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DCA (dichloroacetate) is a naturally occurring, simple and inexpensive compound with significant therapeutic value in disease treatment, especially cancer. Dichloroacetate use in the treatment of disease is not a new concept.

For more than 30 years, dichloroacetate has been used safely and successfully to treat rare metabolic disorders in both children and adults.[1,2]

Recent evidence on the safety and efficacy of dichloroacetate as a cancer treatment makes this novel compound an exciting adjunct in cancer care, especially in those who have advanced (metastatic) and drug-resistant cancers.[3,4]

Oncology experts and researchers agree that one of the biggest challenges facing current and future development of anti-cancer therapy is the difficulty in identifying agents that can selectively induce cancer cell death, but spare normal cells.[5]

Based on the mechanism of dichloroacetate actions and clinical evidence for its tremendous value in cancer treatment, it fits the desirable criteria for a novel anticancer agent that selectively targets cancer cells with little to no adverse effects on healthy cells.[6]




DCA (dichloroacetate) is a novel cancer agent because it doesn’t directly kill cancer cells (the standard mechanism of most chemo agents, which renders their significant toxicity). Rather, it alters the unique metabolic features characteristic of cancer cells.[1,7]

Unlike healthy cells, cancer cells produce vast amounts of energy from glucose in a dysfunctional way. Cancer cells have the unique ability to over-express insulin receptors that transport glucose into the cancer cell. Here, via the process of glycolysis – the primary method of energy production for cancer cells – energy is produced from glucose without oxygen (even if oxygen is present).[8]

This phenomenon was first observed by Nobel Prize laureate Otto Warburg in 1929 (known in science as the “Warburg Effect”). [9]

Rapidly growing tumor cells exhibit rates of glycolysis up to 200 times higher than those of healthy cells. In turn, the energy produced is used to fuel the growth and spread of cancer.[10]

On the other hand, healthy cells do not primarily use glycolysis for energy production, because it’s an inefficient way to produce energy. Instead, healthy cells use oxygen to produce energy from glucose in the mitochondria (the metabolic center) of the cell. The switch to glycolysis as an energy source occurs when cells of a tumor (either benign or pre-cancerous) become deprived of oxygen in their environment. As a result, their mitochondria cannot work properly. These abnormal cells then ‘switch off’ their mitochondria.[11] Mitochondria are essential to the process of inducing apoptosis (the process by which abnormal cells self-destruct). When cells switch off mitochondria, they develop “immortality” and can continue to divide.[12]

Not all cells of a tumor develop ways to turn off their mitochondria and become immortal. Those that do, outlive the other cells in the tumor and these are the dominant cells that are responsible for the growth, spread (metastasis) and recurrence of disease. DCA specifically targets these dominant cells, producing the clinical observation that most individuals having their disease treated with DCA experience a partial or complete response to treatment.[3,13]



Evangelos Michelakis of the University of Alberta and his colleagues tested DCA on human cells cultured outside the body and found that DCA killed lung, breast and brain cancer cells, while sparing healthy cells.

 Glioblastoma Multiforme

Tumors in rats deliberately implanted with human cancer also shrank drastically when they were fed dichloroacetate (DCA) over several weeks. Results of the study were published in the journal Cancer Cell in 2006. Michelakis’s work proved that DCA re-established proper mitochondrial function in cancer cells, thereby re-engaging the cell’s ability to self-destruct, resulting in cancer cell death (apoptosis).[3]

Results of a small human clinical trial were published in Science Translational Medicine in 2010. Five patients with aggressive brain cancer were treated with DCA. DCA was found to extend the lives of four of the five patients. Brain scans and biopsies demonstrated that dichloroacetate arrested the growth of cancer cells by switching them back to normal energy production in the mitochondria.[14]

Colorectal cancer is the third most common cancer in the world and the fourth leading cause of cancer-related death. A study published in the British Journal of Cancer (2010) found DCA caused a significant decrease in cancer cell proliferation associated with apoptosis and cell-cycle arrest in colorectal cancer cells.[15]

