AGI-5198 - CAS 1355326-35-0
Not Intended for Therapeutic Use. For research use only.
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AGI-5198 is the first highly potent and selective inhibitor of IDH1 R132H/R132C mutants with IC50 of 0.07 μM/0.16 μM.
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Molecular Formula:
Isocitrate Dehydrogenase (IDH)
Chemical Structure
CAS 1355326-35-0 AGI-5198

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Reference Reading

1.Radioprotection of IDH1-Mutated Cancer Cells by the IDH1-Mutant Inhibitor AGI-5198.
Molenaar RJ1, Botman D2, Smits MA2, Hira VV2, van Lith SA3, Stap J2, Henneman P4, Khurshed M2, Lenting K3, Mul AN4, Dimitrakopoulou D2, van Drunen CM5, Hoebe RA2, Radivoyevitch T6, Wilmink JW7, Maciejewski JP8, Vandertop WP9, Leenders WP3, Bleeker FE4, va Cancer Res. 2015 Nov 15;75(22):4790-802. doi: 10.1158/0008-5472.CAN-14-3603. Epub 2015 Sep 11.
Isocitrate dehydrogenase 1 (IDH1) is mutated in various types of human cancer to IDH1(R132H), a structural alteration that leads to catalysis of α-ketoglutarate to the oncometabolite D-2-hydroxyglutarate. In this study, we present evidence that small-molecule inhibitors of IDH1(R132H) that are being developed for cancer therapy may pose risks with coadministration of radiotherapy. Cancer cells heterozygous for the IDH1(R132H) mutation exhibited less IDH-mediated production of NADPH, such that after exposure to ionizing radiation (IR), there were higher levels of reactive oxygen species, DNA double-strand breaks, and cell death compared with IDH1 wild-type cells. These effects were reversed by the IDH1(R132H) inhibitor AGI-5198. Exposure of IDH1 wild-type cells to D-2-hydroxyglutarate was sufficient to reduce IDH-mediated NADPH production and increase IR sensitivity. Mechanistic investigations revealed that the radiosensitivity of heterozygous cells was independent of the well-described DNA hypermethylation phenotype in IDH1-mutated cancers.