Imidazole ketone erastin (IKE) is an ferroptosis inducer with inhibitory effects on system Xc-cystine/glutamate transporter proteins. Imidazole ketone erastin has antitumor activity and induces glutathione depletion and lipid peroxidation.

METHODS: Human astrocytoma cells CCF-STTG1 were incubated with Imidazole ketone erastin for 2 h. Glutamate released into the medium was detected using glutamate oxidase, horseradish peroxidase, and Amplex UltraRed fluorimetric assay.
RESULTS: The IC50 for system xc- inhibition by Imidazole ketone erastin was 30 nM. [1]
METHODS: 18 DLBCL cell lines were treated with Imidazole ketone erastin (0.0001-100 µM) for 24 h. Cell viability was measured using the Cell Titor-Glo luminescent cell viability test.
RESULTS: DLBCL cell lines showed different sensitivities to Imidazole ketone erastin inhibition. 7 cell lines with IC50 <100 nM were categorized as sensitive; 5 cell lines with IC50 >10 µM were categorized as resistant; and 6 cell lines with IC50 between 100 nM and 10 µM were categorized as moderately resistant. [2]

METHODS: To detect anti-tumor activity in vivo, Imidazole ketone erastin (23-40 mg/kg, 5% DMSO in HBSS at pH 4) was injected intraperitoneally into NCG mice harboring human diffuse histiocytic lymphoma SUDHL6 once daily for thirteen days.
RESULTS: Imidazole ketone erastin inhibited tumor growth in vivo. [2]
METHODS: To test the antitumor activity in vivo, Imidazole ketone erastin (40 mg/kg every two days) and liproxstatin-1 (10 mg/kg once a day) were intraperitoneally injected into C57BL/6 mice with the hepatocellular carcinoma tumor Hepa1-6 for ten days on either a control (Met+) or a methionine-free (Met-) diet. Met-) diet.
RESULTS: In mice receiving the control diet, Imidazole ketone erastin treatment effectively reduced tumor growth, and this effect was completely blocked by liproxtatin-1. However, in mice receiving a methionine-free diet, Imidazole ketone erastin treatment failed to inhibit tumor growth. [3]