Science in Society Archive

Does DCA Cure Cancer?

A common chemical seems just short of the latest miracle cure for cancer, but its implications for our basic understanding of cancer may be far more important Dr. Mae-Wan Ho

DCA kills cancer cells and shrinks tumours

Cancer researcher Evangelos Michelakis and his team at University of Alberta in Canada created a sensation in 2007 when they published a research paper claiming that a common chemical dichloroacetate (DCA) (see Figure 1) specifically killed cancer cells in culture without affecting normal cells, and inhibited the growth of human cancerous tumours that developed in rats [1]. (NB: it is the sodium salt of DCA that is used in cancer therapy, and not the acid.)

Figure 1   Sodium dichloroacetate

Unfortunately, there was no support forthcoming from pharmaceutical companies for clinical trials because DCA is a widely available chemical and cannot be patented. Nevertheless, it had been in use for more than 30 years with a good safety record, and there was a strong case for testing the drug in human cancer patients.

Results of first clinical trial promising

With funding from private foundations and public donations as well as the Canadian National Institutes of Health, the team carried out the first clinical trial on five patients with glioblastoma (a fast-growing malignant brain tumour nearly always fatal), and the results were published in 2010 [2]. Of the five patients treated, one of the three with terminal cancer died after 3 months on DCA, but the rest were clinically stable at month 15 of DCA therapy, and still alive at month 18. Three of the patients showed some evidence of the tumour shrinking on magnetic resonance imaging. The results were promising.

One noted side effect of higher doses of DCA was peripheral neuropathy, which was reversed when the dosage was lowered. The team concluded: “Indications of clinical efficacy were present at a dose that did not cause peripheral neuropathy and at serum concentrations of DCA sufficient to inhibit the target enzyme of DCA, pyruvate dehydrogenase kinase II, which was highly expressed in all glioblastomas. Metabolic modulation may be a viable therapeutic approach in the treatment of glioblastomas.”

But Michelakis rightly stressed it is too soon to say whether DCA will provide an effective treatment against cancer in humans, and proper placebo-controlled trials were needed [3]. The trial was complicated by the fact that each patient received different treatments and was also simultaneously on other anti-cancer drugs.

What prompted Michelakis and colleagues to use DCA in treating cancer?

Cancer cells have abnormal energy metabolism

The inspiration to use DCA for cancer therapy came from observations made since the 1920s by German physiologist Otto Heinrich Warburg on the energy metabolism of cancer cells compared with normal cells. Normal cells obtain energy by breaking down the 6-carbon  molecule glucose to two 3-carbon pyruvate molecules in a series of reactions in the cytoplasm called glycolysis that does not require oxygen, followed by oxidation reactions in the mitochondria (special ‘power houses’ inside cells)  in which oxygen is needed.

Cancer cells, however, depend heavily on glycolysis to obtain energy, and were thought incapable of oxidative metabolism even though sufficient oxygen is present. This phenomenon – aerobic glycolysis subsequently referred to as the Warburg effect - prompted Warburg to propose that mitochondrial malfunction was the primary cause of cancer [4].

As glycolysis is a much less efficient way of extracting energy from glucose, cancer cells are extra hungry for glucose. Actually, it was later found that not all cancer cells are unable to carry out oxidative metabolisms (see [5] Cancer a Redox Disease? SiS 54). Some cancer cells appear to have working mitochondria, and in the presence of an adequate oxygen supply, they carry out both glycolysis and oxidative phosphorylation simultaneously, and still generate a lot of lactic acid, the end product of pyruvate that does not get oxidized in the mitochondria.

Warburg’s idea fell into disfavour as the view of cancer as a metabolic disease was gradually displaced with one of cancer as a genetic disease caused by mutations in specific cancer related genes, or oncogenes [6]. 

In recent years, positron emission tomography (PET) imaging has confirmed that most malignant tumours have increased glucose uptake and metabolism. But still, this was thought to be an effect of cancer rather than its cause.

