Ruthenium-based anticancer drugs display low general toxicity and specifically accumulate in cancer cells. This is possibly due to the ability of ruthenium to mimic iron in binding to certain biomolecules, including serum transferrin and albumin, which are known to be responsible for solubilisation, transport, and detoxification of iron in mammals. Rapidly growing cancer cells have a greater requirement for iron, which is provided to the proliferating cells by an increase in transferrin receptor expression. This increase in expression allows for uptake of the plasma Fe transport protein, Transferrin, to facilitate more intake of iron for essential cellular processes. Thus, iron mimicking feature of ruthenium compounds eases its access and accumulation in cancer cells [15]. Furthermore, arene complexes provide an ideal metal scaffold to deliver antitumour compounds to tumour cells, because they provide a proper lipophilicity for transport through cell membranes with a relatively high aqueous solubility and stabilize ruthenium(II) [16]. Thus, complexation endowed the employed biologically relevant ligands with higher affinity toward their targets, via increased solubility, increased cellular uptake, higher accumulation in the cell nucleus, the capability of DNA interactions, and the propensity to overcome acquired resistance to the metal-free drugs.