(-)-FINO2 is an organic peroxide that can selectively induce ferroptosis and is used to study the mechanisms of ferroptosis and anticancer therapy[1]. (-)-FINO2 can specifically induce iron-dependent lipid peroxidation by depleting glutathione and inhibiting GPX4 activity to trigger ferroptosis[2]. (-)-FINO2 can be used to investigate the role of ferroptosis in pathological processes such as tumor suppression, neurodegenerative diseases, and ischemia-reperfusion injury[3-4].
In vitro, treatment of human articular chondrocytes (C-28/I2, T/C-28/A2 cell lines, and primary chondrocytes) with (-)-FINO2 (20μM) for 24 hours significantly reduces cell viability by oxidizing unstable Fe²⁺ and indirectly inhibiting GPX4 activity to trigger ferroptosis[5]. Treatment of HT-1080 fibrosarcoma cells with (-)-FINO2 (10μM) for 24 hours significantly induces cell death via an iron-dependent lipid peroxidation pathway[6].
References:
[1] Abrams RP, Carroll WL, Woerpel KA. Five-Membered Ring Peroxide Selectively Initiates Ferroptosis in Cancer Cells. ACS Chem Biol. 2016 May 20;11(5):1305-12.
[2] Lei Y, Peng X, Hu Y, et al. The Calcilytic Drug Calhex-231 Ameliorates Vascular Hyporesponsiveness in Traumatic Hemorrhagic Shock by Inhibiting Oxidative Stress and miR-208a-Mediated Mitochondrial Fission. Oxid Med Cell Longev. 2020 Dec 3;2020:4132785.
[3] JHuang Y, Ru Q, Ruan H, et al. Changyanning tablet alleviates Crohn's disease by inhibiting GPX4-mediated ferroptosis. J Ethnopharmacol. 2025 Feb 27;342:119415.
[4] Van Kessel ATM, Cosa G. Lipid-derived electrophiles inhibit the function of membrane channels during ferroptosis. Proc Natl Acad Sci U S A. 2024 May 21;121(21):e2317616121.
[5] Wipplinger A, Bekric D, Ablinger C, et al. Cannabidiol Is a Potential Inhibitor of Ferroptosis in Human Articular Chondrocytes. J Cell Mol Med. 2025 Jul;29(13):e70592.
[6] Gaschler MM, Andia AA, Liu H, et al. FINO2 initiates ferroptosis through GPX4 inactivation and iron oxidation. Nat Chem Biol. 2018 May;14(5):507-515.
(-)-FINO2一种能够选择性激活铁死亡的有机过氧化物，用于研究铁死亡机制及抗肿瘤治疗[1]。(-)-FINO2可以特异性诱导铁依赖性脂质过氧化反应，通过消耗谷胱甘肽和抑制GPX4活性来触发铁死亡[2]。(-)-FINO2 可用于研究铁死亡在肿瘤抑制、神经退行性疾病和缺血再灌注损伤等病理过程中的作用[3-4]。
在体外，(-)-FINO2（20μM）处理人关节软骨细胞（C-28/I2、T/C-28/A2细胞系及原代软骨细胞）24小时，(-)-FINO2通过氧化不稳定Fe²⁺并间接抑制GPX4活性触发铁死亡，显著降低细胞活力[5]。(-)-FINO2（10μM）处理HT-1080纤维肉瘤细胞24小时，(-)-FINO2通过铁依赖性脂质过氧化途径显著诱导细胞死亡[6]。