Warburg’s metabolic hypothesis of cancer has been revived recently [6] as decades of investment into the ‘war on cancer’ based on the genetic hypothesis has delivered little, and new findings on the remarkable genetic heterogeneity of even a single tumour are raising doubts over the genetic approach to cancer therapy [7] (Personalized Medicine for Cancer Fact or Fiction? SiS 54).

It has been suggested that as cancers typically develop in a hypoxic (low oxygen) microenvironment, transformed (cancerous) cells would have to rely on glycolysis for energy initially. This switch to glycolysis offers the transformed cells a proliferative advantage, at the same time suppressing apoptosis (programmed cell suicide) that would otherwise have occurred [8]. Moreover, the end-product of glycolysis, lactate and associated acidosis, help break down the extracellular matrix, facilitating cell mobility and the invasive (metastatic) potential of the cancer cells.  Thus, even though tumours that eventually develop became richly supplied with blood vessels and plenty of oxygen, aerobic glycolysis persists as it conferred a powerful growth advantage for the evolution of invasive human cancers.

Alternatively, it has been argued that active glycolysis is also important for providing the carbon skeletons for other molecules that make proteins and nucleic acids, all of which are required for rapid growth [9].          

How DCA works

The enzyme pyruvate-dehydrogenase kinase (PDK) normally inactivates the gate-keeper enzyme for the mitochondria, pyruvate dehydrogenase (PDH), which catalyses the conversion of pyruvate into acetyl-CoA that feeds into the citric acid cycle in the mitochondria, so pyruvate becomes converted into lactate. DCA inhibits PDK, thereby reactivating PDH and allowing pyruvate to be oxidized in the mitochondria. At the same time, this induces apoptosis in the cancer cells, with little or no effect on normal, non-cancer cells.

DCA induced suicide in human cancer cells and shrank xenograft tumours in rats

In their 2007 publication, the team reported their first results on experiments with human cancer cells in culture as well as tumours (xenografts) grown from the cells transplanted into rats [1].

DCA increased apoptosis of human lung, brain and breast cancer cells in culture according to several markers: increased expression of annexin, activation of caspase 3 and 9, and ~6-fold increase in TUNEL-positive nuclei in cancer cells. TUNEL (Terminal deoxynucleotidyl transferase dUTP nick end labelling) is a method for detecting DNA fragmentation, the hallmark of apoptosis, by labelling the ends of fragmented nucleic acids.)

DCA also decreased cell proliferation according to standard indices, including BrdU (bromodeoxyuridine) incorporation, and expression of proliferating cell nuclear antigen (PCNA). In addition, DCA decreased the expression of survivin, a mitotic indicator.

 The human lung cancer cells were injected subcutaneously into nude athymic rats with a reduced immune system hence prone to develop cancer, and given free access to water with and without DCA at 75 mg/litre.

In the first set of experiments, 21 animals were divided into three groups: untreated controls; DCA-prevention rats, which received DCA just before cell injection and for the 5 weeks following, and DCA-reversal rats, which received DCA only 2 weeks after cell injection (when tumours had already developed) and for 3 weeks following. The untreated rats rapidly developed tumours, with a constant exponential tumour growth. Both DCA-treated groups had a significant decrease in tumour size measured by tumour weight at sacrifice and maximal diameter using callipers. In some rats, in vivo magnetic resonance imaging allowed the tumour volume to be calculated. There was an inverse correlation between apoptosis and tumour size in treated rats. The voltage-gated potassium channel Kv1.5  (a marker of DCA effect) was up-regulated and survivin down-regulated in the DCA-treated rats.

