MBM-02 (Tempol) for the Treatment of Glioblastoma Multiforme (GBM)

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MBM-02 is an HIF-1 and HIF-2 inhibitor that has shown in animal models to turn back on the apoptosis process (cell death) in cancer. Hypoxia is well documented in most solid tumors (Vaupel et al., 1991). Acute, intermittent, and cycling hypoxia are associated with inadequate blood flow, whereas chro...

MBM-02 is an HIF-1 and HIF-2 inhibitor that has shown in animal models to turn back on the apoptosis process (cell death) in cancer. Hypoxia is well documented in most solid tumors (Vaupel et al., 1991). Acute, intermittent, and cycling hypoxia are associated with inadequate blood flow, whereas chronic hypoxia is the consequence of increased oxygen diffusion distance resulting from tumor expansion (Dewhirst et al., 2008). A study by Chen and colleagues (2015) showed that cycling hypoxia and chronic hypoxia are important tumor microenvironment phenomena that limit tumor response to chemotherapy in GBM. In hypoxic conditions observed in solid state tumors, the hypoxia inducible factors, HIF-1? and HIF-2?, are upregulated and transcribe a panel of genes associated with cancer survival and progression, such as vascular endothelial growth factor receptor (VEGFR), platelet derived growth factor (PDGF), and glucose transporter 1 (GLUT1). These factors are essential for tumor survival, thereby increasing tumor progression and decreasing apoptosis. Without the functions of the HIF family of genes, solid-state tumors could not progress and would not survive. In both Chen et al. (2015) and Sourbier et al. (2012), researchers established that the active compound in MBM-02 is an inhibitor of both HIF-1? and HIF-2?. This is an open label multisite trial that will assess MBM-02's ability to increase progress free survival in patients receiving standard of care for glioblastoma.

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