目前，金属配合物有很多用途，特别是在药物化学和催化领域。因此，制造作为催化剂和化疗药物的新复合物始终是对文献的有益补充。在此，我们报道了三种杂环缩氨基硫脲基Pd(II)配合物[Pd(HL1)Cl] (C1)、[Pd(L2)(PPh3)] (C2)和[Pd(L3)(PPh3)]Cl (C3) )具有共配体Cl和PPh3。使用多种光谱技术系统地表征了缩氨基硫脲配体（H2L1、H2L2 和 HL3）和配合物（C1-C3）。单晶X射线衍射方法表明，C2金属中心周围的结构环境是方形平面，而C1和C3则是稍微扭曲的方形平面。化合物的超分子网络是通过氢键、C-H⋯π和π⋯π相互作用构建的。配合物结构的密度泛函理论（DFT）研究支持了实验结果。这些配合物作为 Suzuki-Miyaura 偶联反应催化剂的应用已经在 PEG 400 溶剂中用各种芳基卤化物和苯基硼酸进行了检验。该复合物与 DNA/蛋白质表现出良好的生物分子相互作用，结合常数值为 105 M-1 量级。与其他复合物相比，C3 对这些生物分子表现出更大的结合效力，这可能是由于 C3 的阳离子性质。此外，还研究了该复合物针对人类三阴性乳腺癌 (TNBC) 细胞系 MDA-MB-231 的抗肿瘤活性。结果发现，C3 对 MDA-MB-231 细胞的毒性（IC50 = 10 ± 2.90 μM）比其他复合物更高。已知的化疗药物 5-氟尿嘧啶作为阳性对照。 C3的程序性细胞死亡机制得到证实。此外，复合物诱导的细胞凋亡已被证实并通过线粒体依赖性（内在）途径发生。

Currently, there are many uses of metal complexes, especially in the fields of medicinal chemistry and catalysis. Thus, fabrication of new complexes which perform as a catalyst and chemotherapeutic drug is always a beneficial addition to the literature. Herein, we report three heterocyclic thiosemicarbazone-based Pd(II) complexes [Pd(HL1)Cl] (C1), [Pd(L2)(PPh3)] (C2) and [Pd(L3)(PPh3)]Cl (C3) having coligands Cl and PPh3. Thiosemicarbazone ligands (H2L1, H2L2 and HL3) and the complexes (C1-C3) were characterized methodically using several spectroscopic techniques. Single-crystal X-ray diffraction methods reveal that the structural environment around the metal center of C2 is square planar, while for C1 and C3 it is a slighty distorted square plane. The supramolecular network of compounds was built via hydrogen bonds, C-H⋯π and π⋯π interactions. Density functional theory (DFT) study of the structure of the complexes supports experimental findings. The application of these complexes as catalysts toward Suzuki-Miyaura coupling reactions has been examined with various aryl halides and phenyl boronic acid in PEG 400 solvent. The complexes displayed good biomolecular interactions with DNA/protein, with a binding constant value of the order of 105 M-1. C3 showed greater binding efficacy toward these biomolecules than the other complexes, which might be due to the cationic nature of C3. Furthermore, antitumor activity of the complexes was studied against the human triple-negative breast cancer (TNBC) cell line MDA-MB-231. It was found that C3 was more toxic (IC50 = 10 ± 2.90 μM) toward MDA-MB-231 cells than the other complexes. A known chemotherapeutic drug, 5-fluorouracil, was included as positive control. The programmed cell death mechanism of C3 was confirmed. Additionally, complex-induced apoptosis was confirmed and occurred via a mitochondria-dependent (intrinsic) pathway.