In a second set of experiments, the researchers studied whether the effects of DCA were sustained for longer periods of time and whether DCA would have a similar effect in more advanced tumours. Three groups of rats 6 in each were followed for 12 weeks; an untreated control group, a prevention group of rats given DCA at the time of tumour cell injection, and a reversal group with rats given DCA at week 10 after injection of tumour cells for 2 weeks. The rats in the prevention group had significantly smaller tumours compared to the untreated controls. DCA at week 10 inhibited tumour growth immediately, with a significant decrease even just after 1 week of treatment. DCA therapy did not have any toxic effects, as measured by several blood tests.

Similarly, in the clinical trial on patients with glioblastomas, Michelakis’ team developed patient-specific cell lines, as well as putative glioblastoma stem cells [2].  They were able to show that DCA induced apoptosis in markers of the cancer cells and their response to DCA treatment. A low dose of DCA that had no side effects was sufficient to inhibit the target enzyme pyruvate dehydrogenase kinase II, which was highly expressed in all glioblastomas.

DCA effective against other cancer cells and tumours

Other researchers have followed up the anti-cancer effects of DCA discovered by the Michelakis team. A report published in 2009 described DCA inhibition of several rat breast cancer cell lines [10]. The researchers found a reversal of the glycolytic phenotype by DCA, accompanied by an inhibition of proliferation, but without any increase in cell death. In vivo, DCA caused a 58 % reduction in the number of lung metastases observed macroscopically after injecting the breast cancer cells into the tail vein of rats.

DCA was found to induce apoptosis and cell-cycle arrest in colorectal cancer cells without reducing the growth of non-cancerous cells [11]. The largest apoptotic effect was found in metastatic LoVo cells, in which DCA induced up to 10-fold increase in apoptotic cell counts after 48 h. The most striking cell cycle arrest was evident in well-differentiated HT29 cells, where DCA caused an 8-fold increase in cells arrested in the G2 phase after 48 h. DCA also reduced lactate levels in the growth media and induced dephosphorylation of the E1a subunit of pyruvate dehydrogenase complex in all cell lines, but the mitochondrial potential was reduced only in cancer cells. (The significance of mitochondrial electrical potential is described in another article in this series [5].)

In a third report, researchers found DCA inhibited neuroblastoma growth by specifically acting against malignant undifferentiated cells [12]. Neuroblastomas are malignant tumours of peripheral nerves most often in adrenal glands [13]. This effect was not expected, because neuroblastoma was one of the tumour types on which DCA was considered ineffective as it is composed of cells with very few mitochondrial anomalies. Despite that, DCA was found to have a selective effect against very malignant neuroblastoma cells, without affecting the more differentiated/less malignant cells.

In addition, DCA was shown to be effective against prostate cancer [14] and endometrial cancer cells [15].

The precise connections between activating the gate-keeping enzyme for oxidative metabolism in the cancer cells and inducing programmed cell suicide are still unclear. But a host of downstream effects consistent with the induction of apoptosis as well as a reduction of cell proliferation have been documented.

The ability of DCA to inhibit cancer and tumour growth is just short of miraculous, and deserves our full attention. It is a cheap, commonly available chemical that selectively kill malignant cells, without hurting normal cells, and with the minimum of side-effects. But its implications for our fundamental understanding of cancer may be even more important. That’s what we shall look at next [5].

