您好,欢迎来到试剂信息网! [登录] [免费注册]
试剂信息网
位置:首页 > 产品库 > CIL56
立即咨询
咨询类型:
     
*姓名:
*电话:
*单位:
Email:
*留言内容:
请详细说明您的需求。
*验证码:
 
CIL56
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
CIL56图片
CAS NO:300802-28-2
规格:98%
分子量:489.61
包装与价格:
包装价格(元)
5mg电议
10mg电议
25mg电议
50mg电议
100mg电议

产品介绍
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。
CAS:300802-28-2
分子式:C23H27N3O5S2
分子量:489.61
纯度:98%
存储:Store at -20°C

Background:

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


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[1]. 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 detectable polyunsaturated fatty acids. A plausible model to account for the accumulation of both nonessential and essential fatty acids species is that CIL56 inhibits the normal breakdown of fatty acids by mitochondrial β-oxidation. CIL56 accelerates the ACC1-dependent production of malonyl-CoA, a metabolite that acts as a negative regulator of this process[2].



[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.