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. Author manuscript; available in PMC: 2020 Feb 4.
Published in final edited form as: Chem Soc Rev. 2019 Feb 4;48(3):771–813. doi: 10.1039/c8cs00304a

Fig. 28.

Fig. 28

(a) Mechanism-based rationale for a dual targeting approach to drug design. (A) Elevated endogenous ROS can be tolerated by cancer cells. (B) Accentuating exogenous ROS by a single mechanism may not reach the cell death threshold. (C) Antioxidant inhibitors reduce the concentrations of reducing metabolites, thus lowering the cell death threshold. (D) The dual targeting approach involves the use of (1) a socalled redox cycling agent to accentuate exogenous ROS that is combined with (2) a reducing metabolite inhibitor to lower the cell death threshold. This combination is expected to overwhelm the system and drive it towards death. (b) Chemical structures of auranofin 132 and dual targeting redox active Au(I) N-heterocyclic carbene-based complexes 133 and 134. The portion of this figure appearing in (a) was first published in ref. 407 and reproduced with permission. Copyright Royal Society of Chemistry.