cuprizone

Cuprizone is a synthetic copper-chelating agent, chemically known as bis-cyclohexanone oxaldihydrazone, primarily used in research as an experimental neurotoxin to induce selective oligodendrocyte death and central nervous system (CNS) demyelination in rodents[1][3][8]. It is orally administered, typically via the diet, to generate animal models of demyelinating diseases such as multiple sclerosis, allowing investigators to study mechanisms of demyelination and remyelination in vivo[1][3]. Cuprizone exerts its effects by disrupting copper-dependent mitochondrial enzymes (including cytochrome c oxidase), inducing oxidative stress, and causing mitochondrial dysfunction in oligodendrocytes[1][7]. This toxicity triggers metabolic injury and apoptosis of oligodendrocytes, followed by demyelination, glial activation, and neuroinflammation[1][7][10]. In addition, cuprizone may also affect iron homeostasis, leading to ferroptosis, and might interact with pyridoxal 5'-phosphate, suggesting both copper-dependent and -independent mechanisms[1]. Cuprizone has no known or approved therapeutic use in humans or animals and is strictly a laboratory research tool[5].

Other names

bis-cyclohexanone oxaldihydrazonebis(cyclohexylidenehydrazide) ethanedioic acidcuprizaneethanedioic acid, bis(cyclohexylidenehydrazide)