Elesclomol induced oxidative stress in cancer cells via rapid generation of reactive oxygen species.1 It preferentially binds copper ions outside the cell and selectively transports inside the mitochondria with subsequent reactive oxygen species generation leading to apoptosis.2,3 Elesclomol can restore copper homeostasis in models of copper deficiency and disorders of copper metabolism.4,5 Copper-induced cell death (Cuproptosis) caused by Elesclomol is now believed to occur via direct binding of copper to lipoylated components of the tricarboxylic acid cycle causing protein aggregation and subsequent iron-sulfur protein loss leading to proteotoxic stress and cell death.6
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