Matrix has FDA approval and is conducting phase II studies administering MBM-02 to increase survival in patients diagnosed with Glioblastoma multiforme (GBM).

GBM is the most malignant form of brain cancer with a high mortality rate (Agnihotri et al., 2013; Holland, 2000; Maher et al., 2001; Schwartzbaum et al., 2006). Despite multimodality aggressive therapies (surgery followed by chemoradiotherapy based on temozolomide (TMZ) and adjuvant TMZ) median overall survival is only 12 to 15 months. This low survival is mainly due to the high invasiveness and proliferation rate of GBM due to upregulation of the master gene HIF-1.

MBM-02 represents a potentially dramatic breakthrough treatment for patients suffering from newly diagnosed and recurrent glioblastoma. MBM-02 not only has the potential to increase patient survival by improving the efficacy of the cancer treatment regimen, but it also has the potential to increase patient quality of life by minimizing and preventing the side effects of the cancer treatment process. This activity is supported by evidence that the active compound in MBM-02 performs the following:

1. Acts synergistically with TMZ, thereby enhancing the efficiency of TMZ’s anti-tumor activity, thus increasing patient overall survival (Chen et al., 2015);
2. Serves as an independent anti-tumor agent by inhibiting both HIF-1α and HIF-2α (Chen et al., 2015; Sourbier et al., 2012). HIF-1α and HIF-2α are critical genes for the progression of all solid state tumors: without HIF-1α and HIF-2α activity, solid state cancer cannot survive;

*This is of critical importance as GBM is one of the most hypoxic tumors due to increased HIF-1α and HIF-2α activity which leads to therapy resistance;

3. Serves as an independent anti-tumor agent for glioma tumors by increasing the number of apoptotic cells and decreasing the rate of neo-vascularization (Gariboldi et al., 2003);
4. When administered with TMZ, increases apoptotic cell death through modulation of the expression of genes involved in the apoptotic process and induces a cell-type specific decrease in GSH levels and GSH-related enzyme activities (Ravizza et al., 2004);
5. Decreases tumorigenesis and carcinogenesis in general (Dickey et al., 2013; Gariboldi et al., 1998; Gariboldi et al., 2003; Gariboldi et al., 2000; Gariboldi et al., 2006; Mitchell et al., 2012; Sourbier et al., 2012);
6. Protects non-cancerous cells’ DNA from damage due to radiation, chemotherapy, and cancer exposure (DeGraff et al., 1992; Mitchell et al., 2012);
7. Prevents and reduces the type of oxidative stress in non-cancerous cells (Wilcox, 2010);
8. Increases the lifespan of mice under various conditions and toxicities, including cancer prone strains (Erker et al., 2005; Mitchell et al., 2012; Schubert et al., 2004; Yamato et al., 2014).