Compounds that modulate H₂O₂ reaction networks have applications as targeted cancer therapeutics, as a subset of cancers exhibit sensitivity to this redox signal. Previous studies to identify therapeutics that induce oxidants have relied upon probes that respond to many different oxidants in cells, and thus do not report on only H₂O₂, a redox signal that selectively oxidizes proteins. Here we use a genetically encoded fluorescent probe for human peroxiredoxin-2 (Prx2) oxidation in screens for small-molecule compounds that modulate H₂O₂ pathways. We further characterize cellular responses to several compounds selected from the screen. Our results reveal that some, but not all, of the compounds enact H₂O₂-mediated toxicity in cells. Among them, SMER3, an antifungal, has not been reported as an oxidant-inducing drug. Several drugs, including cisplatin, that previously have been shown to induce reactive oxygen species (ROS) do not appear to oxidize Prx2, suggesting H₂O₂ is not among the ROS induced by those drugs.

调节 H ₂ O ₂反应网络的化合物可用作靶向癌症治疗剂，因为一部分癌症表现出对该氧化还原信号的敏感性。先前确定诱导氧化剂的治疗剂的研究依赖于对细胞中许多不同氧化剂有反应的探针，因此并没有仅报告 H ₂ O ₂，​​这是一种选择性氧化蛋白质的氧化还原信号。_{在这里，我们使用基因编码的荧光探针来筛选调节 H 2} O ₂的小分子化合物中的人类过氧化还原蛋白-2 (Prx2) 氧化途径。我们进一步描述了细胞对从屏幕上选择的几种化合物的反应。我们的结果表明，一些但不是全部的化合物在细胞中产生 H ₂ O ₂介导的毒性。其中，SMER3，一种抗真菌剂，尚未被报道为一种氧化诱导药物。几种药物，包括顺铂，以前已被证明可诱导活性氧 (ROS)，但似乎不会氧化 Prx2，这表明 H ₂ O ₂不在这些药物诱导的 ROS 中。