Article first published 10/04/12


  1. Bonnet S, Archer SL, Allalunis-Turner J et al and Michelakis ED. A mitochondria-K+ channel axis is suppressed in cancer and its normalization promotes apoptosis and inhibits cancer growth. Cancer Cell 2007, 11, 37-51.
  2. Michelakis ED, Sutendra G, Dromparis P et al. Metabolic modulation of gliobastoma with dichloroacetate. Science Translational Medicine 2010, 2, 31-34.
  3. “Cancer drug resurfaces and threatens false optimism”, Andy Coghlan, New Scientist 16 May 2011,
  4. Warburg O. The Metabolism of Tumours, Richard R Smith, New York, 1931.
  5. Ho MW. Cancer a redox disease? Science in Society 54 2012.
  6. Seyfied TN and Shelton LM. Cancer as a metabolic disease. Nutrition & Metabolism 2010, 7, 7.
  7. Ho MW. Personalized medicine for cancer fact or fiction? Science in Society 54 2012.
  8. Gatenby RA and Gillies RJ. Why do cancers have high aerobic glycolysis? Nature Cancer Reviews 2004, 4, 891-9.
  9. Hamanaka RB and Chandel NS. Warburg effect and redox balance. Science 2011, 334, 1219-20.
  10. Sun RC, Fadia M, Dahlstrom JE, Parish CR, Board PG and Blackburn AC. Reversal of the glycolytic phenotype by dichloroacetate inhibits metastatic breast cancer cell growth in vitro and in vivo. Breast Cancer Res Treat DOI 10.1007/s1-540-009-0435-9.
  11. Madhok BM, Yeluri S, Perry SL, Hughes TA and Jayne DG. Dichloroacetat indces apoptosis and cell-cycle arrest in colorectal cancer cells. British J Cancer 2010, 102. 1746-52.
  12. Vella S, Contin  M, Tasso R, Cancedda R and Pagano A. dichloroacetate inhibits neuroblastoma growth by specifically acting against malignant undifferentiated cells. International J Cancer 2011, 130, 1484-93.
  13. Neuroblastoma, Wikipedia, 31 January 2012,
  14. Cao W, Yacoub S, Shiverick KT, Namiki K, Sakai Y, Porvasnik S, Urbanek C, Rosser CJ. Dichloroacetate (DCA) sensitizes both wild-type and over expressing Bcl-2 prostate cancer cells in vitro to radiation. Prostate 2008, 68, 1223–31.
  15. Wong JY, Huggins GS, Debidda M, Munshi NC, De Vivo I. Dichloroacetate induces apoptosis in endometrial cancer cells. Gynecol Oncol 2008, 109, 394–402.

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There are 34 comments on this article so far. Add your comment above.

Monica Taurel Comment left 10th April 2012 23:11:25
A highly interesting article with striking evidence. I am not a doctor but a conference interpreter and nontheless can estabish a link between white sugar and cancer. This information is of the essence for cancer patients and the public at large, that does not fully understand this link. I look forward to much more information on human trials. Many thanks.

Rory Short Comment left 11th April 2012 06:06:34
The fact that pharmaceutical companies are not interested in DCA speaks volumes about the priority given to money making over and above service to humanity not only in pharmaceutical companies but generally in our modern culture. It is no wonder that psychological depression is on the increase as money just cannot be a reason for living.

Rosemary Kralik Comment left 11th April 2012 06:06:30
I have DCA in powder but when mixed with food for ingestion, has a very strong odour. Is it best ingested or injected? How best in either case? Specifically interested as my Livestock Guardian Dog has an osteo sarcoma & the scent is very strong to the sensitive canine nose. So far I have mixed DCA with raw ground meat from my pasture raised, ancient breed cattle. Thank you for this article. Sinceerely, Rosemary Kralik 613 268-9999 Canada

Danilo Comment left 15th April 2012 04:04:20
I think we need an urgent research about the four PDK isoenzymes: which Laboratory or University is doing that? "We hypothesized that DCA may have differential effects on hypoxic versus normoxic colorectal cancer cells, and found that while some cell lines are refractory to DCA’s effects, most colorectal cancer cells examined actually displayed enhanced survival under hypoxic conditions in the presence of DCA. Consistent with this, DCA treated xenografts showed no anti-tumor effect but instead there was enhanced growth of treated tumors. Our findings suggest that DCA may have differential effects on cancer cell survival depending on the regional microenvironment within treated tumors, which may complicate its usefulness as an adjuvant anti-cancer therapy." (Sodium dichloroacetate (DCA) reduces apoptosis in colorectal tumor hypoxia, ). "Thus, although DCA inhibits growth of a variety of cancer cells, the effect and the underlying mechanisms seem to be cell-type dependent. A likely explanation for these differential effects could be the difference in expression of the PDK isoenzymes in the cancer cells examined. Dichloroacetate is a non-specific inhibitor of PDK (Whitehouse and Randle, 1973), and has a different Ki for each of the four PDK isoenzymes (Bowker-Kinley et al, 1998). In addition, the four PDK isoenzymes are known to be differentially expressed in various tissues. Thus, there is a need to develop inhibitors to the individual PDK isoenzymes that should allow cancer cell-type-specific metabolic manipulation." (Dichloroacetate induces apoptosis and cell-cycle arrest in colorectal cancer cells. , )

