In the xenograft mouse model, a significant delay in tumor growth is observed in the piperazine erastin-treated group compared to the vehicle-treated group. Ptgs2 is upregulated in mouse liver with 10 or 60 mg/kg piperazine erastin administration[1].
In Vitro
Erastin is a ferroptosis activator. It triggers a unique iron-dependent form of non-apoptotic cell death that is termed as ferroptosis. Piperazine erastin is a more effective analog of erastin which is more water-soluble (0.086 mM for erastin versus 1.4 mM for piperazine erastin) and more metabolically stable. Piperazine erastin is affected similarly by cell death modulators as erastin and displays a distinct pattern from other non-FIN lethal compounds[1].
Kinase Assay
Cell Assay
Animal Administration
Mice: Athymic nude mice are injected with four million HT-1080 cells s.c. The next day, 400 μL of vehicle (0.625% DMSO/99.375% HBSS [pH 2]) or 40 mg/kg piperazine erastin is delivered to the s.c. site where cancer cells are injected. Two days later, the s.c. injection is repeated. Three days later, 300 μL of vehicle or 30 mg/kg piperazine erastin is administered to the mice through tail vein. Tail vein injection is repeated three more times, once every other day before the final tumor size is measured in both groups[1].
References
[1]. Yang WS, et al. Regulation of ferroptotic cancer cell death by GPX4. Cell. 2014 Jan 16;156(1-2):317-331.
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