Molecular Weight(MW): 440.88
RSL3 is a ferroptosis activator in a VDAC-independent manner,exhibiting selectivity for tumor cells bearing oncogenic RAS. RSL3 binds, inactivates GPX4 and thus mediates GPX4-regulated ferroptosis.
Cited by 18 Publications
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HK2 cells with elevated PEBP1 are more sensitive to ferroptosis. Inset: ferrostatin-1-inhibitable cell death (means ± SD, *p < 0.05 versus pCMV6, **p < 0.05 versus pCMV6/RSL3, ***p < 0.05 versus pCMV6-PEBP1/RSL3, #p < 0.05 versus pCMV6/RSL3, n = 3/group). Inset: quantitation of ferroptosis as differences in LDH in ± FER-treated cells.
Cell, 2017, 171(3):628-641. RSL3 purchased from Selleck.
(D) Representative western blot and (E) densitometry showing protein levels of HO-1 in HO-1+/+ PTCs treated with RSL3 over time. Data shown represent the Mean ± SEM of three independent experiments performed each time in triplicate; * = p<0.05, ** = p<0.01 compared to lower concentration at each time point.
Am J Physiol Renal Physiol, 2017, doi: 10.1152/ajprenal.00044.2017. RSL3 purchased from Selleck.
ATG3 is required for ferroptosis. ATG3KO MEFs, or ATG3KO cells reconstituted with ectopic ATG3 expression, were treated as indicated for 12 h. Cell death was determined by PI staining coupled with flow cytometry. ATG3 expression was confirmed by immunoblotting. erastin: 1 μM; RSL3: 1 μM.
Cell Res, 2016, 26(9):1021-32. RSL3 purchased from Selleck.
Detection of lipid hydroperoxides by live cell fluorescence imaging of Liperfluo in HBE cells treated with RSL3 (200 nM) or ΔwspF supernatant for 4 hours. Top panel shows time course of changes in the fluorescence intensity from baseline. Bottom panel shows typical changes in fluorescence (of 4 performed) in one stage position (of 10) at 3 time points (0, 2, and 4 hours). Time control used as a negative control and RSL3 as a positive control for ferroptosis. For statistical analysis, each stage position was counted as one data entry.
J Clin Invest, 2018, 128(10):4639-4653. RSL3 purchased from Selleck.
miR-137 negatively regulates ferroptosis in melanoma. a The A375 and G-361 human melanoma cells were treated with erastin (2.5–40 µM) or RSL3 (0.1–10 µM) with or without a cell death inhibitor (ferrostatin-1, 1 µM; ZVAD-FMK, 10 µM; necrosulfonamide, 0.5 µM) for 24 h. Cell death was assayed using a CCK-8 kit. Data shown represent mean ± SD from three independent experiments. ****p < 0.0001. b Overexpression of miR-137 suppressed erastin- and RSL3-induced cell death in human melanoma cells. Indicated cells were treated with erastin (2.5–40 µM) or RSL3 (0.1–10 µM) for 24 h. Cell death was assayed using a CCK-8 kit. Data shown represent mean ± SD from three independent experiments. *p < 0.05; **p < 0.01; ***p < 0.001. c Inhibition of endogenous miR-137 enhanced erastin- and RSL3-induced cell death in human melanoma cells. Indicated cells were treated with erastin (2.5–40 µM) or RSL3 (0.1–10 µM) for 24 h. Cell death was assayed using a CCK-8 kit. Data shown represent mean ± SD from three independent experiments. *p < 0.05; **p < 0.01. d Quantitative RT-PCR showing the relative expression levels of miR-137 in b. Data are mean ± SD from three independent experiments. ***p < 0.001. e Quantitative RT-PCR showing the relative expression levels of miR-137 in d. Data are mean ± SD from three independent experiments. ***p < 0.001
Cell Death Differ, 2018, 1457-1472. RSL3 purchased from Selleck.
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Choose Selective Ferroptosis Inhibitors
|Description||RSL3 is a ferroptosis activator in a VDAC-independent manner,exhibiting selectivity for tumor cells bearing oncogenic RAS. RSL3 binds, inactivates GPX4 and thus mediates GPX4-regulated ferroptosis.|
Ferroptosis-inducing compounds inactivate GPX4 by direct binding or by depleting glutathione.After binding to GPX4, RSL3 inactivates GPX4 to induce ROS production from lipid peroxidation. RSL3's ability to induce synthetic lethality with oncogenic RAS is rapid and quite potent. This compound inhibits the growth of BJ-TERT/LT/ST/RASV12 and DRD cells as low as 10 ng/mland started to kill sensitive cells as early as 8 hr after treatment.
|In vivo||Prostaglandin-endoperoxide synthase (PTGS) is the key enzyme in prostaglandin biosynthesis. There are two isozymes of PTGS: a constitutive PTGS1 and an inducible PTGS2. PTGS2 encoding cyclooxygenase-2 (COX-2) is significantly upregulated after treatment with RSL3 and erastin in mice.|
|In vitro||DMSO||88 mg/mL (199.6 mM)|
|Ethanol||22 mg/mL (49.9 mM)|
|In vivo||Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
2% DMSO+30% PEG 300+2% Tween 80+ddH2O
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