A Cu(I)-based Fenton-like agent inducing mitochondrial damage for photo-assisted enhanced chemodynamic therapy.

Increasing the reactive oxygen species (ROS) content at the tumor site is one of the effective strategies to promote intracellular oxidative stress and improve therapeutic efficiency. Herein, an atomically precise cinnamaldehyde-derived metal-organic Cu(I) complex (denoted as DC-OD-Cu) was rationally constructed. DC-OD-Cu could preferentially accumulate in the mitochondria of HeLa cells due to the mitochondria-targeting ability of triphenylphosphine, which was accompanied by the generation of large amounts of highly toxic hydroxyl radicals (˙OH) Cu(I)-mediated Fenton-like reactions.

A triphenylphosphine coordinated cinnamaldehyde-derived copper(I) Fenton-like agent with mitochondrial aggregation damage for chemodynamic therapy.

Chemodynamic therapy (CDT), which uses agents to induce cell death by decomposing endogenous hydrogen peroxide (HO) into highly toxic hydroxyl radicals (˙OH), has been recognized as a promising approach to treat cancer. However, improving the efficiency of ˙OH production is considered one of the biggest challenges that limits the therapeutic efficacy of CDT. Herein, to controllably and efficiently induce oxidative damage through the production of ˙OH, we developed a new metal complex CDT agent with atomically precise structural characteristics as a deviation from traditional nanomaterial-CDT agents.