由于金属中心，螯合配体和Cpx/芳烃成分对定义其抗癌效力和选择性的重要性，极盛关注半夹心铂族有机金属络合物的生物功效，其化学式为[(η5-Cpx)/(η6-芳烃)M(XY)Cl]0/+（XY = 双齿配体；Cpx = 功能化环戊二烯；M = Ir，Rh，Ru，Os）。我们通过使用烷基铝还原剂对BIAN衍生的亚胺胺配体进行容易获取，本文描述了16个半夹心Ir（III），Rh（III）和Ru（II）络合物的制备及其特征化，这些络合物与混合型sp2-N/sp3-N供体配体螯合。Ir1-Ir3，Ir7，Rh1，Ru1和Ru4的X射线单晶结构证实了非平面五元金属环。使用碱作为脱质基团的去质子剂尝试制备亚胺酰胺络合物导致亚胺胺络合物混合物，其中离去基团Cl-被取代，而不含Cl-的16电子亚胺酰胺络合物。该体系中的半夹心亚胺胺络合物在水溶液中经历快速水解，表现出弱发光性，并具有结合CT-DNA和BSA的能力。采用MTT法确定了所有亚胺胺络合物对A549肺癌细胞系，HeLa宫颈癌细胞系和4T1小鼠乳腺癌细胞的细胞毒性。这些络合物的IC50值在5.71-67.28μM范围内。值得注意的是，与我们先前报道的螯合sp2-N/sp2-N供体配体的相应α-双亚胺络合物相比，这些络合物中大多数显示出改善的对A549癌细胞相对于非癌细胞BEAS-2B的选择性。这些络合物的抗癌选择性与氧化串联反应的机制有关，包括将NADH催化氧化为NAD+，产生活性氧自由基（ROS）和线粒体膜脱极。此外，这些络合物在A549癌细胞和BEAS-2B正常细胞中诱导凋亡与其抗癌选择性相关，表明在该体系中细胞死亡的凋亡模式。此外，这些络合物可以通过能源依赖途径进入A549细胞，并能够阻碍A549细胞的体外迁移。

The biological efficacy of half-sandwich platinum group organometallic complexes of the formula [(η5-Cpx)/(η6-arene)M(XY)Cl]0/+ (XY = bidentate ligands; Cpx = functionalized cyclopentadienyl; M = Ir, Rh, Ru, Os) has received considerable attention due to the significance of the metal center, chelating ligand, and Cpx/arene moieties in defining their anticancer potency and selectivity. With a facile access to the BIAN-derived imine-amine ligands using alkylaluminum as the reductant, we herein described the preparation and characterization of 16 half-sandwich Ir(III), Rh(III), and Ru(II) complexes chelating the hybrid sp2-N/sp3-N donor ligand. A nonplanar five-member metallacycle was confirmed by X-ray single-crystal structures of Ir1-Ir3, Ir7, Rh1, Ru1, and Ru4. The attempt to prepare imine-amido complexes using a base as the deprotonating agent led to the mixture of imine-amine complexes, within which the leaving group Cl- was displaced, and 16-electron imine-amido complexes without Cl-. The half-sandwich imine-amine complexes in this system underwent rapid hydrolysis in aqueous solution, exhibited weak photoluminescence, and showed the ability of binding to CT-DNA and BSA. The cytotoxicity of all imine-amine complexes against A549 lung cancer cell lines, HeLa cervical cancer cell lines, and 4T1 mouse breast cancer cells was determined by an MTT assay. The IC50 values of these complexes were in a range of 5.71-67.28 μM. Notably, most of these complexes displayed improved selectivity toward A549 cancer cells versus noncancerous BEAS-2B cells in comparison with the corresponding α-diimine complexes chelating the sp2-N/sp2-N donor ligand, which have been shown no selectivity in our previous report. The anticancer selectivity of these complexes appeared to be related to the redox-based mechanism including the catalytic oxidation of NADH to NAD+, reactive oxygen species (ROS) generation, and depolarization of the mitochondrial membrane. Further, inducing apoptosis of these complexes in A549 cancer cells and BEAS-2B normal cells also correlated with their anticancer selectivity, indicating the apoptosis mode of cell death in this system. In addition, these complexes could enter A549 cells via energy-dependent pathway and were able to impede the in vitro migration of A549 cells.