells) treatment leads to a time- and dose-dependent decrease in NCI-H2228 cell viability[1].ZX-29 (10 nM; 24 hours; NCI-H2228 cells) treatment causes typical signs of autophagy and the formation of autophagosomes. ZX-29 enhances the expression level of LC3 and Beclin1[1].ZX-29 (10 nM; 0-48 hours; NCI-H2228 cells) inhibits the proliferation of NCI-H2228 cells and arrests the cells in G1 phase[1].ZX-29 (10-40 nM; 24-48 hours; NCI-H2228 cells) treatment induces apoptosis of NCI-H2228 cells. ZX-29 dose-dependently upregulates the expression levels of proapoptotic protein Bax, increases the production of activated forms of caspase 3, and downregulates the expression level of antiapoptotic protein Bcl-2[1].ZX-29 (30-300 nM; 24 hours; NCI-H2228 cells) treatment significantly down-regulates the expression of p-ALK and its downstream signaling proteins, including p-Akt and p-STAT3, in a dose-dependent manner[1].ZX-29 (20 nM; 0-48 hours; NCI-H2228 cells) treatment significantly increases the mRNA level of CHOP[1].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[1]. ZX-29 (50 mg/kg; intragastric administration; every 2 days; for a total of 7 times; female BALB/c nude mice) treatment suppresses tumor growth in a mouse xenograft model[1].
References
[1]. Gou W, et al. 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 Mar 26;1867(7):118712.
ZX-29 Preparation Products And Raw materials
Raw materials
Preparation Products
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