A new series of N-(2-(1H-benzo[d]imidazol-2-yl)phenyl) cinnamides was prepared and evaluated for their in vitro cytotoxic activity using various cancer cell lines viz. A549 (human non-small cell lung cancer), MDA-MB-231 (human triple negative breast cancer), B16-F10 (mouse melanoma), BT-474 (human breast cancer), and 4T1 (mouse triple negative breast cancer). In the series of tested compounds, 12h showed potent cytotoxic activity against non-small cell lung cancer cell line with IC₅₀ value of 0.29 ± 0.02 µM. The cytoxicity of most potent compound 12h was also tested on NRK-52E (normal rat kidney epithelial cell line) and showed less cytotoxicity compared to cancer cells. Tubulin polymerization assay indicated that the compound 12h was able to impede the cell division by inhibiting tubulin polymerization. Moreover, molecular docking study also suggested the binding of 12h at the colchicine-binding site of the tubulin protein. Cell cycle analysis revealed that the compound 12h arrests G2/M phase. In addition, 12h induced apoptosis in A549 cell lines was evaluated by various staining studies like acridine orange, DAPI, analysis of mitochondrial membrane potential, annexin V-FITC, and DCFDA assays.

制备了一系列新的N-（2-（1 H-苯并[ d ]咪唑-2-基）苯基）肉桂酸酯，并使用多种癌细胞系评估了它们的体外细胞毒性活性。A549（人类非小细胞肺癌），MDA-MB-231（人类三阴性乳腺癌），B16-F10（小鼠黑色素瘤），BT-474（人类乳腺癌）和4T1（小鼠三阴性乳腺癌） 。在一系列测试的化合物中，12h对非小细胞肺癌细胞系表现出有效的细胞毒活性，IC ₅₀值为0.29±0.02 µM。最有效的化合物12h的细胞毒性还对NRK-52E（正常大鼠肾上皮细胞系）进行了测试，与癌细胞相比，其细胞毒性更低。微管蛋白聚合测定表明化合物12h能够通过抑制微管蛋白聚合来阻止细胞分裂。此外，分子对接研究还表明在微管蛋白的秋水仙碱结合位点结合了12h。细胞周期分析表明，化合物12h阻滞了G2 / M期。此外，通过各种染色研究（如a啶橙，DAPI，线粒体膜电位分析，膜联蛋白V - FITC和DCFDA分析）评估了A549细胞系在12h诱导的凋亡。