Dichloroacetic acid

Dichloroacetic acid
Dichloroacetic acid
CAS number 79-43-6 YesY
PubChem 6597
ChemSpider 10771217 YesY
DrugBank DB08809
KEGG C11149 YesY
MeSH Dichloroacetate
ChEBI CHEBI:36386 YesY
RTECS number AG6125000
Jmol-3D images Image 1
Molecular formula C2H2Cl2O2
Molar mass 128.94 g mol−1
Appearance Colorless liquid
Density 1.5634 g/cm3 (20 °C)
Melting point

9-11 °C, 282-284 K, 48-52 °F

Boiling point

194 °C, 467 K, 381 °F

Solubility in water miscible
Solubility miscible with ethanol, diethyl ether[1]
Acidity (pKa) 1.25[2]
Std enthalpy of
-496.3 kJ·mol-1[3]
MSDS MSDS (jtbaker)
R-phrases R35 R50
S-phrases (S1/2) S26 S45 S61
NFPA 704
NFPA 704.svg
Related compounds
Related chloroacetic acids Chloroacetic acid
Trichloroacetic acid
Related compounds Acetic acid
Difluoroacetic acid
Dibromoacetic acid
 YesY (verify) (what is: YesY/N?)
Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa)
Infobox references

Dichloroacetic acid, often abbreviated DCA, is the chemical compound with formula CHCl2COOH. It is an acid, an analogue of acetic acid, in which two of the three hydrogen atoms of the methyl group have been replaced by chlorine atoms. The salts and esters of dichloroacetic acid are called dichloroacetates. Salts of DCA have been studied as potential drugs because they inhibit the enzyme pyruvate dehydrogenase kinase.

Cancer cells change the way they metabolize oxygen in a way that promotes their survival. In laboratory studies of isolated cancer cells grown in tissue culture, DCA restores the original metabolism, and promotes their self-destruction. This has led to the use of DCA for treating cancer, by individuals experimenting with it themselves, by doctors administering it to patients as a non-approved drug, by scientists testing it in cancer tissue cultures in cell culture and in mice, and in human Phase II studies. DCA has improved certain biochemical parameters, but it has not demonstrated improved survival.[citation needed]

A study in mice at the University of Alberta showed that "DCA induces apoptosis, decreases proliferation, and inhibits tumor growth, without apparent toxicity."[4] In 2010, a small human trial on 5 cancer patients and 49 samples of tissue was conducted.[5] The results were encouraging, and DCA "appeared to extend the lives of four of the five study participants".[6]


Chemistry and occurrence

The chemistry of dichloroacetic acid is typical for halogenated organic acids. It is a member of the chloroacetic acids family. The dichloroacetate ion is produced when the acid is mixed with water. As an acid with a pKa of 1.48,[7] pure dichloroacetic acid is very corrosive and extremely destructive to tissues of the mucous membranes and upper respiratory tract.[8]

DCA does not occur in nature. It is a trace product of the chlorination of drinking water and is produced by the metabolism of various chlorine-containing drugs or chemicals.[9] DCA is typically prepared by the reduction of trichloroacetic acid.

Therapeutic use

Owing to the highly corrosive action of the acid, only the salts of dichloroacetic acid are used therapeutically, including its sodium and potassium salts, sodium dichloroacetate and potassium dichloroacetate.

Lactic acidosis

The dichloroacetate ion stimulates the activity of the enzyme pyruvate dehydrogenase by inhibiting the enzyme pyruvate dehydrogenase kinase.[10] Thus, it decreases lactate production by shifting the metabolism of pyruvate from glycolysis towards oxidation in the mitochondria. This property has led to trials of DCA for the treatment of lactic acidosis in humans.[11][12][13][14]

A randomized controlled trial in children with congenital lactic acidosis found that while DCA was well tolerated, it was ineffective in improving clinical outcomes.[12] A separate trial of DCA in children with MELAS (a syndrome of inadequate mitochondrial function, leading to lactic acidosis) was halted early, as all 15 of the children receiving DCA experienced significant nerve toxicity without any evidence of benefit from the medication.[13] A randomized controlled trial of DCA in adults with lactic acidosis found that while DCA lowered blood lactate levels, it had no clinical benefit and did not improve hemodynamics or survival.[14]

Thus, while early case reports and pre-clinical data suggested that DCA might be effective for lactic acidosis, subsequent controlled trials have found no clinical benefit of DCA in this setting. In addition, clinical trial subjects were incapable of continuing on DCA as a study medication owing to progressive toxicities.

Potential cancer applications

Cancer cells generally use glycolysis rather than respiration (oxidative phosphorylation) for energy (the Warburg effect), as a result of hypoxia that exists in tumors and malfunctioning mitochondria.[15] Usually dangerously damaged cells kill themselves via apoptosis, a mechanism of self-destruction that involves mitochondria, but this mechanism fails in cancer cells.

