953717-12-9

Basic information

• Product Name: N-(2-aminoethyl)-2-methylbenzamide
• Synonyms: N-(2-aminoethyl)-2-methylbenzamide
• CAS NO: 953717-12-9
• Molecular Formula: C₁₀H₁₄N₂O
• Molecular Weight: 178.24
• Mol File: 953717-12-9.mol

Chemical Properties

• Appearance: /
• CAS DataBase Reference: N-(2-aminoethyl)-2-methylbenzamide(CAS DataBase Reference)
• NIST Chemistry Reference: N-(2-aminoethyl)-2-methylbenzamide(953717-12-9)
• EPA Substance Registry System: N-(2-aminoethyl)-2-methylbenzamide(953717-12-9)

Safety Data

• Hazardous Substances Data: 953717-12-9(Hazardous Substances Data)

Upstream product

• 118-90-1 ortho-methylbenzoic acid 
• 107-15-3 ethylenediamine 

Downstream Products

• 1379000-54-0 C₂₀H₂₉N₃O₃ 

Relevant articles and documents

Expanding the structural diversity of Bcr-Abl inhibitors: Hybrid molecules based on GNF-2 and Imatinib

In order to expand the structural diversity of Bcr-Abl inhibitors, twenty hybrids (series E and P) have been synthesized and characterized based on Imatinib and GNF-2. Their biological activities were evaluated in vitro against human leukemia cells. Most compounds exhibited potent antiproliferative activity against K562 cells, especially for compounds E4, E5 and E7. Furthermore, these new hybrids were also screened for Abl kinase inhibitory activity, and some of them inhibited Abl kinase with low micromolar IC50 values. In particular, compound P3 displayed the most potent activity with IC50 value of 0.017 μM comparable with that of Imatinib. Molecular docking studies indicated that these novel hybrids fitted well with the active site of Bcr-Abl. These results suggested the great potential of these compounds as novel Bcr-Abl inhibitors.

Expanding the structural diversity of Bcr-Abl inhibitors: Dibenzoylpiperazin incorporated with 1 H -indazol-3-amine

A series of N,N'-dibenzoylpiperazine derivatives incorporated with 1H-indazol-3-amine have been designed, synthesized and evaluated as novel Bcr-Abl inhibitors. Several title compounds exhibited potent inhibitory activity against Bcr-Abl wild type as well as T315I mutant. Two compounds, 11a and 12c, strongly suppressed the activity of native and mutant Bcr-Abl. In particular, 11a exhibited comparable potency with that of Imatinib. It potently inhibited both Bcr-AblWT and Bcr-AblT315I with IC50 values of 0.014 μM and 0.45 μM, respectively. Furthermore, compound 11a also inhibited the proliferation of K562 leukemia cancer cells. Therefore, it could serve as promising lead compound for further optimization of Bcr-AblWT and Bcr-AblT315I inhibitors.