Copper is a necessary micronutrient for maintaining the well-being of the human body. The biological activity of organic ligands, especially their anticancer activity, is often enhanced when they coordinate with copper(I) and (II) ions. Copper and its compounds are capable of inducing tumor cell death through various mechanisms of action, including activation of apoptosis signaling pathways by reactive oxygen species (ROS), inhibition of angiogenesis, induction of cuproptosis, and paraptosis. Some of the copper complexes are currently being evaluated in clinical trials for their ability to map tumor hypoxia in various cancers, including locally advanced rectal cancer and bulky tumors. Several studies have shown that copper nanoparticles can be used as effective agents in chemodynamic therapy, phototherapy, hyperthermia, and immunotherapy. Despite the promising anticancer activity of copper-based compounds, their use in clinical trials is subject to certain limitations. Elevated copper concentrations may promote tumor growth, angiogenesis, and metastasis by affecting cellular processes.

Coordination compound (dmapH)₂[Sn(pydc)₃]·2H₂O (where pydc is pyridine-2,6-dicarboxylate and dmapH is 4-dimethylaminopyridine) was prepared from the reaction between the proton-transfer compound, [dmapH]₂[pydc²⁻] and SnCl₄·5H₂O metal salt. The structure was fully characterized by single-crystal X-ray diffraction and distorted tricapped triangular prism geometry was realized for it. The thermal behavior of the complex was investigated by TGA-DTA analyses. Then, inhibitory effect of both the complex and its ligand was tested, using oxaliplatin as a standard, under MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide) method, against U251 (a human glioblastoma), H1299 (a human non-small cell lung carcinoma), βTC (a mouse beta pancreatic), A431 (an epidermoid carcinoma) and HFF (a human foreskin fibroblast) cell lines. Potent and selective anti-proliferative effect of the complex (IC₅₀ = 1 μM, MAE = 65.32%) and also intense decrease of mitochondrial membrane potential (MMP) was exhibited on A431 cells. Evaluation of reactive oxygen species (ROS) in cited cells confirmed that apoptotic pathway may be a possible mode for the death of cells. In order to evaluate the cellular internalization potential of the complex, A431 cells were incubated with it at IC₅₀ concentration. The recorded fluorescent images confirmed successful penetration of the complex.

A ruthenium(III) complex formulated as [Ru(pyc)₃]·H₂O (where pyc is pyridine-2-carboxylate) was prepared through a one-pot reaction of pyridine-2,6-dicarboxylic acid and anhydrous ruthenium(III) chloride. Here, hydrothermal conditions led to decarboxylation from pyridine-2,6-dicarboxylic acid into pyridine-2-carboxylate. The compound was identified by spectroscopic methods and its crystal structure was determined by single-crystal X-ray diffraction. The cytotoxicity of the compounds was evaluated by MTT(3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide) assay against three cancer cell lines containing a human melanoma (A375), a human non-small cell lung carcinoma (H1299), a human colon adenocarcinoma (HT29), and also one normal cell human foreskin fibroblast (HFF). A strong and selective inhibitory effect of the complex (IC₅₀ = 6.50 μM, viability inhibition = 67.12%) was exhibited toward A375 cells. The apoptosis through a mitochondrial pathway was suggested via reactive oxygen species (ROS) production and mitochondria membrane potential (MMP) collapse. The cytostatic effect of the complex in the A375 3 D spheroid model was depicted.