22397-48-4

Basic information

• Product Name: 1H-Imidazole, 4,5-bis(4-methoxyphenyl)-
• CAS NO: 22397-48-4
• Molecular Formula: C17H16N2O2
• Molecular Weight: 280.326
• Mol File: 22397-48-4.mol
• Article Data: 13

Chemical Properties

• CAS DataBase Reference: 1H-Imidazole, 4,5-bis(4-methoxyphenyl)-(CAS DataBase Reference)
• NIST Chemistry Reference: 1H-Imidazole, 4,5-bis(4-methoxyphenyl)-(22397-48-4)
• EPA Substance Registry System: 1H-Imidazole, 4,5-bis(4-methoxyphenyl)-(22397-48-4)

Safety Data

• Hazardous Substances Data: 22397-48-4(Hazardous Substances Data)

Upstream product

• 119-52-8 4,4'-dimethoxybenzoin 
• 77287-34-4 formamide 
• 57-13-6 urea 
• 50-00-0 formaldehyd 
• 1226-42-2 1,2-bis(4-methoxyphenyl)-1,2-ethanedione 
• 15813-09-9 4,5-diiodo-1H-imidazole 
• 5720-07-0 4-methoxyphenylboronic acid 
• 123-11-5 4-methoxy-benzaldehyde 
• 100-97-0 hexamethylenetetramine 

Downstream Products

• 18874-84-5 1-benzyl-4,5-bis-(4-methoxy-phenyl)-1H-imidazole 
• 3360-48-3 4,5-bis(4-methoxyphenyl)-1-methyl-1H-imidazole 
• 1309775-99-2 1-(2-phenyl-2-oxoethyl)-2-benzoyl-4,5-di(4-methoxyphenyl)imidazole 
• 1309776-00-8 1-(2-(4-methoxyphenyl)-2-oxoethyl)-2-benzoyl-4,5-di(4-methoxyphenyl)imidazole 
• 1309776-35-9 2,3-di(4-methoxyphenyl)-6,8-diphenylimidazo[1,2-a]pyrazine 
• 1309776-36-0 2,3,6-tri(4-methoxyphenyl)-8-phenylimidazo[1,2-a]pyrazine 
• 117215-39-1 (4,5-bis(4-methoxyphenyl)-1H-imidazol-2-yl)(phenyl)methanone 
• 117215-49-3 C₂₄H₁₉ClN₂O₃ 
• 110032-88-7 C₂₅H₂₂N₂O₄ 
• 3363-51-7 1-ethyl-4,5-bis(4-methoxyphenyl)-1H-imidazole 
• 1349703-45-2 1,3-diethyl-4,5-bis(4-methoxyphenyl)-1H-imidazolium bromide 
• 1349703-49-6 1,3-diethyl-4,5-bis(4-hydroxyphenyl)-1H-imidazolium bromide 
• 1393109-22-2 bis[1-ethyl-4,5-bis(4-methoxyphenyl)-1H-imidazol-2-yl]methanone 
• 1393109-24-4 bis[1-ethyl-4,5-bis(4-methoxyphenyl)-1H-imidazol-2-yl]methane 

Relevant articles and documents

Design, synthesis and analgesic/anti-inflammatory evaluation of novel diarylthiazole and diarylimidazole derivatives towards selective COX-1 inhibitors with better gastric profile

The inhibition of gastric cyclooxygenase 1 (COX-1) enzyme was believed to be the major cause of non-steroidal anti-inflammatory drugs (NSAIDs)-induced gastric ulcer. Recent studies disproved this belief and showed that the gastric tissues vulnerability is not solely connected to COX-1 inhibition. This work aimed at exploring and rationalizing the differential analgesic and anti-inflammatory activities of novel selective COX-1 inhibitors with improved gastric profile. Two novel series of 4,5-diarylthiazole and diarylimidazole were designed, synthesized in analogy to selective COX-1 inhibitors (mofezolac and FR122047) which lack gastric damaging effects. The new compounds were evaluated in vitro for their COXs inhibitory activity and in vivo for their anti-inflammatory and analgesic potentials. Four compounds; diphenylthiazole glycine derivatives (15a, 15b) and diphenylimidazolo acetic acid derivatives (19a, 19b), which possess carboxylic acid group exhibited significant activity and selectivity against COX-1 over COX-2. Of these compounds, (4,5-bis(4-methoxyphenyl)thiazol-2-yl)glycine 15b was the most potent compound against COX-1 with an inhibitory half maximal concentration (IC50) of 0.32 μM and a selectivity index (COX-2 IC50/COX-1 IC50) of 28.84. Furthermore, an ulcerogenicity study was performed where the tested compounds demonstrated a significant gastric tolerance. Interestingly, the most selective COX-1 inhibitor showed higher analgesic activity in vivo as expected compared to their moderate anti-inflammatory activity. This study underscores the need for further design and development of novel analgesic agents with low tendency to cause gastric damage based on improving their COX-1 affinity and selectivity profile.

Application of N-heterocyclic carbene selenium-gold compound in preparation of carbapenem-resistant acinetobacter baumannii drug

The invention discloses application of an N-heterocyclic carbene selenium-gold compound in preparation of a novel antibacterial drug resistant to carbapenem acinetobacter baumannii infection, and belongs to the technical field of drug preparation. According to the N-heterocyclic carbene selenium-gold compound, selenium-containing imidazole N-heterocyclic carbene selenium is used for replacing a thiosaccharide ligand in a gold nofen structure; the reaction activity of Au-Se in the N-heterocyclic carbene selenium-gold compound is higher than that of an Au-S bond, so that the Au-S bond in a Jinnofen structure can be prevented from being easily damaged by reducing mercaptan to a certain extent; and toxic and side effects are caused by metabolism before reaching a target spot. In-vitro antibacterial activity shows that IC50 of the compounds H7 and H8 in inhibition of carbapenem-resistant acinetobacter baumannii is 3.34 mu M and 4.67 mu M, MIC of the same are both 10 mu M, and MBC of the same are both 20 mu M. The animal in-vivo administration also shows a good anti-drug-resistant bacterium effect, which proves that the compound can significantly prolong the survival time of mice infected by drug-resistant bacteria, and has important practical application value.

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.