作为人类必需的微量元素，铜的代谢受到进化保守的稳态调节机制的精细调控。当铜的浓度超过一定阈值时，会发生铜中毒，这已经被利用于铜离子载体（如elesclomol）作为抗癌治疗药物的开发。elesclomol已被认可为一种强效抗癌药物，并已在众多临床试验中进行评估。然而，elesclomol诱导的细胞死亡机制尚不清楚。发现了杯皮质形态的死亡，这是一种通过靶向铜在线粒体中的积累而触发的新型细胞死亡形式，重新定义了elesclomol在癌症治疗中的重要性。在这里，我们提供铜稳态和其相关病理疾病（特别是癌症发生过程中的铜代谢）的概述。我们总结了当前对elesclomol的肿瘤抑制机制的了解，重点介绍了杯皮质死亡。最后，我们讨论了可能有助于更好应用elesclomol于癌症治疗的策略。版权所有 ©2023年，由Elsevier B.V.出版。

As an essential micronutrient for humans, the metabolism of copper is fine-tuned by evolutionarily conserved homeostatic mechanisms. Copper toxicity occurs when its concentration exceeds a certain threshold, which has been exploited in the development of copper ionophores, such as elesclomol, for anticancer treatment. Elesclomol has garnered recognition as a potent anticancer drug and has been evaluated in numerous clinical trials. However, the mechanisms underlying elesclomol-induced cell death remain obscure. The discovery of cuproptosis, a novel form of cell death triggered by the targeted accumulation of copper in mitochondria, redefines the significance of elesclomol in cancer therapy. Here, we provide an overview of copper homeostasis and its associated pathological disorders, especially copper metabolism in carcinogenesis. We summarize our current knowledge of the tumor suppressive mechanisms of elesclomol, with emphasis on cuproptosis. Finally, we discuss the strategies that may contribute to better application of elesclomol in cancer therapy.Copyright © 2023. Published by Elsevier B.V.