1430720-15-2

Upstream product

• 1446846-60-1 6-(2-ethoxyphenyl)benzo[d]thiazol-2-amine 
• 530-62-1 1,1'-carbonyldiimidazole 
• 156-87-6 propan-1-ol-3-amine 
• 213211-69-9 (2-ethoxyphenyl)boronic acid 
• 471240-50-3 2′-ethoxybiphenyl-3,4-diamine 
• 1575-37-7 4-Bromo-benzene-1,2-diamine 

Relevant academic research and scientific papers

Discovery of new benzothiazole-based inhibitors of breakpoint cluster region-abelson kinase including the T315i mutant

The existence of drug resistance caused by mutations in the break-point cluster region-Abelson tyrosine kinase (Bcr-Abl) kinase domain remains a clinical challenge due to limited effective treatment options for chronic myeloid leukemia (CML). Herein we report a novel series of benzothiazole-based inhibitors that are effective against wild-type and T315I mutant Bcr-Abl kinases. The original hit compound, nocodazole, was extensively modified through a structure-based drug design strategy, especially by varying the groups at the C2 and C6 positions of the scaffold. In addition, the introduction of water-solubilizing groups at the terminal ethyl group resulted in enhanced physicochemical properties and potency in cellular inhibition. Several compounds inhibited the kinase activity of both wild-type Bcr-Abl and the T315I mutant with IC50 values in the picomolar range and exhibited good antiproliferative effects on Ba/F3 cell lines transformed with either wild-type or T315I mutant Bcr-Abl.