合成了新型香豆素衍生物并测试了其对人类癌细胞（PC-3 和 MDA-MB-231）的细胞毒性。化合物 5、4b 和 4a 对 PC-3 细胞具有有效的细胞毒活性，IC50 分别为 3.56、8.99 和 10.22 µM。化合物 4c 在 MDA-MB-231 细胞中的细胞毒性高于厄洛替尼，IC50 为 8.5 µM。此外，化合物 5 对 EFGR 表现出有效的抑制活性，IC50 为 0.1812 µM，PI3Kβ 抑制活性比 LY294002 高出两倍，表明该化合物具有 EGFR 和 PI3Kβ 双重抑制活性。对接与体外结果一致，并揭示了双重靶向的分子机制。此外，化合物 5 降低了 PC-3 细胞中 AKT 和 m-TOR 的表达，表明它通过 EGFR/PI3K/Akt/m-TOR 信号通路特异性靶向这些细胞。同时，化合物 5 引起细胞周期停滞在 S 期，并诱导内在和外在凋亡途径的激活。

Novel coumarin derivatives were synthesised and tested for their cytotoxicity against human cancer cells (PC-3 and MDA-MB-231). Compounds 5, 4b, and 4a possessed potent cytotoxic activity against PC-3 cells with IC50 3.56, 8.99, and 10.22 µM, respectively. Compound 4c displayed cytotoxicity more than erlotinib in the MDA-MB-231 cells with IC50 8.5 µM. Moreover, compound 5 exhibited potent inhibitory activity on EFGR with IC50 0.1812 µM, as well as PI3Kβ inhibitory activity that was twofold higher than LY294002, suggesting that this compound has a dual EGFR and PI3Kβ inhibiting activity. Docking aligns with the in vitro results and sheds light on the molecular mechanisms underlying dual targeting. Furthermore, compound 5 decreased AKT and m-TOR expression in PC-3 cells, showing that it specifically targets these cells via the EGFR/PI3K/Akt/m-TOR signalling pathway. Simultaneously, compound 5 caused cell cycle arrest at S phase and induced activation of both intrinsic and extrinsic apoptotic pathways.