Previously we reported the capacity of the bio-inspired Fe(III) complexes, Fe 2 PO and Fe 2 PC, to mimic the activity of superoxide dismutase and peroxidase enzymes, as well as their capacity to reduce the cytotoxicity generated by superoxide radicals in human peripheral blood mononuclear cells, under stress conditions. Based on those findings, we decided to evaluate the cytotoxicity, antioxidant and redox state modulation capacity of Fe 2 PO and Fe 2 PC complexes, pondering them as drug candidates against free radicals unbalance disorders. Fe 2 PO and Fe 2 PC deactivated the ABTS synthetic radical with an IC 50 value of 38.4 ± 0.9 µM and 28.9 ± 0.2 µM, respectively, while against the DPPH radical, the IC 50 value was over the higher concentration tested (>200 µM) for both complexes. As desirable for any drug candidate, none of the metallic complexes (at 25, 50 and 100 µM) induced cytotoxicity on M12.C3.F6 cells (a murine B-cell lymphoma model), but differences in the redox state modulation were observed on the basis of fluorescence detection of a 2′,7′-dichlorofluorescin probe by flow cytometry. Cells under normal conditions and preincubated with Fe 2 PO and Fe 2 PC complexes slightly augmented the reactive oxygen species concentration, meanwhile, cells under stress condition preincubated with H 2 O 2 and metallic complexes, showed a higher augmentation in the reactive oxygen species concentration, in comparison to the controls. Finally, a cellular internalisation assay was performed, showing that Fe 2 PO and Fe 2 PC exert those effects from the outside of the cells. All these results suggest the ability of Fe 2 PO and Fe 2 PC complexes to selectively increase the reactive oxygen species concentration in cells with a free radical unbalance, without inducing mortality in cells under normal conditions.