1440754-07-3

Usage

General Description

1-Piperidinecarboxylic acid, 4-[1-(2-phenyl-1H-benziMidazol-1-yl)-2-[4-[1-(phenylMethyl)-1H-benziMidazol-2-yl]phenoxy]ethyl]-, 1,1-diMethylethyl ester is a chemical compound commonly known as Midazolam. It is a potent short-acting benzodiazepine drug used for sedation, anxiety, agitation, and muscle relaxation. 1-Piperidinecarboxylic acid, 4-[1-(2-phenyl-1H-benziMidazol-1-yl)-2-[4-[1-(phenylMethyl)-1H-benziMidazol-2-yl]phenoxy]ethyl]-, 1,1-diMethylethyl ester works by enhancing the effects of a certain natural chemical in the body (GABA). Midazolam is commonly used before medical procedures and surgery to relieve anxiety and induce drowsiness, and it is also used for the treatment of acute seizures and as a premedication for anesthesia. This chemical compound should be used under the guidance of a medical professional and with caution, as it can cause dizziness, drowsiness, and potential addiction or withdrawal symptoms with prolonged use.

Upstream product

• 1440753-63-8 tert-butyl 4-(2-(benzyl(tert-butoxycarbonyl)amino)-2-oxo-1-(2-phenyl-1H-benzo[d]imidazol-1-yl)ethyl)piperidine-1-carboxylate 
• 1440753-42-3 2-(4-(allyloxy)phenyl)-1-benzyl-1H-benzo[d]imidazole 
• 100-39-0 benzyl bromide 
• 1440753-74-1 tert-butyl 4-(2-hydroxy-1-(2-phenyl-1H-benzo[d]imidazol-1-yl)ethyl)piperidine-1-carboxylate 
• 10206-01-6 4-(1-benzyl-1H-benzo[d]imidazol-2-yl)phenol 
• 146651-75-4 tert–butyl (2–aminophenyl)carbamate 
• 65-85-0 benzoic acid 
• 40663-68-1 4-(2-propenyloxy)benzaldehyde 
• 137076-22-3 tert butyl 4-formylpiperidine-1-carboxylate 
• 95-54-5 1,2-diamino-benzene 
• 425365-62-4 2-(4-(allyloxy)phenyl)-1H-benzo[d]imidazole 

Relevant academic research and scientific papers

Structure guided design and kinetic analysis of highly potent benzimidazole inhibitors targeting the PDEδ prenyl binding site

K-Ras is one of the most frequently mutated signal transducing human oncogenes. Ras signaling activity requires correct cellular localization of the GTPase. The spatial organization of K-Ras is controlled by the prenyl binding protein PDEδ, which enhances Ras diffusion in the cytosol. Inhibition of the Ras-PDEδ interaction by small molecules impairs Ras localization and signaling. Here we describe in detail the identification and structure guided development of Ras-PDEδ inhibitors targeting the farnesyl binding pocket of PDEδ with nanomolar affinity. We report kinetic data that characterize the binding of the most potent small molecule ligands to PDEδ and prove their binding to endogenous PDEδ in cell lysates. The PDEδ inhibitors provide promising starting points for the establishment of new drug discovery programs aimed at cancers harboring oncogenic K-Ras.

Benzimidazoles for the treatment of cancer

The present invention relates to novel substituted benzimidazoles and stereoisomeric forms, prodrugs, solvates, hydrates and/or pharmaceutically acceptable salts of these compounds as well as pharmaceutical compositions containing at least one of these substituted benzimidazoles together with pharmaceutically acceptable carrier, excipient and/or diluents. Said novel substituted benzimidazoles binding to the prenyl binding pocket of PDEδ have been identified as useful for the prophylaxis and treatment of cancer by the inhibition of the binding of PDEδ to K-Ras and of oncogenic Ras signalling in cells by altering its localization leading to cell death or inhibition of proliferation.

BENZIMIDAZOLES FOR THE TREATMENT OF CANCER

The present invention relates to novel substituted benzimidazoles and stereoisomeric forms, prodrugs, solvates, hydrates and/or pharmaceutically acceptable salts of these compounds as well as pharmaceutical compositions containing at least one of these substituted benzimidazoles together with pharmaceutically acceptable carrier, excipient and/or diluents. Said novel substituted benzimidazoles binding to the prenyl binding pocket of PDEδ have been identified as useful for the prophylaxis and treatment of cancer by the inhibition of the binding of PDEδ to K-Ras and of oncogenic Ras signalling in cells by altering its localization leading to cell death or inhibition of proliferation.