882408-16-4

Upstream product

• 630125-84-7 N-(4-bromomethyl-3-trifluoromethylphenyl)-2,2,2-trifluoroacetamide 
• 1408000-40-7 tert-butyl N-[4-(bromomethyl)-3-(trifluoromethyl)phenyl]carbamate 
• 1408000-39-4 tert-butyl N-[4-methyl-3-(trifluoromethyl)phenyl]carbamate 
• 65934-74-9 3-(trifluoromethyl)-4-methylaniline 

Downstream Products

• 882408-06-2 [4-(1-pyrrolidinylmethyl)-3-(trifluoromethyl)phenyl]carbamic acid phenyl ester 
• 1408000-41-8 3-azido-4-methyl-N-(4-(pyrrolidin-1-ylmethyl)-3-(trifluoromethyl)phenyl)benzamide 

Relevant academic research and scientific papers

ISOQUINOLINE DERIVATIVES AND PHARMACEUTICAL COMPOSITIONS THEREOF FOR THE TREATMENT OF DISEASES

The present invention discloses compounds according to Formula (I) wherein R1, R2, R3, L1, L2, and L3 are as defined herein. The present invention relates to compounds inhibiting discoidin domain receptors (DDRs), methods for their production, pharmaceutical compositions comprising the same, and methods of treatment using the same, for the prophylaxis and/or treatment of fibrotic diseases, inflammatory diseases, respiratory diseases, autoimmune diseases, metabolic diseases, cardiovascular diseases, and/or proliferative diseases by administering a compound of the invention.

Design and Development of a Series of Potent and Selective Type II Inhibitors of CDK8

Using Sorafenib as a starting point, a series of potent and selective inhibitors of CDK8 was developed. When cocrystallized with CDK8 and cyclin C, these compounds exhibit a Type-II (DMG-out) binding mode.

Design, synthesis, and biological evaluation of 3-(1H-1,2,3-triazol-1-yl) benzamide derivatives as potent pan Bcr-Abl inhibitors including the threonine315←isoleucine315 mutant

A series of 3-(1H-1,2,3-triazol-1-yl)benzamide derivatives were designed and synthesized as new Bcr-Abl inhibitors by using combinational strategies of bioisosteric replacement, scaffold hopping, and conformational constraint. The compounds displayed significant inhibition against a broad spectrum of Bcr-Abl mutants including the gatekeeper T315I and p-loop mutations, which are associated with disease progression in CML. The most potent compounds 6q and 6qo strongly inhibited the kinase activities of Bcr-AblWT and Bcr-AblT315I with IC50 values of 0.60, 0.36 and 1.12, 0.98 nM, respectively. They also potently suppressed the proliferation of K562, KU812 human CML cells, and a panel of murine Ba/F3 cells ectopically expressing either Bcr-AblWT or any of a panel of other Bcr-Abl mutants that have been shown to contribute to clinical acquired resistance, including Bcr-AblT315I, with IC50 values in low nanomolar ranges. These compounds may serve as lead compounds for further development of new Bcr-Abl inhibitors capable of overcoming clinical acquired resistance against imatinib.