22889-08-3

Basic information

• Product Name: 2-((1H-benzo[d]imidazol-2-yl)thio)-1-(thiophen-2-yl)ethan-1-one
• Synonyms: 2-((1H-benzo[d]imidazol-2-yl)thio)-1-(thiophen-2-yl)ethan-1-one
• CAS NO: 22889-08-3
• Molecular Formula: C13H10N2OS2
• Molecular Weight: 274.3613
• Mol File: 22889-08-3.mol
• Article Data: 2

Chemical Properties

• Appearance: /
• CAS DataBase Reference: 2-((1H-benzo[d]imidazol-2-yl)thio)-1-(thiophen-2-yl)ethan-1-one(CAS DataBase Reference)
• NIST Chemistry Reference: 2-((1H-benzo[d]imidazol-2-yl)thio)-1-(thiophen-2-yl)ethan-1-one(22889-08-3)
• EPA Substance Registry System: 2-((1H-benzo[d]imidazol-2-yl)thio)-1-(thiophen-2-yl)ethan-1-one(22889-08-3)

Safety Data

• Hazardous Substances Data: 22889-08-3(Hazardous Substances Data)

Upstream product

• 88-15-3 2-Acetylthiophene 
• 134469-07-1 Benzimidazol-2-thiol 
• 95-54-5 1,2-diamino-benzene 
• 10531-41-6 2-Bromoacetylthiophene 

Relevant articles and documents

Synthesis, crystal study, and anti-proliferative activity of some 2-benzimidazolylthioacetophenones towards triple-negative breast cancer MDA-MB-468 cells as apoptosis-inducing agents

On account of its poor prognosis and deficiency of therapeutic stratifications, triple negative breast cancer continues to form the causative platform of an incommensurate number of breast cancer deaths. Aiming at the development of potent anticancer agents as a continuum of our previous efforts, a novel series of 2-((benzimidazol-2-yl)thio)-1-arylethan-1-ones 5a–w was synthesized and evaluated for its anti-proliferative activity towards triple negative breast cancer (TNBC) MDA-MB-468 cells. Compound 5k was the most active analog against MDA-MB-468 (IC50 = 19.90 ± 1.37 μM), with 2.1-fold increased activity compared to 5-fluorouracil (IC50 = 41.26 ± 3.77 μM). Compound 5k was able to induce apoptosis in MDA-MB-468, as evidenced by the marked boosting in the percentage of florecsein isothiocyanate annexin V (Annexin V–FITC)-positive apoptotic cells (upper right (UR) + lower right (LR)) by 2.8-fold in comparison to control accompanied by significant increase in the proportion of cells at pre-G1 (the first gap phase) by 8.13-fold in the cell-cycle analysis. Moreover, a quantitative structure activity relationship (QSAR) model was established to investigate the structural requirements orchestrating the anti-proliferative activity. Finally, we established a theoretical kinetic study.