SML2234
1S,3R-RSL 3
≥98% (HPLC), powder, GPx4 inhibitor
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RAS-selective lethal, RSL3, (1S, 3R)-2-(2-Chloroacetyl)-2,3,4,9-tetrahydro-1-[4-(methoxycarbonyl)phenyl]-1H-pyrido[3,4-b]indole-3-carboxylic acid methyl ester
C23H21ClN2O5
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Assay
≥98% (HPLC)
form
powder
color
white to beige
solubility
DMSO: 2 mg/mL, clear
storage temp.
−20°C
General description
Ras-selective lethal small molecule 3 (RSL3) induces ferroptosis by inhibiting the activity of glutathione peroxidase 4 (GPx4). RSL3 not only activates ferroptosis but also blocks the activation of the mammalian target of rapamycin (mTOR) signaling pathway through interactions with GPX4. In thyroid cancer cell lines, RSL3 decreases cell viability, inhibits spheroid formation, and disrupts cell migration in vitro.
Application
1S,3R-RSL 3 has been used:
- as a glutathione peroxidase 4 (GPX4) inhibitor to study its effects on cell death in subventricular glioblastoma multiforme (GBM) lines
- GPX4 inhibitor and ferroptosis inducer to study its effects on cardiomyocyte death and heart failure in mice
- as a ferroptosis inducer in HT-1080 cellsin cell viability assay
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
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Cancer science, 108(11), 2187-2194 (2017-08-25)
In cancer cells the small compounds erastin and RSL3 promote a novel type of cell death called ferroptosis, which requires iron-dependent accumulation of lipid reactive oxygen species. Here we assessed the contribution of lipid peroxidation activity of lipoxygenases (LOX) to
Inactivation of the glutathione peroxidase GPx4 by the ferroptosis-inducing molecule RSL3 requires the adaptor protein 14-3-3?
Febs Letters (2020)
Chemistry & biology, 15(3), 234-245 (2008-03-22)
We screened small molecules to identify two compounds, which we named RSL3 and RSL5, that have increased lethality in the presence of oncogenic RAS. Counter screening with biologically active compounds defined aspects of the mechanism of action for RSL3 and
RSL3 and Erastin differentially regulate redox signaling to promote Smac mimetic-induced cell death.
Oncotarget, 7(39), 63779-63792 (2016-09-03)
Redox mechanisms play an important role in the control of various signaling pathways. Here, we report that Second mitochondrial activator of caspases (Smac) mimetic-induced cell death is regulated by redox signaling. We show that RSL3, a glutathione (GSH) peroxidase (GPX)
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