| 名称 | FIN56 |
| 描述 | FIN56 is an iron death-specific inducer that binds to and activates squalene synthase, inducing ferroptosis by triggering GPX4 degradation. FIN56 can be used in studies of ferroptosis regulatory mechanisms, autophagy-ferroptosis crosstalk, and tumor therapy. |
| 细胞实验 | 1000 cells/36 μL are seeded in each well in 384-well plates. Lethal compounds are dissolved and a 2-fold, 12-point dilution series are prepared in DMSO. Compound solutions are further diluted with media at 1:25 and 4 μL/well of the diluted solutions are added to cell cultures immediately after cells are seeded. When ferroptosis inhibitors (100 μM α-tocopherol, 152 μM deferoxamine, or 10 μM U-0126) are co-treated with lethal inducers, they are supplemented to cell culture at the same time as lethal compounds are added, and the cells are incubated for 24 hrs. When other cell death modulating compounds (100 nM sodium selenite, 1 μM cerivastatin, 100 μg/mL mevalonic acid) are co-treated, they are first supplemented to cell culture for 24 hrs before lethal compounds are added to cell culture and further incubated for 24 hrs at 37°C under 5% CO2. On the day of the viability measurement, 10 μL/well of 50% Alamar Blue diluted in media is added and further incubated at 37°C for 6 hrs. Fluorescence intensity (ex/em: 530/590) is measured with a Victor 3 plate reader and the normalized viability is calculated by VL = (IL-I0)/(IV-I0), where VL, I0, IV, and IL are the normalized viability, raw fluorescence intensities from the wells containing media, cells treated with a vehicle (negative control), and cells with the lethal compound (L), respectively. When the effect of a chemical modulator (M) on L is calculated, we instead used the equation: VL|M = (IM, L-I0)/(IM, V-I0), where VL|M, IM, L and IM, V are the normalized viability, and fluorescence intensity from cells treated with M and V, and from cells with M and L. respectively. The viability is typically measured in biological triplicates unless otherwise specified. A representative dose-response curve, the mean and standard error of normalized viability from one replicate are plotted. |
| 体外活性 | 方法：人膀胱癌细胞 J82， 253J， T24， RT-112，加入浓度梯度 （0.3， 1， 3， 10 μM） FIN56，处理 3， 6， 9， 24， 72 h，CCK-8 法检测细胞活力。
结果： FIN56 在所有 4 种细胞中均诱导细胞死亡。[1]
方法：253J， T24 细胞中加入 FIN56 （10 μM），α-生育酚 （铁死亡抑制剂），Liproxstatin-1 （铁死亡抑制剂），处理 24 小时，CCK-8 法检测细胞活力。
结果：两种铁死亡抑制剂均显著阻止 FIN56 诱导的细胞死亡，证实其通过铁死亡发挥作用。[1]
方法：采用人胶质母细胞瘤 LN229、U118 细胞，以 1 μM FIN56 处理 24 h，1 μM Ferrostatin-1 预处理 1 h 后联合 FIN56 处理，通过 BODIPY 581/591 C11、CellRox green、4‑HNE 免疫荧光、透射电镜检测脂质过氧化与铁死亡水平。
结果：FIN56 可显著诱导 LN229、U118 细胞发生脂质过氧化及铁死亡，该效应可被 Ferrostatin‑1 阻断。[2] |
| 体内活性 | 方法：构建 LN229 细胞裸鼠皮下移植瘤模型，腹腔注射 FIN56 10 mg/kg 或对照试剂，连续给药 30 天，检测肿瘤体积、Ki67（增殖）、4-HNE（铁死亡）。
结果：FIN56 显著缩小肿瘤体积，降低 Ki67 阳性细胞比例，升高 4-HNE 水平，在体内抑制胶质母细胞瘤生长并诱导铁死亡。[2] |
| 存储条件 | The compound is unstable in solution. Please use soon
Powder: -20°C for 3 years | In solvent: -80°C for 1 year
Shipping with blue ice/Shipping at ambient temperature. |
| 溶解度 | DMSO : 247.5 mg/mL (478.11 mM), The compound is unstable in solution, please use soon.
10% DMSO+90% Corn Oil : 3.3 mg/mL (6.37 mM), Sonication is recommended.
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| 关键字 | synthase | squalene | Inhibitor | inhibit | GPX4 | FIN-56 | FIN56 | FIN 56 | Ferroptosis | degradation |
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| 相关库 | 经典已知活性库 | 已知活性化合物库 | 细胞凋亡化合物库 | 抗COVID-19化合物库 | NO PAINS 化合物库 | 铁死亡化合物库 |