SKOG102 and other compounds that exhibited anti-GBM activity are chemically tractable and suitable for structural modification to (1) enhance OLIG2 selectivity which may be important as other targets in addition to OLIG2 may be variously engaged by SKOG102 in its current form, and (2) optimize pharmacokinetics and the toxicity profile of SKOG102, and assess its survival extending effect, in order to pursue the development of this scaffold as a potential GBM and CNS therapeutic. The gene discussed is OLIG2; the disease is glioblastoma.