1408000-19-0

Basic information

• Product Name: C₂₆H₁₉F₃N₁₀O
• CAS NO: 1408000-19-0
• Molecular Weight: 544.498
• Mol File: 1408000-19-0.mol

Chemical Properties

• CAS DataBase Reference: C₂₆H₁₉F₃N₁₀O(CAS DataBase Reference)
• NIST Chemistry Reference: C₂₆H₁₉F₃N₁₀O(1408000-19-0)
• EPA Substance Registry System: C₂₆H₁₉F₃N₁₀O(1408000-19-0)

Safety Data

• Hazardous Substances Data: 1408000-19-0(Hazardous Substances Data)

Upstream product

• 875781-17-2 5-bromo-7-azaindazole 
• 54962-75-3 [3-bromo-5-(trifluoromethyl)phenyl]amine 
• 1207351-15-2 5-ethynyl-1H-pyrazolo[3,4-b]pyridine 
• 1408000-54-3 3-azido-4-methyl-N-(3-(3-methyl-1H-1,2,4-triazol-1-yl)-5-(trifluoromethyl)phenyl)benzamide 
• 18595-18-1 3-amino-4-methyl benzoic acid methyl ester 
• 1207351-08-3 5-((trimethylsilyl) ethynyl)-1H-pyrazolo[3,4-b]pyridine 
• 855304-57-3 methyl 3-azido-4-methylbenzoate 
• 1290090-15-1 C₁₀H₉F₃N₄ 

Relevant articles and documents

Heterocyclic benzoyl amide compounds, medicinal composition and use thereof

The invention discloses heterocyclic benzamide compounds with structural characteristics of formula (1) or pharmaceutically acceptable salts or steric isomers or prodrug molecules thereof. The heterocyclic benzamide compounds as well as pharmaceutically acceptable salts thereof can effectively restrain growth of a plurality of tumor cells, can generate inhibiting effect to proteases such as BCR-ABL, c-Kit and PDGFR, can be used for preparing anti-tumor drugs and can be used for overcoming existing drug (Gleevec)-induced drug resistance.

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.