We report the synthesis and photochemical and biological characterization of Ru(II) complexes containing πexpansive ligands derived from dimethylbenzo[i]dipyrido[3,2a:2′,3′-c]phenazine (Me 2 dppn) adorned with flanking aryl substituents. Late-stage Suzuki couplings produced Me 2 dppn ligands substituted at the 10 and 15 positions with phenyl (5), 2,4-dimethylphenyl (6), and 2,4-dimethoxyphenyl (7) groups. Complexes of the general formula [Ru(tpy)(L)(py)](PF 6 ) 2 (8− 10), where L = 4−7, were characterized and shown to have dual photochemotherapeutic (PCT) and photodynamic therapy (PDT) behavior. Quantum yields for photodissociation of monodentate pyridines from 8−10 were about 3 times higher than that of parent complex [Ru(tpy)(Me 2 dppn)(py)](PF 6 ) 2 (1), whereas quantum yields for singlet oxygen ( 1 O 2 ) production were ∼10% lower than that of 1. Transient absorption spectroscopy indicates that 8−10 possess long excited state lifetimes (τ = 46−50 μs), consistent with efficient 1 O 2 production through population and subsequent decay of ligand-centered 3 ππ* excited states. Complexes 8−10 displayed greater lipophilicity relative to 1 and association to DNA but do not intercalate between the duplex base pairs. Complexes 1 and 8−10 showed photoactivated toxicity in breast and prostate cancer cell lines with phototherapeutic indexes, PIs, as high as >56, where the majority of cell death was achieved 4 h after treatment with Ru(II) complexes and light. Flow cytometric data and rescue experiments were consistent with necrotic cell death mediated by the production of reactive oxygen species, especially 1 O 2 . Collectively, this study confirms that DNA intercalation by Ru(II) complexes with π-expansive ligands is not required to achieve photoactivated cell death.