Cuproptosis, a recently identified copper-dependent programmed cell death pathway, has emerged as a promising strategy in cancer therapy. Its effectiveness is closely linked to intracellular copper accumulation but is mitigated by elevated levels of glutathione (GSH) in tumor cells. A significant barrier to its clinical application lies in the challenge of facilitating the cellular uptake of copper ions. Additionally, intracellular copper ions rapidly bind with GSH, further complicating the induction of tumor cell death. Notably, no existing ionophore drug simultaneously acts as both a copper ionophore and a GSH scavenger to effectively induce cuproptosis.
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