68163-71-3

Basic information

• Product Name: 4,5-BIS-(P-FLUOROPHENYL)IMIDAZOLE
• Synonyms: 4,5-BIS-(P-FLUOROPHENYL)IMIDAZOLE
• CAS NO: 68163-71-3
• Molecular Formula: C₁₅H₁₀F₂N₂
• Molecular Weight: 256.2501064
• Mol File: 68163-71-3.mol
• Article Data: 6

Chemical Properties

• Appearance: /
• CAS DataBase Reference: 4,5-BIS-(P-FLUOROPHENYL)IMIDAZOLE(CAS DataBase Reference)
• NIST Chemistry Reference: 4,5-BIS-(P-FLUOROPHENYL)IMIDAZOLE(68163-71-3)
• EPA Substance Registry System: 4,5-BIS-(P-FLUOROPHENYL)IMIDAZOLE(68163-71-3)

Safety Data

• Hazardous Substances Data: 68163-71-3(Hazardous Substances Data)

Upstream product

• 459-57-4 4-fluorobenzaldehyde 
• 53458-16-5 1,2-bis(4-fluorophenyl)-2-hydroxyethan-1-one 
• 77287-34-4 formamide 

Downstream Products

• 1349703-55-4 1-ethyl-4,5-bis(4-fluorophenyl)-1H-imidazole 
• 1349703-48-5 1,3-diethyl-4,5-bis(4-fluorophenyl)-1H-imidazolium bromide 
• 1349703-50-9 3-benzyl-1-ethyl-4,5-bis(4-fluorophenyl)-1H-imidazolium chloride 
• 74767-58-1 1-(tetrahydropyran-2-yl)-4,5-bis(4-fluorophenyl)imidazole 
• 68163-73-5 1-benzenesulfonyl-4,5-bis-(4-fluoro-phenyl)-1H-imidazole 
• 96226-00-5 2-Bromo-4,5-bis(4-fluorophenyl)-1H-imidazole, Hydrobromide 
• 139981-69-4 4-Fluoro-N-[2-(4-fluoro-phenyl)-3-methyl-5,5-bis-trifluoromethyl-3,5-dihydro-imidazol-(4Z)-ylidene]-benzamide 
• 81659-38-3 α,α-bis(trifluoromethyl)-4,5-bis(4-fluorophenyl)-1-methyl-1H-imidazole-2-methanamine 
• 178553-80-5 4,5-Bis-(4-fluoro-phenyl)-1-methyl-1H-imidazole 

Relevant articles and documents

Synthesis and in vitro anticancer activities of selenium N-heterocyclic carbene compounds

Fourteen novel selenium N-heterocyclic carbene (Se-NHC) compounds derived from 4,5-diarylimidazole were designed, synthesized, and evaluated as antiproliferative agents. Most of them were more effective toward A2780 ovarian cancer cells than HepG2 hepatocellular carcinoma cells. Among them, the most active compound 2b was about fourfold more active than the positive control ebselen against A2780 cells. In addition, this compound displayed twofold higher cytotoxicity to A2780 cells than to IOSE80 normal ovarian epithelial cells. Further studies revealed that 2b could induce reactive oxygen species production, damage mitochondrial membrane potential, block the cells in the G0/G1 phase, and finally promote A2780 cell apoptosis.

A new rhodium(I) NHC complex inhibits TrxR: In vitro cytotoxicity and in vivo hepatocellular carcinoma suppression

Thioredoxin reductase (TrxR) is often overexpressed in different types of cancer cells including hepatocellular carcinoma (HCC) cells and regarded as a target with great promise for anticancer drug research and development. Here, we have synthesized and characterized nine new designed rhodium(I) N-heterocyclic carbene (NHC) complexes. All of them were effective towards cancer cells, especially complex 1e was more active than cisplatin and manifested strong antiproliferative activity against HCC cells. In vivo anticancer studies showed that 1e significantly repressed tumor growth in an HCC nude mouse model and ameliorated liver lesions in a chronic HCC model caused by CCl4. Notably, a mechanistic study revealed that 1e can strongly inhibit TrxR system both in vitro and in vivo. Furthermore, 1e promoted intracellular ROS accumulation, damaged mitochondrial membrane potential, promoted cancer cell apoptosis and blocked the cells in the G1 phase.

NHC gold halide complexes derived from 4,5-diarylimidazoles: Synthesis, structural analysis, and pharmacological investigations as potential antitumor agents

A series of novel neutral NHC gold halide complexes derived from 4,5-diarylimidazoles were synthesized, characterized, and analyzed for biological effects. High growth inhibitory effects in MCF-7 and MDA-MB 231 breast cancer as well as HT-29 colon cancer cell lines depended on the presence of the C4,C5-standing aromatic rings. Methoxy groups at these rings did not change the growth inhibitory properties, while F-substituents in the ortho-position (5d) increased the activity in MCF-7 and MDA-MB 231 cells. The substituents at the nitrogen atoms and the oxidation state of the metal play a subordinate role. The most active bromo[1,3-diethyl-4,5-bis(2-fluorophenyl)-1,3- dihydro-2H-imidazol-2-ylidene]gold(I) (5d) was distinctly more active than cisplatin. All complexes caused thioredoxin reductase (TrxR) inhibition (EC 50 = 374-1505 nM) distinctly lower than auranofin (EC50 = 18.6 nM) excluding this enzyme as main target. Because of the low nuclear content, a participation of DNA interaction on the mode of action is very unlikely. The missing ER binding and the missing correlation of growth inhibition and inactivation of COX enzymes exclude these targets, too. (Figure presented)