| 名稱 | 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. |
| 細胞實驗 | 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. |
| 體外活性 | 方法：人膀胱癌細胞 J82， 253J， T24， RT-112，加入濃度梯度 （0.3， 1， 3， 10 μM） FIN56，處理 3， 6， 9， 24， 72 h，CCK-8 法檢測細胞活力。
結(jié)果： FIN56 在所有 4 種細胞中均誘導(dǎo)細胞死亡。[1]
方法：253J， T24 細胞中加入 FIN56 （10 μM），α-生育酚 （鐵死亡抑制劑），Liproxstatin-1 （鐵死亡抑制劑），處理 24 小時，CCK-8 法檢測細胞活力。
結(jié)果：兩種鐵死亡抑制劑均顯著阻止 FIN56 誘導(dǎo)的細胞死亡，證實其通過鐵死亡發(fā)揮作用。[1]
方法：采用人膠質(zhì)母細胞瘤 LN229、U118 細胞，以 1 μM FIN56 處理 24 h，1 μM Ferrostatin-1 預(yù)處理 1 h 后聯(lián)合 FIN56 處理，通過 BODIPY 581/591 C11、CellRox green、4?HNE 免疫熒光、透射電鏡檢測脂質(zhì)過氧化與鐵死亡水平。
結(jié)果：FIN56 可顯著誘導(dǎo) LN229、U118 細胞發(fā)生脂質(zhì)過氧化及鐵死亡，該效應(yīng)可被 Ferrostatin?1 阻斷。[2] |
| 體內(nèi)活性 | 方法：構(gòu)建 LN229 細胞裸鼠皮下移植瘤模型，腹腔注射 FIN56 10 mg/kg 或?qū)φ赵噭?，連續(xù)給藥 30 天，檢測腫瘤體積、Ki67（增殖）、4-HNE（鐵死亡）。
結(jié)果：FIN56 顯著縮小腫瘤體積，降低 Ki67 陽性細胞比例，升高 4-HNE 水平，在體內(nèi)抑制膠質(zhì)母細胞瘤生長并誘導(dǎo)鐵死亡。[2] |
| 存儲條件 | The compound is unstable in solution. Please use soon,
Powder: -20°C for 3 years
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.
|
| 關(guān)鍵字 | synthase | squalene | Inhibitor | inhibit | GPX4 | FIN-56 | FIN56 | FIN 56 | Ferroptosis | degradation |
| 相關(guān)產(chǎn)品 | L-Cystine | Coenzyme Q10 | Gallic Acid Monohydrate | Sodium Molybdate | L-Glutamic acid | Baicalein | (-)-Epigallocatechin Gallate | Rosiglitazone | Hemin | Curcumin | L-Glutamine | Sorafenib |
| 相關(guān)庫 | 經(jīng)典已知活性庫 | 已知活性化合物庫 | 細胞凋亡化合物庫 | 抗COVID-19化合物庫 | NO PAINS 化合物庫 | 鐵死亡化合物庫 |