Written by Timm Hoeres, Markus Horneber and the CAM-Cancer Consortium.
Updated July 13, 2016


What is it?


Dichloroacetate (DCA) is a xenobiotic, meaning that it does not occur naturally in our bodies or in the environment. However, DCA is widely present in the environment in minute quantities because it is a by-product of the process of water chlorination. It is also a product of the breakdown of certain industrial chemicals and medicinal drugs. DCA is also used as an intermediate for chemical syntheses 1. The U.S. Environmental Protection Agency (EPA) has classified DCA as a hazardous environmental chemical (group B2, probable human carcinogen) 2. On the other hand, it is being used as an investigational drug for the treatment of cancer 3 and of rare diseases associated with disturbances of cellular energy metabolism, such as congenital lactic acidosis 4,5.

Scientific name/ingredients

DCA mostly refers to the sodium or potassium salts of dichloroacetic acid. DCA salts can be easily solved in water. Pure dichloroacetic acid is a strong organic acid and should not be ingested.

Application and dosage

DCA has been administered to patients with genetic mitochondrial diseases for more than 30 years and its pharmacology has been extensively studied 6,7. DCA is rapidly absorbed after oral intake, has a plasma half-life time of approximately 1 hour and inhibits its own metabolic breakdown leading to increasing plasma concentrations over time 8. There is evidence that the clearance of DCA and possibly neurotoxic degradation products correlates with age and depends on the subject’s genotype of the glutathione transferase zeta-1 9,10. The doses of DCA applied orally in clinical studies range between 4 mg/kg body weight twice daily to 25mg mg/kg body weight twice daily. A dosage of 6.25 mg/kg body weight twice daily leads to plasma concentrations at values required for the inhibition of pyruvate dehydrogenase kinase 11.

In addition, variations in the rate at which DCA is metabolized in humans suggest that genetics-based personalized dosing of DCA may offer an improved means of administering safe doses 12.


DCA made its way into the press and media due to results that were derived from laboratory and animal studies 13.

The principal commercial supplier of DCA for laboratory and clinical research subsequently marketed DCA as being “the best new approach to cancer treatment in years”) via its Website. The Food and Drug Administration (FDA) banned the web­site in 2007 and shut down sales of DCA.

Claims of efficacy

The DCA story and the associated claims raised hope for a cancer cure and received widespread attention. Therefore, DCA is often being labeled as a wonder drug against cancer in the lay media, whereas other critical voices described it as yet another way to make money 14.

Mechanisms of action

DCA's supposed mechanisms of action against cancer cells relate to Warburg’s observations in the late 1920s that the metabolism of cancer cells is different from that of most normal cells 15,16.

Shifting the metabolism from glucose oxidation within the mitochondria towards aerobic glycolysis in the cytosol might confer several survival advantages for the malignant cell: adaptation to a hypoxic microenvironment 13, resistance to apoptosis 17, and facilitated uptake of nutrients needed to proliferate 16.It seems that to establish this altered metabolic phenotype multiple changes and molecular mechanisms around the signalling cascade of the hypoxia-inducible factors (HIFs) that mediate the effects of hypoxia on the cellular level are necessary8.

DCA inhibits pyruvate dehydrogenasekinase (PDK), which, in turn, inhibits the mitochondrial pyruvate dehydrogenase complex (PDC) by reversible phosphorylation. PDC catalyses the mitochondrial oxidative decarboxylation of pyruvate to acetyl–coenzyme A, allowing its entry into the Krebs cycle and away from lactate production 18. Therefore, by inhibiting PDK, DCA maintains PDC in its active form, facilitating the mitochondrial oxidation of glucose. Chronic administration of the drug also may help stabilize PDC and decrease its rate of degradation 8.

Bonnet et al. found that the metabolic shift from glycolysis to glucose oxidation triggered by DCA in cancer cells subsequently led to a number of pro-apoptotic changes of the mitochondria: decreased membrane potential, increased reactive oxygen species, and activated specific potassium channels 1. By decreasing the expression of HIF-1 through a yet undetermined mechanism, DCA confers further apoptotic signals 8. Kankotia and Stacpoole hypothesized that the decreased generation and release of lactic acid through DCA may alter the tumour-microenvironment and improve functions of immune cells. They further reported synergistic effects in vitro when DCA is combined with different drugs (e.g. bortezomib and arsenic trioxide) or radiation on a various cancer cell lines and supposed that DCA may not only promote apoptosis but also reverse resistance to chemotherapy and radiation 8.

Prevalence of use

No data exists regarding the prevalence of use of DCA in cancer patients.

Legal issues

DCA is not legally available as a drug or supplement in the USA or in Europe other than through clinical trials, but is listed as an orphan drug 19.

There has been an application for a patent for the use of DCA for the treatment of cancer which was subsequently withdrawn 13. The FDA banned the purveyors from producing and selling DCA in the USA on July 17, 2007.

Costs and expenditures

Capsules labeled to contain 300 mg Sodium Dichloroacetate are available on the Internet for €0.60 – 1 per capsule. Monthly expenses for a typical dose of 6.25 mg/kg body weight twice daily would add up to approximately €50–60.

Citation Timm Hoeres, Markus Horneber, CAM-Cancer Consortium. Dichloroacetate [online document]. http://ws.cam-cancer.org/The-Summaries/Dietary-approaches/Dichloroacetate. July 13, 2016.


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