Dichloroacetate (DCA), the prototypic PDK inhibitor, readily crosses the blood-brain barrier
and represents an entirely new class of small molecule metabolic modulators that act in
mitochondria to reset cellular homeostasis in various congenital and acquired metabolic
disorders. Indeed, pharmacological inhibition of PDK in cancer cells by DCA restores PDC
activity, reverses the Warburg effect and induces a caspase-mediated selective apoptosis of
tumors. The central hypothesis is that patients treated with DCA prior to surgery will have a
significant (p ≤ 0.05) mean decrease in phosphorylated PDC protein expression in tumor
tissue, compared to tissue from patients who are not treated before surgery.
Phase:
Phase 2
Details
Lead Sponsor:
Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins