1219810-16-8

Basic information

• Product Name: RSL3
• Synonyms: RSL3;RSL3 (1S,3R-);1S,3R-RSL3
• CAS NO: 1219810-16-8
• Molecular Formula: C23H21ClN2O5
• Molecular Weight: 440.87624
• Product Categories: API
• Mol File: 1219810-16-8.mol
• Article Data: 0

Chemical Properties

• Boiling Point: 641.3±55.0 °C(Predicted)
• Appearance: /
• Density: 1.368±0.06 g/cm3(Predicted)
• Storage Temp.: Inert atmosphere,Store in freezer, under -20°C
• Solubility: Soluble in DMSO (45 mg/ml)
• PKA: 16.09±0.60(Predicted)
• Stability: Stable for 2 years from date of purchase as supplied. Solutions in DMSO may be stored at -20°C for up to 1 month.
• CAS DataBase Reference: RSL3(CAS DataBase Reference)
• NIST Chemistry Reference: RSL3(1219810-16-8)
• EPA Substance Registry System: RSL3(1219810-16-8)

Safety Data

• Hazardous Substances Data: 1219810-16-8(Hazardous Substances Data)

Usage

Description

RSL3, with the chemical formula 1219810-16-8, is a small molecule compound that inhibits glutathione peroxidase (GPX4), thereby inducing ferroptosis, a form of regulated cell death. It has been found to effectively induce ferroptosis in glioblastoma cells and, when combined with Everolimus, synergistically inhibits the viability of renal cell carcinoma (RCC) cells, suggesting a potential mechanism to overcome drug resistance in RCC.

Uses

Used in Oncology Research:
RSL3 is used as a research tool for studying the mechanisms of ferroptosis and its role in cancer cell death. It aids in understanding the underlying pathways and potential therapeutic targets for cancer treatment.
Used in Drug Development:
RSL3 is utilized in the development of novel cancer therapies, particularly for glioblastoma and renal cell carcinoma. Its ability to induce ferroptosis and overcome drug resistance makes it a promising candidate for combination therapies and targeted treatments.
Used in Pharmaceutical Industry:
In the pharmaceutical industry, RSL3 is used as a lead compound for the design and synthesis of new drugs targeting glutathione peroxidase (GPX4) and other related enzymes. This can lead to the development of more effective and targeted cancer treatments with fewer side effects.

in vitro

rsl3, which was a glutathione peroxidase (gpx) 4 inhibitor, had been cooperated with the smac mimetic bv6 to induce reactive oxygen species (ros)-dependent cell death in acute lymphoblastic leukemia cells. it was found that addition of the caspase inhibitor failed to rescue ros-induced cell death, suggesting that rsl3-induced cell death occured in a caspase-independent manner. moreover, the iron chelator deferoxamine inhibited rsl3/bv6-induced cell death significantly, however, it could not rescue cell death by erastin/bv6, indicating that rsl3/bv6-, but not erastin/bv6-mediated cell death depended on iron. in addition, it was shown that ros production was required for both rsl3/bv6- and erastin/bv6-induced cell death. in contrast, genetic or pharmacological inhibition of lipid peroxidation by gpx4 overexpression significantly decreased rsl3/bv6-induced cell death. of importance, inhibition of lipid peroxidation could protect from rsl3/bv6-stimulated ros production [1].

IC 50

100 nm

References

Yang et al. (2014), Regulation of ferroptotic cancer cell death by GPX4; Cell 156 317 Kagan et al. (2017), Oxidized arachidonic and adrenic PEs navigate cells to ferroptosis; nAT. Chem. Biol. 13 81 Shengbiao et al. (2021), RSL3 Drives Ferroptosis through NF-kB Pathway Activation and GPX4 depletion in Glioblastoma; oXID. Med. Cell. Longev. 2021 2915019 Yangyun et al. (2022), Everolimus accelerates Erastin and RSL3-induced ferroptosis in renal cell carcinoma; Gene 809 145992