Clioquinol and PBT2 are 8-hydroxyquinoline Copper deriv […]
Clioquinol and PBT2 are 8-hydroxyquinoline Copper derivatives. Clioquinol was previously indicated for intestinal amebiasis until the 1970s, however, a severe side effect, subacute myelocytic-neuropathy, resulted in the drug being withdrawn from sale in 1985. This side effect was only observed in Japan and has been disputed. It was later found that clioquinol was a moderate chelator of iron, copper, and zinc. However, the affinity of clioquinol for copper and zinc is moderate (KdCu is 1.2 × 10−10 M, KdZn is 7 × 10−8 M), and no in vivo data has demonstrated a reduction in copper and zinc levels in the brain of clioquinol-treated animals. Clioquinol has more recently been shown to exhibit ionophore activity, which instead of removing copper and zinc from the cell, it redistributes these metals into the cell. The ability for clioquinol to redistribute metal ions possibly underlies its neuroprotective properties in AD.
Clioquinol was effective in reducing Aβ deposition, rescuing memory impairment in an AD mouse model. Importantly, clioquinol improved cognitive performance in Phase II clinical trial and a case study, however, complications with large-scale manufacturing of the compound prevented its further development.
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