25433-10-7

Basic information

• Product Name: 1H-Imidazole, 2-(methylthio)-4-phenyl-
• Synonyms: 1H-Imidazole,2-(methylthio)-4-phenyl;2-Methylthio-4-phenylimidazol;2-Mercaptomethyl-4-phenyl-imidazol;2-Methylmercapto-4-phenyl-1(3)H-imidazol;2-(methylsulfanyl)-4-phenyl-1H-imidazole;2-methylsulfanyl-4-phenyl-1(3)H-imidazole;2-Methylmercapto-4-phenyl-imidazol
• CAS NO: 25433-10-7
• Molecular Formula: C10H10N2S
• Molecular Weight: 190.26500
• Mol File: 25433-10-7.mol
• Article Data: 2

Chemical Properties

• CAS DataBase Reference: 1H-Imidazole, 2-(methylthio)-4-phenyl-(CAS DataBase Reference)
• NIST Chemistry Reference: 1H-Imidazole, 2-(methylthio)-4-phenyl-(25433-10-7)
• EPA Substance Registry System: 1H-Imidazole, 2-(methylthio)-4-phenyl-(25433-10-7)

Safety Data

• Hazardous Substances Data: 25433-10-7(Hazardous Substances Data)

Usage

Heterocyclic organic compound

contains an imidazole ring with a methylthio group and a phenyl group attached to it

Common uses

Organic synthesis and pharmaceutical research

Biological activity

Potential antimicrobial and antifungal properties

Potential applications

Development of novel drugs and therapeutic agents

Upstream product

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Relevant articles and documents

Trisubstituted Pyridinylimidazoles as Potent Inhibitors of the Clinically Resistant L858R/T790M/C797S EGFR Mutant: Targeting of Both Hydrophobic Regions and the Phosphate Binding Site

Inhibition of the epidermal growth factor receptor represents one of the most promising strategies in the treatment of lung cancer. Acquired resistance compromises the clinical efficacy of EGFR inhibitors during long-term treatment. The recently discovered EGFR-C797S mutation causes resistance against third-generation EGFR inhibitors. Here we present a rational approach based on extending the inhibition profile of a p38 MAP kinase inhibitor toward mutant EGFR inhibition. We used a privileged scaffold with proven cellular potency as well as in vivo efficacy and low toxicity. Guided by molecular modeling, we synthesized and studied the structure-activity relationship of 40 compounds against clinically relevant EGFR mutants. We successfully improved the cellular EGFR inhibition down to the low nanomolar range with covalently binding inhibitors against a gefitinib resistant T790M mutant cell line. We identified additional noncovalent interactions, which allowed us to develop metabolically stable inhibitors with high activities against the osimertinib resistant L858R/T790M/C797S mutant.