A study published in 2009 looked at the effects of combination therapy with DCA on hepatocellular carcinoma (HCC). The researchers found the combination therapy synergistically suppressed tumor growth.[16]

There are several published in vivo (cultured cell) and in vitro (human, animal) data on the benefits of DCA in breast cancer, including metastatic disease. [17-19]

At Medicor Cancer Centres (Toronto, Canada), Dr. Khan MD has treated numerous patients with DCA since 2009.[20] He published several papers on the subject and data collection with clinical observation is ongoing. Some published data include:

  • Glioblastoma: tumor shrinkage in 2 patients treated with DCA alone (plus several reports of complete response in glioblastoma, unpublished data)[14]

  • Cholangiocarcinoma: 1 case, response to DCA with omeprazole and tamoxifen[21]

  • Renal small cell carcinoma: cured by DCA and palliative radiation therapy[22]

  • Prostate cancer: PSA reduction in androgen depletion therapy (castration) resistant prostate cancer[20]

  • Colon Cancer (with liver metastasis): reduction in CEA and liver enzymes when treated with DCA and other natural substances (unpublished data)[20]


Other published and unpublished clinical reports from Khan include:

  • Non-Hodgkins lymphoma (NHL): 1 case of complete remission with DCA alone, after chemo failure[23]

  • T-cell Non-Hogdkins Lymphoma with CNS involvement: stable disease after 1 year when treated with DCA and other natural substances[20]

  • Acute myeloid leukemia (AML) and chronic myeloid leukemia (CML): several case reports of response to DCA[20]

  • Metastatic melanoma: CT scan confirmed partial response to DCA and other natural substances[20]


A study published in June 2008 in the journal Gynecology Oncology confirmed that DCA induces apoptosis (cancer cell death) in endometrial cancer cells.[24] Another study, published in 2008 in the journal Prostate found DCA sensitized cancer cells to radiation, enhancing the effects of radiotherapy.[25]

In 2011, the journal Reproductive Science published results of a study that found DCA induced apoptosis of exposed epithelial ovarian cancer cells.[26] Results of an unpublished report demonstrated a complete response in stage 4 ovarian cancer when DCA was used in conjunction with carboplatin.


Other cancers successfully treated with DCA (alone or in conjunction with conventional therapies) include neuroblastoma [27], lung (carcinoid and non-small cell)[28,20], pancreas, cervical, melanoma, stomach, head and neck, salivary, esophagus, stomach, vaginal and several others.[20]


DCA can be administered orally or by the intravenous method. Based on clinical evidence thus far, DCA appears to be more efficacious when given intravenously. In addition, side effects are significantly less with IV DCA than with oral DCA. These observations make IV DCA the preferred method of drug delivery.


IV DCA is administered 2x/wk. Oral DCA is taken 2-3x/day, 2 weeks on and 1 week off.


About 45% of patients will experience side effects to DCA treatment. You must be under the supervision of an ND or MD who is well trained in the delivery and administration of DCA and other cancer natural cancer treatments.

Side effects to DCA are all reversible. With oral DCA, the most common side effects include peripheral neuropathy (numbness in an area of the body, with or without associated nerve pain; experienced in 15% of patients), fatigue (15%) and confusion/reduced memory (15%). IV DCA has fewer side effects and whatever side effects are experienced, are short-lived. No true allergy to DCA has ever been observed.


If taking cannabinoids and other CNS drugs that cause delirium, dichloroacetate must be used cautiously (start with low dose and gradually increase).

It is important that the source of DCA be obtained from a reputable supplier for optimal effect and to ensure safety. Various clinics obtain DCA from reputable sources and discourage anyone considering DCA treatment from seeking online or other suppliers of DCA. Those who do, run the serious risk of compromising efficacy, and more importantly, the safety of the treatment.

Certain natural medicines (such as alpha lipoic acid and several others) act synergistically with DCA and reduce the potential for side effects. Use of the right agents in conjunction with DCA is essential – especially to prevent neuropathy.

