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Novel anticancer effect of substituted imidazole derivatives against urothelial carcinoma: integrating In vitro screening and molecular docking for target kinases
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Novel anticancer effect of substituted imidazole derivatives against urothelial carcinoma: integrating In vitro screening and molecular docking for target kinases
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Journal Article
Novel anticancer effect of substituted imidazole derivatives against urothelial carcinoma: integrating In vitro screening and molecular docking for target kinases
2025
Overview
Four novel substituted imidazole derivatives—5a (Kim-161), 5b (Kim-111), 5c (Kim-261), and 5d (Kim-231) were evaluated for their antiproliferative activity against urothelial carcinoma. Among these, the two derivatives Kim-161 (5a) and Kim-111 (5b) demonstrated potent cytotoxicity against the T24 transitional carcinoma cell line, with IC
50
values of 56.11 µM and 67.29 µM, respectively, as determined by MTT assay. Further mechanistic investigations revealed that these compounds modulate key pathways involved in cancer progression including cell cycle regulation; (p53), oncogenic signaling (Kras), cell apoptosis; (BAX and caspase 3), inflammatory response (Interleukin 6 (IL6), Tumor Necrosis Factor alpha (TNFα), and Nuclear Factor kappa B (NF-κB), autophagy regulation (phosphoinositide 3-kinase signaling (PIK3CA) and its targets protein kinase Akt and mammalian target of rapamycin (mTOR) and metastasis (Matrix metalloproteinase-9 (MMP-9)). Molecular docking and dynamic simulations against key cancer targets PTK6, FLT3, and BCL-2 revealed exceptional binding affinity and stable protein-ligand complexes. Furthermore, these compounds exhibited favorable drug-like properties, including optimal physicochemical and pharmacokinetic profiles. This integrated approach, combining the in vitro validation and computational modeling, places Kim-161 and Kim-111 as promising lead compounds for targeted urothelial carcinoma therapy. The findings underscore the therapeutic potential of dual kinase/tubulin inhibition in combating aggressive malignancies, offering a robust foundation for further preclinical development.
Publisher
BioMed Central,BioMed Central Ltd,Springer Nature B.V,BMC
Subject
/ Antineoplastic Agents - chemistry
/ Antineoplastic Agents - pharmacology
/ Biomedical and Life Sciences
/ Carcinoma, Transitional Cell - drug therapy
/ Carcinoma, Transitional Cell - metabolism
/ Carcinoma, Transitional Cell - pathology
/ Cell Proliferation - drug effects
/ Design
/ Drug Screening Assays, Antitumor
/ Health Promotion and Disease Prevention
/ Humans
/ Kinases
/ Molecular Docking Simulation
/ NMR
/ Oncology
/ Protein Kinase Inhibitors - chemistry
/ Protein Kinase Inhibitors - pharmacology
/ Signal Transduction - drug effects
/ Toxicity
/ Tubulin
/ Urinary Bladder Neoplasms - drug therapy
