37466-89-0Relevant articles and documents
Ni@Pd core-shell nanoparticles immobilized on yolk-shell Fe 3O4@polyaniline composites as a highly efficient, magnetically separable and atom-economical catalyst for reduction of nitrobenzenes
Nabid, Mohammad Reza,Bide, Yasamin,Ghalavand, Nastaran,Niknezhad, Mahvash
, p. 389 - 395 (2014)
The preparation of Ni@Pd core-shell nanoparticles immobilized on yolk-shell Fe3O4@polyaniline composites is reported. Fe 3O4 nanoclusters were first synthesized through the solvothermal method and then the SiOs
Design, Synthesis, Biological Evaluation, and Molecular Modeling of 2-Difluoromethylbenzimidazole Derivatives as Potential PI3Kα Inhibitors
Wang, Xiangcong,Wang, Zhonghua,Wu, Fanhong,Wu, Zhongshan,Yu, Yanyan,Zhang, Moxuan,Zhu, Ranran
, (2022/01/13)
PI3Kα is one of the potential targets for novel anticancer drugs. In this study, a series of 2-difluoromethylbenzimidazole derivatives were studied based on the combination of molecular modeling techniques 3D-QSAR, molecular docking, and molecular dynamic
Overcoming imatinib resistance in chronic myelogenous leukemia cells using non-cytotoxic cell death modulators
Schoepf, Anna M.,Salcher, Stefan,Obexer, Petra,Gust, Ronald
supporting information, (2019/10/22)
Recent studies examined the possibility to overcome imatinib resistance in chronic myeloid leukemia (CML) patients by combination therapy with peroxisome proliferator-activated receptor gamma (PPARγ) ligands. Pioglitazone, a full PPARγ agonist, improved the survival of patients by the gradual elimination of the residual CML stem cell pool. To evaluate the importance of the pharmacological profile of PPARγ agonists on the ability to circumvent resistance, the partial PPARγ agonist 4‘-((2-propyl-1H-benzo[d]imidazol-1-yl)methyl)-[1,1’-biphenyl]-2-carboxylic acid, derived from telmisartan, and other related derivatives were investigated. The 4-substituted benzimidazole derivatives bearing a [1,1′-biphenyl]-2-carboxamide moiety sensitized K562-resistant cells to imatinib treatment. Especially the derivatives 18a-f, which did not activate PPARγ to more than 40% at 10 μM, retrieved the cytotoxicity of imatinib in these cells. The cell death modulating properties were higher than that of pioglitazone. It is of interest to note that all novel compounds were not cytotoxic neither on non-resistant nor on resistant cells. They exerted antitumor potency only in combination with imatinib.