This study investigates the anticancer cytotoxic mechanism of action of benzoyloxy‐ethyl‐carbamic acid (BECA) produced by Streptomyces globosus VITLGK011. Flow cytometry analysis confirmed that BECA (at IC50: 3.12 µg/ml) treatment for 24 h induced apoptosis in 60% of cells. Schrodinger Maestro tools such as QikProp and DFT were used to confirm that BECA is an eligible drug‐like molecule, with suitable physiochemical properties. Glide XP tool was used to perform induced‐fit docking between BECA and 30 cancer drug target proteins. The highest significance was observed for VEGFR2 protein (−6.7 kcal/mol). GROMACS tool was used to perform molecular dynamic simulation between BECA and VEGFR2 protein for 40 ns. Root mean square deviation, root mean square fluctuation, H‐bond, and trajectory analysis, confirmed that BECA is a suitable inhibitor of VEGFR2 protein. Results conclude that BECA is a valid VEGFR2 inhibitor, and it thus exerts the observed anticancer cytotoxicity against MCF‐7 cells.

中文翻译：

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海洋球状链霉菌 VITLGK011 衍生化合物 BECA 靶向 VEGFR2 蛋白：体外和计算机分析

本研究调查了由球形链霉菌 VITLGK011 产生的苯甲酰氧基乙基氨基甲酸 (BECA) 的抗癌细胞毒作用机制。流式细胞术分析证实 BECA（IC50：3.12 µg/ml）处理 24 小时可诱导 60% 的细胞凋亡。Schrodinger Maestro 工具如 QikProp 和 DFT 被用于确认 BECA 是一种合格的类药物分子，具有合适的理化特性。Glide XP 工具用于在 BECA 和 30 种癌症药物靶蛋白之间进行诱导拟合对接。观察到 VEGFR2 蛋白的最高显着性（-6.7 kcal/mol）。GROMACS 工具用于进行 BECA 和 VEGFR2 蛋白之间的分子动力学模拟 40 ns。均方根偏差、均方根波动、氢键和轨迹分析，证实 BECA 是一种合适的 VEGFR2 蛋白抑制剂。结果得出结论，BECA 是一种有效的 VEGFR2 抑制剂，因此它对 MCF-7 细胞发挥了观察到的抗癌细胞毒性。