Further, work by Tateishi and colleagues showed that treating patient-derived IDH1R132H glioma tumour spheres with the S-enantiomer of the AGI-5198 does not block cell proliferation despite the decrease in 2-HG levels, and in vivo data using an orthotopic xenograft glioblastoma IDH mutant model showed similar survival of mice treated with the AGI-5198 S-enantiomer compared to the mice treated with vehicle [168]. This evidence concerns the gene IDH2 and central nervous system cancer.