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Genetic ablation and pharmacological inhibition of HEXB elicits substantial therapeutic effects in preclinical GBM models, while targeting HEXB doesnt induce significant reduction in IDH1 mutant glioma and inhibiting IDH1 mutation-derived 2-hydroxyglutaric acid (2-HG) significantly restores HEXB expression in glioma cells
When butyrate is lacking, colon cells turn to less efficient fuels
Studies show the compound crosses the blood-brain barrier efficiently despite its peptide structure, achieving central nervous system concentrations sufficient for biological activity following systemic administration
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