Brain tumor cells depend on glycolysis for their metabolism of glucose to produce energy. This metabolic tumor cell dependence requires approximately 18 times more glucose than a normal cell to produce the same amount of energy.

This led to the theory that if tumor cells are fed a “glucose decoy” (one that can’t convert into energy) to block specific tumor glucose metabolism, we can “starve” (kill) the tumor. 2-Deoxyglucose (2-DG) has been used as a decoy, but studies demonstrated that it does not have drug-like properties. To improve pharmacokinetics and increase specific organ and tumor uptake a new prodrug WP1122 was designed. While distinctively different from WP1122, WP1234 is a prodrug of 2-DG that increases half-life, has longer circulation time, but also enables release of an HDAC inhibiting short fatty acid, namely ethyl-butyric acid and higher uptake by the specific organs. Studies have demonstrated a high uptake of the drug by the pancreas indicating a unique opportunity to target pancreatic cancer due to its highly glycolytic nature.