Blood work should be performed regularly on all patients receiving DCA or other cancer treatments, in order to monitor safety and efficacy of treatment. These include lab tests such as liver enzymes, markers of kidney function, serum chemistry, complete blood count, glucose levels and relevant tumor markers.


Beyond the anti-cancer effects of DCA, there are additional benefits observed in those who undergo DCA treatment. These include:

  • Safety in renal failure

  • Good in angina and heart failure (increased cardiac pumping efficiency with no increase in oxygen demand)[29]

  • Safe in those with pre-existing heart disease with or without concurrent medications[30]

  • Does not interact with warfarin or low molecular weight heparin (LMWH)

  • Improves diabetes [31]


Yes, DCA can be safely used with conventional therapies (hormones, chemo, radiation). In fact, research thus far has demonstrated DCA enhances the effectiveness of conventional therapies, generating better response rates and providing more favorable disease outcomes. Most published data indicate it is most effective when used as combination therapy.

To summarize, clinical and scientific findings published to-date, in addition to observational data, indicate that DCA:

  • Can be an effective component of a cancer treatment program;

  • Is a viable option for patients who have exhausted conventional therapies;

  • May be effective for chemo-resistant cancers;

  • Is effective against many types of cancers;

  • Is relatively safe and any side effects experienced are reversible;

  • Can improve other co-morbidities in individuals with pre-existing disease (such as diabetes and heart disease)

  • Is more effective in healthier patients than those with advanced stage disease;

  • Is most effective when used as combination therapy;

  • Palliative benefits are significant and can be effective in the treatment of advanced stage cancer.


  1. Stacpoole PW. The pharmacology of dicholoracetate. Metabolism. 1989; 38:1124-1144.

  2. Stacpoole PW, et al. Controlled clinical trial of dichloroacetate for treatment of congenital lactic acidosis in children. Pediatrics. 2006; 117:1519-1531.

  3. Bonnet S, et al. A mitochondria-K+ channel axis is suppressed in cancer and its normalization promotes apoptosis and inhibits cancer growth. Cancer Cell. 2007; 11:37-51.

  4. Sutendra G, et al. Mitochondrial activation by inhibition of PDKII suppressers HIF1a signaling and angiogenenisis in cancer. Oncogene. 2012 May 21. doi: 10.1038/onc.2012.198. [Epub ahead of print]

  5. Kamb A, Wee S, Lengauer C. Why is cancer drug discovery so difficult? Nat Rev Drug Discov. 2007; 6:115-120.

  6. Michelakis ED, Webster L, Mackey JR. Dichloroacetate (DCA) as a potential metabolic-targeting therapy for cancer. British J Cancer. 2008; 99:989-994.

  7. Cornett R, et al. Inhibition of glutathione S-transferase zeta and tyrosine metabolism by dichloroacetate: a potential unifying mechanism for its altered biotransformation and toxicity. Biochem Biophys Res Commun. 1999; 262(3):752-6.

  8. Semenza GL, Roth PH, Fang HM, Wang GL. Transcriptional regulation of genes encoding glycolytic enzymes by hypoxia-inducible factor 1. J Biol Chem. 1994; 269:23757-23763.

  9. Warbug O. Uber den stoffwechsel der tumoren. Constable: London.

  10. Gatenby RA; Gillies RJ. Why do cancers have high aerobic glycolysis? Nature Reviews Cancer. 2004; 4(11).

  11.  Kim JW, et al. HIF-1-mediated expression of pyruvate dehydrogenase kinase: a metabolic switch required for cellular adaptation to hypoxia. Cell Metab. 2006; 3:177-185.

  12. Zamzami N. Kroemer G. The mitochondrion in apoptosis: how Pandora’s box opens. Nat Rev Mol Cell Biol. 2001; 2:67-71.

  13. Pan JG, Mak TW. Metabolic targeting as an anticancer strategy: dawn of a new era? Sci STKE. 2007; 381:pe14.

  14. Michelakis ED, Sutendra G, et al. Metabolic modulation of glioblastoma with dichloroacetate. Sci Transl Med. 2010; 2(31):31ra34.

