癌症干细胞（CSCs）被认为在肿瘤转移和癌症复发中起部分作用。目前，在临床安全剂量下没有有效的治疗选择可以去除CSCs。在这里，我们报告了一系列铜（I）配合物的合成、表征和抗乳腺CSC特性，包括非类固醇抗炎药（NSAIDs）和三苯基膦配体（1-3）。铜（I）配合物能够在毫摩尔浓度下降低在二和三维培养中生长的乳腺CSC的存活率。铜（I）配合物对乳腺CSC的效力类似于沙利霉素（一种用于抗乳腺CSC的已知药物）和顺铂（一种临床使用的金属药物）。细胞研究表明，乳腺CSC能够轻易、并且类似地吸收铜（I）配合物。铜（I）配合物显著增加乳腺CSC内源性活性氧（ROS）水平，并且与NSAID组分有关的时间内ROS产生的谱特征。铜（I）配合物通过产生细胞内ROS可能是引发乳腺CSC死亡的潜在机制的一部分。据我们所知，这是第一项研究探讨铜（I）配合物的抗乳腺CSC特性。

Cancer stem cells (CSCs) are thought to be partly responsible for metastasis and cancer relapse. Currently, there are no effective therapeutic options that can remove CSCs at clinically safe doses. Here, we report the synthesis, characterisation, and anti-breast CSC properties of a series of copper(I) complexes, comprising of non-steroidal anti-inflammatory drugs (NSAIDs) and triphenylphosphine ligands (1-3). The copper(I) complexes are able to reduce the viability of breast CSCs grown in two- and three-dimensional cultures at micromolar concentrations. The potency of the copper(I) complexes towards breast CSCs was similar to salinomycin (an established anti-breast CSC agent) and cisplatin (a clinically used metallopharmaceutical). Cell-based studies showed that the copper(I) complexes are readily, and similarly, internalised by breast CSCs. The copper(I) complexes significantly increase the intracellular reactive oxygen species (ROS) levels in breast CSCs, and their ROS generation profile with respect to time is dependent on the NSAID component present. The generation of intracellular ROS by the copper(I) complexes could be part of the underlying mechanism by which they evoke breast CSC death. As far as we are aware, this is the first study to explore the anti-breast CSC properties of copper(I) complexes.