Potassium DCA shares its entire mechanism of action with sodium DCA. Both deliver the dichloroacetate anion, which inhibits pyruvate dehydrogenase kinase (PDK). This reactivates pyruvate dehydrogenase (PDH), shifting cellular metabolism from anaerobic glycolysis back to mitochondrial oxidative phosphorylation.

In cancer cells, this matters because of the Warburg effect: tumours preferentially use aerobic glycolysis even in oxygen-rich environments. This metabolic shift protects cancer cells from apoptosis by maintaining a hyperpolarised mitochondrial membrane. DCA reverses this, depolarising the membrane and triggering programmed cell death.

The published cancer research base for potassium DCA specifically is minimal — most studies use sodium DCA. However, given that the active moiety is identical, the mechanistic and preclinical evidence for sodium DCA is directly relevant.

Studies showing DCA’s effects on glioblastoma, breast cancer, colorectal cancer, B-CLL, and cervical cancer lines all used the sodium salt, but the dichloroacetate anion is the same. Researchers who prefer the potassium form for sodium restriction reasons can reasonably apply equivalent molar dosing.

Larger human trials are needed. DCA — in either salt form — is not an approved cancer treatment.

This article is for informational and educational purposes only. AuraDCA products are intended for research use only.