  15. Madhok BM, et al. Dichloroacetate induces apoptosis and cell-cycle arrest in colorectal cancer cells. British J Cancer. 2010; 102:1746-1752.

  16. Ying-Chun S, Hsiang-Hsuan F, et al. Abstract B97: Dichloroacetate (DCA) enhances activities of sorafenib against hepatocellular carcinoma (HCC) via modulation of aberrant cellular metabolism of HCC cells. Mol Cancer Ther. 2009; 8(12) Supplement

  17. Ramon CS, Mitali F, et al. Reversal of the glycolytic phenotype by dichloroacetate inhibits metastatic breast cancer cell growth in vitro and in vivo. Breast Cancer Res Treat. 2009; 120(1):253-60.

  18. Sun RC, Board PG, Blackburn AC. Targeting metabolism with arsenic trioxide and dichloroacetate in breast cancer cells. Mol Cancer. 2011; 10:142.

  19. Stander XX, et al. In vitro effects of an in silico-modelled 17β-estradiol derivative in combination with dichloroacetic acid on MCF-7 and MCF-12A cells. Cell Prolif. 2011; 44(6):5567-81.

  20. Khan, A. Medicor Cancer Clinic: Dec 2007 DCA Efficacy Report

  21. Ishiguro T, Ishiguro R, et al. Co-treatment of dichloroacetate, omeprazole and tamoxifen exhibited synergistically antiproliferative effect on malignant tumors: in vivo experiments and a case report. Hepatogastroenterology. 2012; 59(116):994-6.

  22. Khan, A. Case Report of Long Term Complete Remission of Metastatic Renal Squamous Cell Carcinoma after Palliative Radiotherapy and Adjuvant Dichloroacetate. Advances in Cancer: Research & Treatment. 2012; 2012, Article ID 441895, 7.

  23. Strum SB, Adalsteinsson O, et al. Case Report: Sodium dichloroacetate (DCA) inhibition of the “Warburg Effect” in a human cancer patient: complete response in non-Hodgkin’s Lymphoma after disease progression with rituximab-CHOP. J Bioenerg Biomembr. 2012 Dec 20. [Epub ahead of print]

  24. Wong JY, Huggins GS, et al. Dichloroacetate induces apoptosis in endometrial cancer cells. Gyne Oncology. 2008; 109(3):394-402.

  25. Cao W, Yacoub S, et al. Dichloroacetate (DCA) sentizes both wild-type and overexpressing Bcl-2 proatate cancer cells in vitro to radiation. Prostate. 2008; 68(11):1223-1231.

  26. Saed GM, Fletcher NM, et al. Dichloroacetate induces apoptosis of epithelial ovarian cancer cells through a mechanism involving modulation of oxidative stress. Reprod Sci. 2011; 18(12):1253-61.

  27. Vella S, Conti M, et al. Dichloroacetate inhibits neuroblastoma growth by specifically acting against malignant undifferentiated cells. Int J Cancer. 2012; 130(7):1484-93.

  28. Fiebiger W, Olszewski U, et al. In vitro cytotoxicity of novel platinum-based drugs and dichloroacetate against lung carcinoid cell lines. Clin Tranl Oncol. 2011; 13(1):43-9.

  29. Pauly DF, Pepine CJ. Ischemic heart disease: metabolic approaches to management. Clin Cardiol. 2004; (27)8:439-41.

  30. Piao L, Fang YH, et al. The inhibition of pyruvate dehyrogenase kinase improves impaired cardiac function and electrical remodeling in two models of right ventricular hypertrophy: resuscitating the hibernating right ventricle. J Mol Med (Berl). 2010; 88(1):47-60.

  31. Stacpoole PW, Henderson GN, et al. Pharmacokinetics, metabolism and toxicology of dichloroacetate. Drug Metab Rev. 1998; 30(3):449-539.

  32.  Anti-cancer synergy of dichloroacetate and EGFR tyrosine kinase inhibitors in NSCLC cell lines.

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