产品说明书
CIL56
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同义名 : | CA3 |
| CAS号 : | 300802-28-2 | |
| 货号 : | A720858 | |
| 分子式 : | C23H27N3O5S2 | |
| 纯度 : | 99%+ | |
| 分子量 : | 489.608 | |
| MDL号 : | MFCD00323348 | |
| 存储条件： |
粉末 Inert atmosphere,Room Temperature 液体 -20°C:3-6个月-80°C:12个月 |
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| 溶解度 : |
DMSO: 40 mg/mL(81.7 mM)，配合低频超声，并水浴加热至45℃助溶，注意：DMSO长时间开封后，会吸水并导致溶解能力下降，请避免使用长期开封的DMSO |
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| 动物实验配方： |
| 生物活性 | |||
|---|---|---|---|
| 描述 | Ferroptosis is a non-apoptotic and iron-dependent form of regulated cell death. Ferroptosis is characterized by extensive lipid peroxidation, which can be suppressed by iron chelators or lipophilic antioxidants. CIL56 acts as a potent ferroptosis inducer with novel scaffold. CIL56 showed some degree of selectivity towards oncogenic-RAS-expressing cells in the BJ series. CIL56 induced iron-dependent ROS (reactive oxygen species). CIL56 was capable of engaging two independent death pathways: ferroptosis at low concentrations, and a necrotic, non-suppressible phenotype at higher concentrations. Antioxidants and iron chelators only suppressed the lethality of low concentrations of CIL56[1]. Two clonal ACACA (acetyl-CoA carboxylase alpha; encoding ACC1) null HT-1080 cells lines lacked ACC1 expression and exhibited 5-fold resistance to CIL56. Furthermore, the lethality of CIL56 was suppressed by the small molecule ACC1 inhibitor. These results suggest that CIL56 triggers cell death dependent upon the rate-limiting de novo lipid synthetic enzyme ACC1[2]. | ||
| 实验方案 | |||
|---|---|---|---|
| 1mg | 5mg | 10mg | |
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1 mM 5 mM 10 mM |
2.04mL 0.41mL 0.20mL |
10.21mL 2.04mL 1.02mL |
20.42mL 4.08mL 2.04mL |
| 参考文献 |
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[1]Global Survey of Cell Death Mechanisms Reveals Metabolic Regulation of Ferroptosis [2]Human Haploid Cell Genetics Reveals Roles for Lipid Metabolism Genes in Nonapoptotic Cell Death |