Michelle McDonough Comment left 20th April 2012 15:03:23
How can we get a campaign going to raise this money? Its possible, but where would we have money sent to, would it be tax deductible? People need saved. Insurance companies should be all over this. Its would save them that amount within months! Very interested in helping. Im not rich but I can invest time and my voice!

Danilo Comment left 24th June 2012 01:01:44
Recent words by Dr. Michelakis: "(...)So where does DCA sit now, five years after the original excitement? Stalled, due to lack of interest, according to Dr. Michelakis. "We have not initiated another clinical trial with DCA in cancer," he told me in an email this week, "It was my hope that other centres, independent of us, will be inspired to do similar trials, but I have not seen any signs that this is the case." "I am also disappointed that other investigators have not been interested to test this drug with proper trials on their patients," he added, "but I understand that without funding (although DCA itself is very cheap) this is very difficult. As I had said in the beginning of this work, taking a generic drug to patients with a deadly disease is as difficult a task as one can imagine in modern medicine, and it requires many people to participate and push the agenda. One person in one centre cannot do it." But he has not abandoned research on DCA. Just this week, he has had another paper published in the Journal Oncology, online ahead of print. The paper describes another discovery about DCA, that suggests it can inhibit angiogenesis, (the development of blood vessels), and possibly cut off a tumor’s blood supply, a goal of drugs like Avastin, that have so far failed to live up to their early, and much publicized, promise (...)"

susan Comment left 13th July 2012 20:08:09
There is a lot of unanswered questions, the biggest one has to be the funding, we can all understand the lack of interest by big Pharma, no conspiracy just business. However the question i have that has not been raised here is what about the cancer charities? they are all raising funds "to find a cure" are they not, and what about the tax payer funded government agencies why no funding from them? The study that Danilo refers to on his April 14th post is a study paid for by the Canadian Cancer Society conducted at the U of Guelph and had a protocol specifically designed to discredit DCA.This paper was published in Cancer cell journal in April of 2010. How do you prove the protocol for this study was rigged against DCA working? Actually very easy, and i am sure they had no idea but the U of Leeds in the UK completed their own study on DCA as a treatment for colorectal cancer and published their results in the BJC(British Journal of Cancer) in May of 2010. Amazingly they had great results! Here is the link to that paper The truth is that with just a basic understanding of how DCA causes apoptosis in cancer cells you would know the results of the U of Guelph study before even starting. The most recent paper by Dr. Michelakis (May 2012) referred to by Danilo in his June 23rd post, also disproves the U of Guelph paper. In summary the science behind DCA is solid, and fortunately for us Dr. Michilakas is steadfast in his belief, it is up to the rest of us to do our research and keep this story alive. By the way every time you goggle search DCA, a paid ad by the Canadian cancer Society shows up that is linked to the results of this flawed study. Why would the CCS continue to misinform people, when they surely by now must realize that their study has been proven inaccurate? i will leave that up to you to decide. Is DCA safe? well there are published medical Journal studies of patients using DCA for more then 5 years with no adverse effects. There is a site that has gathered all the published medical journal papers on DCA going back to the 60's, confused by all the info out there. Then take the time to go and read the peer reviewed papers. DCA is the biggest breakthrough in cancer research since Warburgs discovery 85 years ago. if you don't know who Warburg was wikipedia actually has a fairly accurate post on him, goggle Otto Warburg.

