AGI-5198 is the first highly potent and selective inhibitor of IDH1 R132H/R132C mutants with IC50 of 0.07 μM/0.16 μM.

>98%

Store at -20℃ for one year（Powder）；Store at 2-4℃ for two weeks；Store at -20℃ for six months after dissolution.

IDH-C35,AGI5198,AGI 5196

Powder

DMSO 24 mg/mL (51.88 mM)

Ethanol 14 mg/mL (30.26 mM)

Isocitrate Dehydrogenase (IDH)

Measurements of R-2HG concentrations in pellets of TS603 glioma cells demonstrates dose-dependent inhibition of the mutant IDH1 enzyme by AGI-5198. AGI-5198 does not impair colony formation of two patient-derived glioma lines that express only the wild-type IDH1 allele (TS676 and TS516). Cancer cells heterozygous for the IDH1(R132H) mutation exhibits less IDH-mediated production of NADPH, such that after exposure to ionizing radiation (IR), there are higher levels of reactive oxygen species, DNA double-strand breaks, and cell death compared with IDH1 wild-type cells. These effects are reversed by the IDH1(R132H) inhibitor AGI-5198.

AGI-5198 (450 mg/kg, p.o.) causes 50 to 60% growth inhibition of the tumor growth from human glioma xenografts. Tumors from AGI-5198- treated mice show reduced staining with an antibody against the Ki-67 protein. AGI-5198 does not affect the growth of IDH1 wild-type glioma xenografts.