Sodium dichloroacetate (BCA) , a specific inhibitor of pyruvate dehydrogenase kinase (PDK) with IC50 values of 183 and 80 μM for PDK2 and PDK4 respectively, has been shown to derepress a mitochondrial potassium-ion channel axis, trigger apoptosis in cancer cells, and inhibit tumor growth.

PDK2:183 μM, PDK4:80 μM

METHODS: Tumor cells A549, MO59K and MCF-7 and normal cells SAEC were treated with Sodium dichloroacetate (0.5 mM) for 48 h. Mitochondrial membrane potential ΔΨm was detected using fluorescent dye.
RESULTS: Incubation of all three types of tumor cells with Sodium dichloroacetate reversed hyperpolarization and restored ΔΨm to the level of normal cells. In contrast, Sodium dichloroacetate did not alter ΔΨm in SAEC. [1]
METHODS: OSCC cell lines HSC-2, HSC-3 and PE15 were treated with Sodium dichloroacetate (1-10 mM) for 24 h. Cell viability was measured using the MST assay.
RESULTS: HSC-2 and HSC-3 showed more significant unique sensitivity to the drugs. Compared with HEK 293, the viability of both HSC-2 and HSC-3 was about 30% at 10 mM Sodium dichloroacetate, while the viability of PE15 was 75-80%. [2]

METHODS: To study the effect on energy expenditure in ApoE-/- mice, Sodium dichloroacetate (100-150 mg/kg) was administered by gavage once daily for four weeks to ApoE-/- mice fed the western diet model of atherosclerosis.
RESULTS: Western diet-fed ApoE-/- mice developed atherosclerotic plaques and hyperlipidemia, as well as obesity, which were significantly ameliorated by the administration of Sodium dichloroacetate. Enhanced glucose oxidation by Sodium dichloroacetate protects against atherosclerosis by inducing hepatic FGF21 expression and BAT activation, thereby increasing the risk of atherosclerosis. atherosclerosis, thereby increasing energy expenditure for calorie production. [3]