ZX-29 是一种选择性ALK抑制剂，对ALK、ALK L1196M和ALK G1202R的IC50分别为 2.1 nM、1.3 nM 和 3.9 nM。它还可诱导保护性自噬并具有抗肿瘤作用。它通过诱导内质网应激来诱导细胞凋亡，并克服了由ALK突变引起的细胞抗性。

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.

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 a mouse xenograft model, ZX-29 treatment suppresses tumor growth[1].

2254805-62-2

C23H28ClN7O3S

518.03

DMSO:42.5 mg/mL (82.04 mM)
Powder: -20°C for 3 years
In solvent: -80°C for 2 years