Danilo Comment left 27th July 2012 23:11:49
Last May Michelakis' study ("Mitochondrial activation by inhibition of PDKII suppresses HIF1a signaling and angiogenesis in cancer" , ) mentions DCA-Vidaza increased therapeutic efficacy: "Another mechanism of potential resistance maybe the recently reported decrease of the DCA transporter SLC5A8, via methylation, is cancer tissues.75 Babu et al. reversed this by increasing the expression of SLC5A8 with the DNA methylation inhibitor 50-Azadc, potentiating the anticancer effects of DCA." In fact the referred Babu et al. document ("Role of SLC5A8, a plasma membrane transporter and a tumor suppressor, in the antitumor activity of dichloroacetate" , ) reports "The findings that dichloroacetate induces cell death selectively in tumor cells at low concentrations but only if SLC5A8 is expressed have clinical and therapeutic significance. The ability of dichloroacetate to activate PDC via inhibition of PDK in cancer cells provides a mechanistically rational basis for the antitumor activity of the compound. But cancer cells are resistant to the drug because of the absence of an effective transporter for the drug, necessitating requirement of high concentrations of the compound to induce cell death, which unfortunately causes detrimental side effects such as neuropathy. We have demonstrated in the present study that SLC5A8 serves as an active transporter for dichloroacetate. However, since the expression of the transporter is silenced in tumor cells, how can the present findings be relevant to the potential therapeutic use of the drug? The silencing of SLC5A8 in cancer cells occurs via epigenetic mechanisms involving DNA methylation; treatment of cancer cells with 5′-azacytidine, an inhibitor of DNA methylation, re-activates the expression of the gene (Li et al., 2003; Ueno et al., 2004; Hong et al., 2005; Porra et al., 2005; Thangaraju et al., 2006; Park et al., 2007, 2008). DNA methylation plays a critical role in silencing tumor suppressor genes in a variety of cancers, and DNA methylation inhibitors hold promise as anticancer drugs (Baylin, 2005). Two compounds with DNA methylation inhibition activity are in clinical use for treatment of hematologic malignancies. These are 5′-aza-2′-deoxycytidine, also known as decitabine (trade name, Dacogen) and 5′-azacytidine (trade name, Vidaza). In vitro studies have shown that treatment of a variety of cancer cell lines with these compounds re-activates the expression of SLC5A8. We speculate that the same phenomenon would also occur in vivo. Therefore, a combination of a DNA methylation inhibitor and dichloroacetate is likely to be effective for treatment of cancer because the DNA methylation inhibitor would induce the expression of SLC5A8 in tumors, which would then effectively transport dichloroacetate into tumor cells to elicit its antitumor activity. This mode of treatment would reduce considerably the concentration of dichloroacetate necessary for in vivo efficacy as an anticancer agent, thus potentially providing tumor selectivity and also avoiding the detrimental side effects such as neuropathy. The findings of the present study provide a rational basis for such a combination therapy."

Danilo Comment left 11th August 2012 22:10:45
I believe we need extended and deep clinical trials of DCA to find out its best therapeutic efficacy. In case DCA-Vidaza_like (DNMT inhibitors) combination works fine since SLC5A8 gene (DCA transporter to the cells) is activated again, might it happen that other bad genes (e.g., oncogenes) could also be activated again? As another issue, even if I’m not an expert about, it sounds quite surprising the results of a previously cited study (“Sodium dichloroacetate selectively targets cells with defects in the mitochondrial ETC.” , ): it refers to in vitro and in vivo cell lines research of DCA, not in a whole organism/humans, but in my opinion that should make even more urgent DCA clinical trials: “In this study, we undertook a retrospective of DCA in vitro activity to verify and extend previously reported mechanistic data.19 We conclude that (i) DCA is relatively inactive in vitro and inhibits cell viability with an IC50 similar to that observed with sodium pyruvate and sodium acetate, (ii) the anti-cancer activity is not selective as DCA displays similar activity toward normal cells, (iii) growth suppression generally occurs without apoptosis induction, (iv) DCA depolarizes mitochondria of both normal and tumor cells, and (v) the potassium transporter Kv1.5 has less overall involvement. However, DCA showed increased activity against cells with mitochondrial defects and effectively synergized with agents known to target mitochondria or interfere with glucose metabolism. These data suggest that clinical evaluation of DCA may benefit from selecting patient populations or combination regimes in accordance with the mechanism described here.”

