(-)-FINO2
目录号 : GC45248A ferroptosis inducer
Cas No.:869298-31-7
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
(-)-FINO2 is a ferroptosis-inducing peroxide compound that indirectly inhibits glutathione peroxidase 4 (GPX4) and oxidizes iron.[1] It decreases GPX4 activity and protein levels in vitro but does not act as an active site, allosteric, or covalent inhibitor of GPX4 or alter GPX homeostasis. It also oxidizes iron in vitro, leading to degradation of the endoperoxide moiety, but does not affect the protein levels of iron regulatory proteins, such as IRP2, FTL1, or TFR. (-)-FINO2 induces lipid peroxidation of a large subset of the lipidome in HT-1080 cells when used at a concentration of 10 µM and induces ferroptosis in an arachidonic acid lipoxygenase-independent manner. It inhibits cell growth (mean GI50 = 5.8 µM) and induces lethality (mean LC50 = 46 µM) in the NCI-60 panel of cancer cell lines. [2] It is selective for oncogenically transformed BJ-ELR cells over noncancerous BJ-hTERT cells when used at concentrations of 15 and 20 µM. (-)-FINO2 (6 µM) induces oxidative stress, including lipid peroxidation, in RS4;11 B-lymphoblastic leukemia cells. It induces iron-dependent cell death, an effect that can be blocked by pretreatment with the lipophilic antioxidants ferrostatin-1 and liproxstatin-1 , and does not induce markers of apoptosis, necrosis, or autophagy in RS4;11 cells.
Reference：
[1]. Gaschler, M.M., Andia, A.A., Liu, H., et al. FINO2 initiates ferroptosis through GPX4 inactivation and iron oxidation. Nat. Chem. Biol. 14(5), 507-515 (2018).
[2]. Abrams, R.P., Carroll, W.L., and Woerpel, K.A. Five-membered ring peroxide selectively initiates ferroptosis in cancer cells. ACS Chem. Biol. 11(5), 1305-1312 (2016).
| Cas No. | 869298-31-7 | SDF | |
| 化学名 | (5α,8α)-8-(1,1-dimethylethyl)-3-methyl-1,2-dioxaspiro[4.5]decane-3-ethanol | ||
| Canonical SMILES | CC(C)(C)[C@@H](CC1)CC[C@]21CC(CCO)(C)OO2 | ||
| 分子式 | C15H28O3 | 分子量 | 256.4 |
| 溶解度 | 30 mg/ml in DMSO, 30 mg/ml DMF, 30 mg/ml in Ethanol | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 3.9002 mL | 19.5008 mL | 39.0016 mL |
| 5 mM | 0.78 mL | 3.9002 mL | 7.8003 mL |
| 10 mM | 0.39 mL | 1.9501 mL | 3.9002 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Pre-exposure to hyperoxic air does not enhance power output during subsequent sprint cycling
Eur J Appl Physiol 2010 Sep;110(2):301-5.PMID:20473681DOI:10.1007/s00421-010-1507-6.
Previous studies have indicated that aerobic pathways contribute to 13-27% of the energy consumed during short-term (10-20 s) sprinting exercise. Accordingly, the present investigation was designed to test the hypothesis that prior breathing of oxygen-enriched air (F(in)O(2) = 60%) would enhance power output and reduce fatigue during subsequent sprint cycling. Ten well-trained male cyclists (mean +/- SD age, 25 +/- 3 years; height, 186.1 +/- 6.9 cm; body mass, 79.1 +/- 8.2 kg; maximal oxygen uptake [VO(2max)]: 63.2 +/- 5.2 ml kg(-1) min(-1)) took 25 breaths of either hyperoxic (HO) or normoxic (NO) air before performing 15 s of cycling at maximal exertion. During this performance, the maximal and mean power outputs were recorded. The concentration of lactate, pH, partial pressure of and saturation by oxygen, [H(+)] and base excess in arterial blood were assessed before and after the sprint. The maximal (1,053 +/- 141 for HO vs. 1,052 +/- 165 W for NO; P = 0.77) and mean power outputs (873 +/- 123 vs. 876 +/- 147 W; P = 0.68) did not differ between the two conditions. The partial pressure of oxygen was approximately 2.3-fold higher after inhaling HO in comparison to NO, while lactate concentration, pH, [H(+)] and base excess (best P = 0.32) after sprinting were not influenced by exposure to HO. These findings demonstrate that the peak and mean power outputs of athletes performing short-term intense exercise cannot be improved by pre-exposure to oxygen-enriched air.