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Copper chelation targets refer to molecular processes or agents that bind and remove copper ions from the body. Chelation therapy involves small molecules (chelators) forming stable complexes with copper ions, which can then be excreted, lowering tissue copper levels. Chelation is essential in treating diseases of copper overload, like Wilson disease, and is also investigated for roles in neurodegenerative diseases (due to copper’s role in amyloid aggregation and oxidative stress) and cancer (where copper modulates proliferation and angiogenesis)[2][3][4][5]. However, "copper ion binding and removal via chelation" describes a therapeutic mechanism or pathway, not a specific, canonical molecular target such as a receptor, enzyme, or transporter; it typically refers to the collective action of chelating agents on copper ions. Additional context and correctness: - is_incorrect: true. The phrase does not correspond to a unique, single molecule or receptor but rather describes a class of molecules (chelators) and a molecular process (chelation). The true drug targets are either the free copper ions themselves or copper-binding/buffering proteins like metallothioneins, ceruloplasmin, or copper-transporters, but these are not explicitly named in the provided entry[1]. - Many chelating agents (D-penicillamine, trientine, tetrathiomolybdate, clioquinol) are clinically used and studied for copper excess conditions, and some are in trials for other indications[3][4]. Summary: "Copper ion binding and removal via chelation" reflects a mechanism and therapeutic action rather than a single canonical target molecule or receptor. Copper chelation is central to the treatment of diseases caused by copper overload. The actual targets in therapy are free copper ions and, in some cases, copper-binding proteins or organelle-localized copper pools.
Chelation and removal of free or loosely bound copper ions from tissues, blood, or organs[2][5] - Restoration of copper homeostasis[5]
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