Danilo Comment left 5th October 2012 05:05:44
Just for info, the University of Alberta web site ( doesn’t report anymore any clear mention to DCA (you have to find it in “search” page but many result pages don't have DCA content and just point again to the home page).

Diana Comment left 20th November 2012 19:07:40
I need more inf about the DCA is Urgent I had a good frend in the last step of Dishaused she have brain cancer I will like to try please helpme where can I find these sustance who can make it ?? anyway if is everything is lost?? Please for God Helpme!!!!.....waiting for

maewan ho Comment left 20th November 2012 19:07:48
Diana, you must contact Evangelos Michelakis and his team at University of Alberta in Canada in the first instance.

Len Clement Sr. Comment left 1st December 2012 00:12:35
Public funding for the Cancer Society is a farce. Most of the money donated goes to administration. Check out ALL the Charities and discover where is the best place to donate your charity dollars

fernanda Comment left 1st December 2012 00:12:57
como acceder al dicloroacetato?

Brendan Gardam Comment left 2nd January 2013 06:06:25
I have a family member who was diagnosed with terminal lung cancer recently. He has been on d.c.a capsules for a month and a recent biopsy found no cancer. He is getting a second biopsy on the 14/01/13 and the doctor thinks he will not need any treatment if the results are the same. The doctors were amazed as the first tests definately showed advanced cancer. We don't know if this turn around is a result of the d.c.a but he has had no other treatment yet.

John Comment left 10th January 2013 03:03:53
Brendan, where can you get DCA capsules? How about a slick kickstarter campaign to raise research funds.?

Danilo Comment left 10th January 2013 03:03:42
Brendan, may I please ask you to add your interesting event also in where cancer patients and doctors try to find help on DCA.

Hans Wiemer Comment left 20th January 2013 22:10:42
If DCA is a glycolytic inhibitor. It should be effective as an anticancer agent. The simple ingestion of citric acid in sufficient quantity seems to inhibit glycolysis (shut down the Warburg effect), restore apototic signals from mitochondria and neutralize cancer cells. No negative effect on normal cells. Anti-acids may be necessary for some (some sour stuff to be sure). Search for info on a Dr Bucay. He practices in Mexico for more details. His work with citric acid may give more info on why/how DCA operates.

loris reggiani Comment left 27th February 2013 01:01:59
Please, someone can give me the contact of Dr Michelakis. I have my sister (58) with a very bad polmon and brain cancer, the italian doctors (where we live) gave her only a few months of life. I'd like to understand if we can try this theraphy and how. Thanks, Loris

miguel godoy bravo Comment left 28th February 2013 03:03:54
HOLA: me gustaria a conseguir los protocolos del tratamiento y donde comprar el dicloroacetato de sodio.....agradecido ...saludos para todos...miguel,

Danilo Comment left 13th March 2013 06:06:02
Loris, you may find here, at the bottom, his e-mail: Carole, just in case you already not know about pulmonary arterial hypertension (PAH) and cancer research by Dr. Michelakis:

CaroleDenise Comment left 12th March 2013 07:07:48
I am currently undergoing a trial of DCA in the UK bit whose main hospital is of the one in Alberta and the doctor who wants to go all out for this drug. My condition is NOT cancer but idiopathic pulmonary hypertension, this is a terminal disease and causes cancer like growths in the lungs. I am about to go for the last of the first four months testing tomorrow, should then have some idea if this drug is working, will post results.

