inhibitor. Among all metabolic modulators, inhibition of glycolysis by 2-DG, a compound previously reported for the targeting of gliomas and currently in clinical testing, significantly compromised the self-renewal properties of transformed iNPCs (Fig. 3d). Then, we performed MTS assays to assess cell viability in the presence of metabolic chemical modulators. Interestingly, FCCP did not show any consistent effect across the different groups whereas the use of Rot/AA affected cell viability in all iNPCs (Fig. 3e and Supplementary Fig. 8a). Importantly, inhibition of glycolysis demonstrated a dramatic effect across the different groups of transformed iNPCs, whereas WTiNPCs remained largely unaffected (Fig. 3e). In view of these results, we next decided to perform a proof-of-concept screening with 101 FDA-approved anti-cancer compounds (Supplementary Fig. 8b and Supplementary Table 4). MTS assays highlighted 16 different compounds compromising cell viability (Supplementary Fig. 8c and Supplementary Table 4, highlighted in red). Among the different compounds, nelarabine, letrozole and capecitabine, currently under testing for the treatment of gliomas, demonstrated specificity against transformed iNPCs and primary GTICs, whereas cabazitaxel also hampered WTiNPC viability (Fig. 4a).
