FIN56 is a specific inducer of ferroptosis, a non-apoptotic form of cell death characterized by iron-dependent accumulation of lipid peroxidation products and lethal reactive oxygen species (ROS). FIN56 has an EC50 value of 240 nM, and is believed to act though two separate pathways. The first requires the enzymatic activity of acetyl-CoA carboxylase (ACC),and results in degradation of glutathione peroxidase 4 (GPX4), which acts as a negative regulator of ferroptosis by reducing lipid hydroperoxides. The second pathway involves FIN56 binding to and activing squalene synthase, which leads to coenzyme Q10 depletion.
FIN56 is a specific inducer of ferroptosis.
Ferroptosis inducer 56 (FIN56) is a member of the class 3 ferroptosis inducers.[1]
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Understanding the mechanisms underlying how T cells become dysfunctional in a tumor microenvironment (TME) will greatly benefit cancer immunotherapy. We found that increased CD36 expression in tumor-infiltrating CD8+ T cells, which was induced by TME cholesterol, was associated with tumor progression and
Cell death and differentiation, 27(3), 1008-1022 (2019-07-20)
Ferroptosis is a specialized iron-dependent cell death that is associated with lethal lipid peroxidation. Modulation of ferroptosis may have therapeutic potential since it has been implicated in various human diseases as well as potential antitumor activities. However, much remains unknown
β-Propeller protein-associated neurodegeneration (BPAN) is a rare X-linked dominant disease, one of several conditions that manifest with neurodegeneration and brain iron accumulation. Mutations in the WD repeat domain 45 (WDR45) gene encoding WIPI4 lead to loss of function in BPAN
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