RSL3 Chemical Properties

Boiling point:

641.3±55.0 °C(Predicted)

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)

form 

solid

color 

Off-white

optical activity

[α]/D 9.0 to 15.0°, c =0.5 in methanol

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.

InChIKey

TXJZRSRTYPUYRW-NQIIRXRSSA-N

SMILES

N1C2=C(C=CC=C2)C2C[C@H](C(OC)=O)N(C(CCl)=O)[C@@H](C3=CC=C(C(OC)=O)C=C3)C1=2

Safety Information

WGK Germany 

WGK 3

HS Code 

2933998090

Storage Class

11 - Combustible Solids

RSL3 Usage And Synthesis

Description

RSL3 (1219810-16-8) Inhibits glutathione peroxidase (GPX4) inducing ferroptosis.1,2 Effectively induces ferroptosis in glioblastoma cells.3 Everolimus in combination with RSL3 synergistically inhibits the viability of renal cell carcinoma (RCC) cells suggesting a mechanism by which RCC drug resistance may be overcome.4

Uses

RSL3 ((1S,3R)-RSL3) is an inhibitor of glutathione peroxidase 4 (GPX4) (ferroptosis activator), reduces the expression of GPX4 protein, and induces ferroptotic death of head and neck cancer cell. RSL3 increases the expression of p62 and Nrf2 and inactivates Keap1 in HN3-rslR cells[1].

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].

in vivo

IC 50

100 nm

storage

Store at -20°C

References

[1] WAN SEOK YANG. Regulation of ferroptotic cancer cell death by GPX4.[J]. Cell, 2014: 317-331. DOI:10.1016/j.cell.2013.12.010
[2] VALERIAN E KAGAN. Oxidized arachidonic and adrenic PEs navigate cells to ferroptosis[J]. Nature chemical biology, 2016, 13 1: 81-90. DOI:10.1038/nchembio.2238
[3] SHENGBIAO LI. RSL3 Drives Ferroptosis through NF-κB Pathway Activation and GPX4 Depletion in Glioblastoma.[J]. Oxidative Medicine and Cellular Longevity, 2021: 2915019. DOI:10.1155/2021/2915019
[4] WANG YANGYUN . Everolimus accelerates Erastin and RSL3-induced ferroptosis in renal cell carcinoma[J]. Gene, 2022, 809: Article 145992. DOI:10.1016/j.gene.2021.145992

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