SML1740
FIN56
≥98% (HPLC)
Synonyme(s) :
N2,N7-Dicyclohexyl-9-(hydroxyimino)-9H-fluorene-2,7-disulfonamide
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A propos de cet article
Formule empirique (notation de Hill) :
C25H31N3O5S2
Numéro CAS:
Poids moléculaire :
517.66
UNSPSC Code:
12352200
NACRES:
NA.77
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Laissez-nous vous aiderQuality Level
assay
≥98% (HPLC)
form
powder
color
white to beige
solubility
DMSO: 20 mg/mL, clear
storage temp.
room temp
SMILES string
[S](=O)(=O)(NC5CCCCC5)c1cc2c(cc1)c3c(cc(cc3)[S](=O)(=O)NC4CCCCC4)C2N=O
InChI
1S/C25H31N3O5S2/c29-26-25-23-15-19(34(30,31)27-17-7-3-1-4-8-17)11-13-21(23)22-14-12-20(16-24(22)25)35(32,33)28-18-9-5-2-6-10-18/h11-18,25,27-28H,1-10H2
InChI key
OYLSCKVHQYAZEE-UHFFFAOYSA-N
Biochem/physiol Actions
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.
Classe de stockage
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
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Unsolved mysteries: How does lipid peroxidation cause ferroptosis?.
Feng H and Stockwell BR
PLoS Biology, 16(5), e2006203-e2006203 (2018)
Po-Han Chen et al.
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
Xingzhe Ma et al.
Cell metabolism, 33(5), 1001-1012 (2021-03-11)
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