Danilo Comment left 19th March 2013 02:02:58
Last Michelakis doc. ( about DCA reports "the greatest effect may be synergistic with existing chemotherapy as DCA “unlocks” cancer cells from a state of apoptosis resistance.". About colon cancer he mentions also this doc. that reports "colon cancer progression is only possible when cancer cells repress the biogenesis and functional activity of mitochondria." (restored by DCA).

aharon feuerstein Comment left 23rd September 2013 21:09:38
do u know wher we can buy pure DCA. a place we can trust?

Danilo Comment left 29th October 2013 01:01:38
Just for info, current DCA clinical trial about “Study of the Safety and Efficacy of Dichloroacetate (DCA) in Glioblastoma and Other Recurrent Brain Tumors”. “Detailed Description: Malignant brain tumors are defined as any World Health Organization grade III-IV glioma and any solid tumor metastasis (spread) to the brain. Recurrent malignant brain tumors (RMBTs) are defined as either: 1) malignant tumors, originating in the brain, that have recurred at least once or 2) malignant tumors originating elsewhere in the body that have spread to the brain at least once. They share an increasing incidence, clinical and radiographic characteristics, lack of effective therapies, tendency to recur, and poor outcome. Importantly, recurrent malignant brain tumor’s shared characteristics may be usefully exploited by an emerging class of biologic agents called metabolic modulators of which Dichloroacetate (DCA) is the drug in the class most thoroughly investigated clinically. DCA’s mechanism of action and tolerability have been extensively demonstrated in the treatment of chronic metabolic disorders. Furthermore, the preciseness of DCA’s mechanism of action appears to target abnormal tumor cell metabolism.”

Danilo Comment left 12th November 2013 08:08:06
By Thomas Seyfried (Professor of biology, Boston College): “I attribute the absence of any real progress in the war of cancer over the last 40 years to the flawed concepts of the somatic mutation theory, and to the failure in recognizing mitochondrial dysfunction as a credible scientific explanation for the origin of the disease. This failure is an inexcusable tragedy ultimately responsible for the deaths of millions of cancer patients”. ( )

Danilo Comment left 13th December 2013 00:12:45
As far as I know, the first published doc. about extended (15 adults) DCA trial: “Phase 1 trial of dichloroacetate (DCA) in adults with recurrent malignant brain tumors” ( ).

Ana Gorski Comment left 5th May 2014 05:05:46
I would like to know if this therapy works for medullar metastasis from breast cancer. And if you have any studies or knowledge on side effects from the therapy itself. Thank you very much. Ana

Danilo Comment left 18th May 2014 23:11:46
DCA is not an official therapy, at least for now. There're a few clinical trials ongoing or terminated: You may find here a study in vitro and on mice: "Reversal of the glycolytic phenotype by dichloroacetate inhibits metastatic breast cancer cell growth in vitro and in vivo" ( )

Danilo Comment left 21st July 2014 14:02:23
Just for info, in vitro “Sodium dichloroacetate exhibits anti-leukemic activity in B-chronic lymphocytic leukemia (B-CLL) and synergizes with the p53 activator Nutlin-3.” ( )

navin Comment left 18th August 2014 21:09:40
Can a person use this DCA for breat cancer lump stage 2? And what is teh best dose? Plse help. Many thanks Nav

Daniel Comment left 22nd August 2014 00:12:26
@navin: there is a chance to work for any cancer type. all the info you need regarding DCA on dosage, source, synergies, etc. is on the DCA site:

Danilo Comment left 2nd September 2014 23:11:22
For info, recent study: “Dichloroacetate and Cancer: New Home for an Orphan Drug?” ( )

Danilo Comment left 7th November 2014 07:07:53
Medicor document about patients treated with intravenous DCA: “A novel form of dichloroacetate therapy for patients with advanced cancer: a report of 3 cases” ( ).