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. Author manuscript; available in PMC: 2014 Apr 14.
Published in final edited form as: Science. 2013 Apr 4;340(6132):626–630. doi: 10.1126/science.1236062

Fig. 4. Dose-dependent inhibition of histone methylation in IDH1-mutant gliomas after shortterm treatment with AGI-5198.

Fig. 4

(A) Intratumoral concentrations of R-2HG in TS603 xenografts treated for 2 weeks with vehicle (n = 10 mice per cohort), 150 mg/kg AGI-5198 (n = 10 mice per cohort), or 450 mg/kg AGI-5198 (n = 8 mice per cohort) (*P < 0.05, two-tailed t test). Error bars, mean ± SEM. (B) Genome-wide distribution of DNA methylation in TS603 glioma xenografts treated for 2 weeks with vehicle, 150 mg/kg AGI-5198, or 450 mg/kg AGI-5198. (C) Effect of AGI-5198 on H3K9 trimethylation in TS603 glioma xenografts. Shown is the quantification of IHC results (****P < 0.00001) (see also fig. S11). Error bars, mean ± SEM of triplicates. (D) RNA levels of astrocytic (GFAP, AQP4, and ATP1A2) and oligodendrocytic (NG2 and CNP) differentiation markers in vehicle-versus AGI-5198– treated TS603 xenografts (P = 4 × 10−8, ANOVA). RNA expression was measured by RT-PCR. Error bars, mean ± SEM for 7 or 8 repeats (7 for vehicle, 8 for 150 mg/kg, and 7 for 450 mg/kg). (E) Tumor volumes of TS603 xenografts in mice treated with vehicle, 150 mg/kg AGI-5198, or 450 mg/kg AGI-5198 (*P < 0.05, two-tailed t test); n = 10 mice per cohort. Error bars, mean ± SEM.