109811-95-2

Upstream product

• 15813-09-9 4,5-diiodo-1H-imidazole 
• 5720-06-9 2-Methoxyphenylboronic acid 
• 135-02-4 ortho-anisaldehyde 
• 6706-96-3 2,2'-dimethoxybenzoin 
• 77287-34-4 formamide 

Downstream Products

• 1349703-39-4 1-ethyl-4,5-bis(2-methoxyphenyl)-1H-imidazole 
• 1349703-41-8 1,3-diethyl-4,5-bis(2-methoxyphenyl)-1H-imidazol-3-ium bromide 

Relevant academic research and scientific papers

A three-way switchable process for suzuki cross-coupling, hydrodehalogenation, or an assisted tandem hydrodehalogenation and suzuki cross-coupling sequence

A three-way switchable Pd-catalyzed and microwave assisted process appropriate for selective arylation or hydrodehalogenation of the imidazole backbone was discovered and entirely optimized. The "arylation switch position" was adapted and optimized for the synthesis of 4,5-diaryl-1H-imidazoles, while the "hydrodehalogenation switch position" was used for the preparation of 4(5)-iodo-1H-imidazole. The hydrodehalogenation and the cross-coupling reactions were also successfully combined in "the third switch position" that performs an assisted tandem reaction sequence that produced 4(5)-aryl-1H-imidazole. All of the three pathways produced their corresponding products in excellent yield. Copyright

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)