Aiming at obtaining new copper complexes with good cytotoxicity against cancer cells, triphenylphosphine (TPP) was introduced to obtain insight into the influence of the co-ligands. In this paper, two copper complexes, Cu(2-pbmq)(CH₃OH)Br₂ (1) and [Cu(2-pbmq)(TPP)Br]₂ (2) were designed, synthesized, and characterized by X-ray crystallography, 2-((2-(pyrazin-2-yl)-1H-benzo[d]imidazol-1-yl)methyl))quinolone (2-pbmq), to investigate the influence of the TPP group on the anticancer activity of the metal complex. Although the presence of the TPP group diminished the intensity of the interaction properties of the complex with DNA, the in vitro anticancer activity and cellular uptake of the TPP-containing complex were markedly superior to those of its TPP-lacking counterpart. Detailed studies on the more potently cytotoxic complex 2 revealed that it accumulated in nucleus, arrested the cell cycle at the G0-G1 phase, causing mitochondrial dysfunction, involving the potential simultaneous mitochondrial membrane collapse, cellular ATP level depletion, and Ca²⁺ leakage, eventually inducing cell apoptosis. In summary, the introduction of a TPP group enhances the biological activity and cytotoxicity of the complex.

为了获得对癌细胞具有良好细胞毒性的新型铜配合物，引入了三苯膦（TPP）以深入了解共配体的影响。本文设计，合成并表征了两种铜配合物Cu（2-pbmq）（CH ₃ OH）Br ₂（1）和[Cu（2-pbmq）（TPP）Br] ₂（2）。射线晶体学研究2-（（（2-（吡嗪-2-基）-1H-苯并[ d ]咪唑-1-基）甲基））喹诺酮（2-pbmq），以研究TPP基团对苯丙氨酸的影响金属配合物的抗癌活性。尽管TPP基团的存在降低了复合物与DNA相互作用的强度，但在体外含有TPP的复合物的抗癌活性和细胞摄取显着优于缺乏TPP的对应物。对更有效的细胞毒性复合物2的详细研究表明，其在细胞核中积累，使细胞周期停滞在G0-G1期，导致线粒体功能障碍，涉及潜在的同时线粒体膜塌陷，细胞ATP水平耗竭和Ca ²⁺泄漏，最终诱导细胞凋亡。总之，TPP基团的引入增强了复合物的生物活性和细胞毒性。