A phase I study published in January 2007 by researchers at the University of Alberta, who had tested DCA on cancer cells grown in mice, found that DCA restored mitochondrial function, thus restoring apoptosis, allowing cancer cells to self-destruct and shrink the tumor.[16]

These results received extensive media attention, beginning with an article in New Scientist titled "Cheap, ‘safe’ drug kills most cancers".[17] Subsequently, the American Cancer Society and other medical organizations have received a large volume of public interest and questions regarding DCA.[18] Clinical trials in humans with cancer have not been conducted in the USA and are not yet final in Canada, emphasizing the need for caution in interpreting the preliminary results.[18][19]

Results of phase II clinical trials

In in vitro studies, Evangelos Michelakis of University of Alberta found that in tissue samples from 49 patients, DCA caused depolarization of mitochondria in GBM tissue but not in normal brain tissue.[5]

Five palliative patients with primary GBM were entered into a phase II trial. Three had not responded to several chemotherapies; two were newly diagnosed. After surgical removal of tumor mass, they were treated with DCA and chemotherapy.[5]

Of the five patients tested, one died after three months. The surviving four were followed for 15 months. Their Karnofsky scores were unchanged in two cases, and decreased by 10 points in two patients.[5]

DCA was associated with tumor regression and had a good safety profile. DCA side effects were minimal.[5]

Michelakis is proceeding with phase three human studies with private funding from philanthropic groups and individuals. DCA's legal status as a discovery is public domain because it was made or discovered as far back as 1864[20] and has been used in the treatment of canine and human lactic acidosis, some who presented at the beginning of treatment with cancer.

Off-label use

Akbar and Humaira Khan have since March 2007 treated cancer patients using DCA off-label at their private clinic, Medicor Cancer Centres, in Toronto.[21] They have treated several types of cancer and said on their web site that some patients "are showing varied positive responses to DCA including tumor shrinkage, reduction in tumor markers, symptom control, and improvement in lab tests".[22] Although they have not reported results at medical conferences, they have published one peer-reviewed paper in The Journal of Palliative Medicine [23] and uploaded details of patient responses and overall statistics on their web site.[24] They report that two patients who had DCA added to traditional chemotherapy had complete remission of metastatic cancer. Medicor states that the clinical results they have been getting are in agreement with clinical trials.[25]

Concerns about pre-trial use

Following its initial publication, The New Scientist later editorialized, "The drug may yet live up to its promise as an anti-cancer agent – clinical trials are expected to start soon. It may even spawn an entirely new class of anti-cancer drugs. For now, however, it remains experimental, never yet properly tested in a person with cancer. People who self-administer the drug are taking a very long shot and, unlikely as it may sound, could even make their health worse."[26]

In 2010, it was found that for human colorectal tumours grown in mice, under hypoxic conditions, DCA decreased rather than increased apoptosis, resulting in enhanced growth of the tumours.[27] These findings suggest that at least in some cancer types DCA treatment could be detrimental to patient health, highlighting the need for further testing before it can be considered a safe and effective cancer treatment.[27]

Planned and ongoing clinical trials

DCA is non-patentable as a compound, though a patent has been filed for its use in cancer treatment.[28] Research by Evangelos Michelakis has received no support from the pharmaceutical industry. Concerns have been raised that without strong intellectual property protection, the financial incentive for drug development is reduced, and therefore clinical trials of DCA may not be funded.[17][18][19][29] However, other sources of funding exist; previous studies of DCA have been funded by government organizations such as the National Institutes of Health, the Food and Drug Administration, the Canadian Institutes of Health Research and by private charities (e.g. the Muscular Dystrophy Association). Recognizing anticipated funding challenges, Michelakis's lab took the unorthodox step of directly soliciting online donations to fund the research.[30] After 6 months, his lab had raised over $800,000, enough to fund a small Clinical Phase 2 study. Michelakis and Archer have applied for a patent on the use of DCA in the treatment of cancer.[31][32]

On 24 September 2007, the Department of Medicine of Alberta University reported that after the trial funding was secured, both the Alberta local ethics committee and Health Canada approved the first DCA clinical trial for cancer.[33] This initial trial was relatively small with enrollment of up to 50 patients. The trial was completed in August 2009.[34] In May 2010 the team published a press release[35] stating no conclusions could be drawn as a result of the trial. A paper describing the results was published[36] but not linked from the press release. Only five patients had been treated with the drug during the trial.

