合成了可光诱导细胞毒性的铂(IV)前药cis,cis,trans-[Pt(NH3)2Cl2(biotin)(L)] (1)，源自顺铂，其中HL是PEG化的红光活性的二吡咯甲烷 (BODIPY) 配体。通过表征其结构并评估其光细胞毒性。在二甲基亚砜和杜氏磷酸盐缓冲盐水 (1 : 1 v/v, pH 7.2) 中，该配合物显示了一个近红外吸收带，在 653 nm (ε ∼9.19 × 104 M-1 cm-1)。在 DMSO 中以 630 nm 光激发时，呈现出在 677 nm 的发光带，其荧光量子产率为 0.13。通过1,3-二苯基异苯并呋喃滴定实验，获得的单线态氧量子产率 (ΦΔ) 约为 0.32。通过DNA 光解实验，揭示了单线态氧作为反应性氧自由基 (ROS)。荧光流式细胞术显示，与非癌细胞 Beas-2B 相比，在A549 癌细胞中具有较高的生物素和 PEG化的二苯乙烯-BODIPY 细胞内摄取，表明对癌细胞具有选择性。二氯二羟荧光素醋酸酯实验显示细胞内有 ROS 生成。共聚焦成像显示主要内化在线粒体中。该前药在癌细胞 A549 和耐多药 MDA-MB-231 细胞中表现出显著的光动力治疗 (PDT) 活性，具有高的光细胞毒性指数值 (半数抑制浓度 (IC50): 0.61-1.54 μM 在红光下)，而在黑暗条件下无毒性。化疗-PDT 活性在非肿瘤肺上皮细胞 (Beas-2B) 中显著较低。该前药有效地引发了细胞凋亡，通过Annexin V-FITC/丙间啶碘化物实验证实，并通过JC-1染料实验证实线粒体膜电位的改变。β-微管蛋白免疫荧光实验证实，将细胞与光处理的配合物共培养后，导致细胞骨架结构破裂和凋亡小体的形成。结果表明，该前药通过 DNA 损伤、线粒体功能减退和细胞骨架框架破坏引发细胞凋亡。

A platinum(IV) prodrug, cis,cis,trans-[Pt(NH3)2Cl2(biotin)(L)] (1), derived from cisplatin, where HL is the PEGylated red-light active boron-dipyrromethene (BODIPY) ligand, was synthesized, characterized and its photocytotoxicity evaluated. The complex showed a near-IR absorption band at 653 nm (ε ∼9.19 × 104 M-1 cm-1) in dimethyl sulfoxide and Dulbecco's phosphate-buffered saline (1 : 1 v/v) at pH 7.2. When excited at 630 nm, it showed an emission band at 677 nm in DMSO with a fluorescence quantum yield of 0.13. The 1,3-diphenylisobenzofuran titration experiment gave a singlet oxygen quantum yield (ΦΔ) of ∼0.32. A mechanistic DNA photocleavage study revealed singlet oxygen as the reactive oxygen species (ROS). The complex with biotin and PEGylated-distyryl-BODIPY showed significantly higher cellular uptake in A549 cancer cells as compared to non-cancerous Beas-2B cells from flow cytometry, indicating selectivity towards cancer cells. A dichlorodihydrofluorescein diacetate assay showed cellular ROS generation. Confocal images revealed predominant internalization in the mitochondria. The prodrug showed remarkable photodynamic therapy (PDT) activity in cancerous A549 and multidrug-resistant MDA-MB-231 cells with a high photocytotoxicity index value (half-maximal inhibitory concentration (IC50): 0.61-1.54 μM in red light), while being non-toxic in the dark. The chemo-PDT activity was significantly less in non-tumorigenic lung epithelial cells (Beas-2B). The prodrug effectively triggered cellular apoptosis, which was confirmed by the Annexin V-FITC/propidium iodide assay, and the alteration of the mitochondrial membrane potential was substantiated by the JC-1 dye assay. The β-tubulin immunofluorescence assay confirmed that incubating the cells with a light-treated complex resulted in the rapture of the cytoskeletal structure and the formation of apoptotic bodies. The results demonstrate that the prodrug triggered apoptosis via DNA damage, a reduction in mitochondrial function and disruption of the cytoskeletal framework.