| Name | ZX-29 |
| Description | ZX-29 is a potent and selective inhibitor of ALK with IC50 values of 2.1 nM, 1.3 nM, and 3.9 nM for ALK, ALK [L1196M], and ALK [G1202R] mutations, respectively. It also induces protective autophagy and exhibits antitumor effects. |
| 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[1]. |
| In vivo | In a mouse xenograft model, ZX-29 treatment suppresses tumor growth[1]. |
| Storage | Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice. |
| Solubility Information | DMSO : 42.5 mg/mL (82.04 mM)
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| Keywords | arrest | antitumor | ZX29 | Resistance | ZX-29 | Anaplastic lymphoma kinase | Bcl-2 | Apoptosis | Inhibitor | CD246 | p-Akt | caspase-3 | endoplasmic | inhibit | CHOP | Anaplastic lymphoma kinase (ALK) | ALK tyrosine kinase receptor | ERS | Cluster of differentiation 246 | Autophagy | reticulum | p-STAT3 | ZX 29 |
| Inhibitors Related | Alectinib hydrochloride | Lorlatinib | SB-431542 | DMH-1 | RepSox | Crizotinib | Vactosertib | Ceritinib | LDN-193189 2HCl | Brigatinib | A 83-01 | ALK-IN-1 |
| Related Compound Libraries | Bioactive Compound Library | Membrane Protein-targeted Compound Library | Tyrosine Kinase Inhibitor Library | Kinase Inhibitor Library | Angiogenesis related Compound Library | Inhibitor Library | Anti-Aging Compound Library | Bioactive Compounds Library Max | Anti-Cancer Compound Library | Anti-Cancer Active Compound Library |
United States
