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Overview
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Background
Sodium dichloroacetate (DCA) is a specific inhibitor of pyruvate dehydrogenase kinase (PDK), with IC50 values of 183 μM and 80 μM for PDK2 and PDK4, respectively. DCA can inhibit the mitochondrial potassium channel axis, cause cancer cell apoptosis and inhibit tumor growth[1].
After DCA treatment, ROS levels in cancer cells increased, MMP depolarization, which can increase apoptosis both in vivo and in vitro[2].
In C57BL/6 mice, in vivo administration of DCA induced a 20% increase in survival and reduced tumor diameter, volume, and weight without affecting its weight and avoiding metastasis[3].[1]. Structure-guided Development of Specific Pyruvate Dehydrogenase Kinase Inhibitors Targeting the ATP-binding Pocket. Journal of Biological Chemistry, 2014, 289(7): 4432-4443.
[2]. Sun R C, Board P G, Blackburn A C. Targeting metabolism with arsenic trioxide and dichloroacetate in breast cancer cells. Molecular Cancer, 2011, 10(1): 142.
[3]. Franco-Molina M A, Mendoza-Gamboa E, Sierra-Rivera C A, et al. In vitro and in vivo antitumoral activitiy of sodium dichloroacetate (DCA-Na) against murine melanoma. African journal of microbiology research, 2012, 6(22): 4782-4796.
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