CIL56 是一种有效的选择性ferroptosis 诱导剂。Ferroptosis 是铁依赖性的调控细胞死亡 (RCD) 的非细胞凋亡形式。

CIL56 is a potent and selective ferroptosis inducer. Ferroptosis is an iron-dependent form of regulated cell death (RCD).

Solid

Ferroptosis is a non-apoptotic form of regulated cell death observed in cancer cells, kidney cells and neurons.CIL56 induces iron-dependent reactive oxygen species (ROS). Antioxidants and iron chelators only suppress the lethality of low concentrations of CIL56. CIL56 triggers cell death dependent upon the rate-limiting de novo lipid synthetic enzyme ACC1.Using mass spectrometry, the metabolome of HT-1080 cells treated with CIL56 (6.5 μM)±TOFA (4 μM) is analyzed, compared to vehicle-treated controls. Among the 298 polar and nonpolar metabolites identified in this analysis, the levels of 141 metabolites are significantly altered by CIL56 treatment, with 82 metabolites significantly increased and 59 significantly decreased (FDR q<0.01). CIL56 triggers the striking TOFA-sensitive accumulation of all detectable long chain saturated and monounsaturated fatty acids and all

Room temperature in continental US; may vary elsewhere.

Powder -20°C 3 years；4°C 2 years

[1]. Shimada K, et al. Global survey of cell death mechanisms reveals metabolic regulation of ferroptosis. Nat Chem Biol. 2016 Jul;12(7):497-503.
[2]. Dixon SJ, et al. Human Haploid Cell Genetics Reveals Roles for Lipid Metabolism Genes in Nonapoptotic Cell Death. ACS Chem Biol. 2015 Jul 17;10(7):1604-9.

In Vitro: DMSO : 41.67 mg/mL (85.11 mM; ultrasonic and warming and heat to 60°C)H₂O : < 0.1 mg/mL (insoluble)配制储备液