A majority of glioblastomas are caused by either activating mutations or amplifications of a gene that produces a protein called the epidermal growth factor receptor (EGFR) located on the surface of brain cells called astrocytes. The result of these abnormalities is that there is too much EGFR activity in the astrocyte that causes them to become cancerous. Most therapeutic efforts for glioblastoma have targeted the EGFR. Specifically, chemical inhibitor or antibodies that reduce the activity of EGFR have been clinically tested. However, these trials have been unsuccessful because the glioblastoma cells become resistant to these therapeutic agents most often by utilizing other receptors that can substitute for the EGFR and thus bypasssing the EGFR. Recent research has found that a protein that EGFR activates within glioblastoma cells called STK17A or DRAK1 might be a better target for therapy. Studies conducted in cell culture and fly models have shown that knocking down of STK17A / DRAK1 levels in glioblastoma cells kills them.
Neugeneron has identified a highly specific chemical inhibitor of STK17A / DRAK1 and has applied for a patent for the use of NGN-006 to treat glioblastoma and other cancers.