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. 2022 Apr 14;29(6):1094–1106. doi: 10.1038/s41418-022-00998-x

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — Some of these compounds are clinically available therapeutics that may additionally induce ferroptosis and/or sensitize cells to ferroptosis (cisplatin, metformin, sulfasalazine, sorafenib, immune checkpoint inhibitors HMG-CoA reductase inhibitors, ionizing radiation, artesunate, haloperidol, lapatinib, ibuprofen, acetaminophen, temozolomide), while others may prevent ferroptosis (selenium, idebenone, CoQ10, zileuton, rosiglitazone, vitamin E, DFO, CPX, resveratrol). In addition, several compounds currently limited to experimental studies carry potential for optimization toward clinical utilization in ferroptosis induction (erastin, RSL3, FIN56, BSO, ML-210, IKE, apocynin, DPI, dioscin) and ferroptosis blockade (baicalein, triascin C, ferrostatin 1, liproxstatin 1, BHT, BH4). RSL3, RAS synthetic lethal 3; BSO, buthionine sulfoximine; IKE, imidazole ketone erastin; DPI, diphenyleneiodonium chloride; BHT, butylated hydroxytoluene; BH4, tetrahydrobiopterin; DFO, deferoxamine; CPX, ciclopirox olamine. Created with BioRender.