In May 2011, online reports[37] suggested that the Alberta group had released new data which the media "had not reported". However, this appeared to be caused by confusion between dates (the previous update was May 2010[38]) and cancer charities moved quickly to counter these rumours,[39][40] which were subsequently covered in New Scientist magazine.[41]

Side effects

Reports in the lay press after the 2007 University of Alberta announcement claim that dichloroacetate "has actually been used safely in humans for decades",[42] DCA is generally well-tolerated, even in children.[43] Short-term, infused, bolus doses of DCA at 50 mg/kg/day have been well-tolerated.[44] The Medicor Cancer Centre reports on its website the use of 20–25 mg/kg/day on a two-week on, one week off cycle. This cycling helps determine which side effects are due to DCA, which are due to cancer, and if treatment should be discontinued.[45]

At sustained, higher doses(generally 25 mg/kg/day taken orally, or greater), there is increased risk of several reversible toxicities, especially peripheral neuropathy, neurotoxicity, and gait disturbance.[42][46] Studies have also shown that it can be carcinogenic at high doses.[47]


A clinical trial where DCA was given to patients of MELAS (a form of genetically inherited lactic acidosis) at 25 mg/kg/day was ended prematurely due to excessive peripheral nerve toxicity.[48] Dichloroacetate can also have anxiolytic or sedative effects.[9]

Animal studies suggest that the neuropathy and neurotoxicity during chronic dichloroacetate treatment may be partly due to depletion of thiamine, and thiamine supplementation in rats reduced these effects.[49] However, more recent studies in humans suggest that peripheral neuropathy is a common side effect during chronic DCA treatment, even with coadministration of oral thiamine.[50][51] An additional study reported that 50 mg/kg/day DCA treatment resulted in unsteady gait and lethargy in two patients, with symptoms occurring after one month for one patient and two months for the second. Gait disturbance and consciousness were recovered with cessation of DCA, however sensory nerve action potentials did not recover in one month.[52]

It has been reported that animals and patients treated with DCA have elevated levels of delta-aminolevulinic acid (delta-ALA) in the urine. A study published in 2008 suggests that this product may be the cause of the neurotoxic side effect of DCA by blocking peripheral myelin formation.[53][54]


Long term use (a year or more) of high doses (> 77 mg/kg/day) of DCA has been shown to increase risk of liver cancer in mice.[47] Studies of the trichloroethylene (TCE) metabolites dichloroacetic acid (DCA), trichloroacetic acid (TCA), and chloral hydrate suggest that both DCA and TCA are involved in TCE-induced liver tumorigenesis and that many DCA effects are consistent with conditions that increase the risk of liver cancer in humans.[55]


The promise of DCA as a cheap, effective and safe treatment for cancer generated a great deal of public interest. Many people turned to self-medication.[56][57]

Doctors warned of potential problems if people attempt to try DCA outside a controlled clinical trial. "If it starts going badly, who is following you before it gets out of control? By the time you realize your liver is failing, you're in big trouble", said Laura Shanner, Associate Professor of Health Ethics at the University of Alberta.[58]


  1. ^ Lide, David R. (1998). Handbook of Chemistry and Physics (87 ed.). Boca Raton, FL: CRC Press. pp. 3–164. ISBN 0-8493-0594-2 
  2. ^ Lide, David R. (1998). Handbook of Chemistry and Physics (87 ed.). Boca Raton, FL: CRC Press. pp. 1278. ISBN 0-8493-0594-2 
  3. ^ Lide, David R. (1998). Handbook of Chemistry and Physics (87 ed.). Boca Raton, FL: CRC Press. pp. 5–30. ISBN 0-8493-0594-2 
  4. ^ Bonnet, SéBastien; Archer, Stephen L.; Allalunis-Turner, Joan; Haromy, Alois; Beaulieu, Christian; Thompson, Richard; Lee, Christopher T.; Lopaschuk, Gary D. et al. (2007). "A Mitochondria-K+ Channel Axis Is Suppressed in Cancer and Its Normalization Promotes Apoptosis and Inhibits Cancer Growth". Cancer Cell 11 (1): 37–51. doi:10.1016/j.ccr.2006.10.020. PMID 17222789. 
  5. ^ a b c d e Michelakis, E. D.; Sutendra, G.; Dromparis, P.; Webster, L.; Haromy, A.; Niven, E.; Maguire, C.; Gammer, T. L. et al. (2010). "Metabolic Modulation of Glioblastoma with Dichloroacetate". Sci Transl Med 2 (31): 31ra34–31ra34. doi:10.1126/scitranslmed.3000677. PMID 20463368. http://dca-information.pbworks.com/f/Metabolic%20Modulation%20of%20Glioblastoma%20with%20Dichloroacetate.pdf. 
  6. ^ "Is Big Pharma Ignoring a Potential Cancer Cure?". Fox News. 18 May 2011. http://www.foxnews.com/health/2011/05/18/big-pharma-ignoring-potential-cancer-cure. 
  7. ^ Lide, D. R. (Ed.) (1990). CRC Handbook of Chemistry and Physics (70th Edn.). Boca Raton (FL):CRC Press.
  8. ^ MSDS (jtbaker)
  9. ^ a b Stacpoole P, Henderson G, Yan Z, James M (1998). "Clinical pharmacology and toxicology of dichloroacetate". Environ Health Perspect (Environmental Health Perspectives, Vol. 106) 106 Suppl 4: 989–994. doi:10.2307/3434142. JSTOR 3434142. PMC 1533324. PMID 9703483. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1533324.  Free full text
  10. ^ Stacpoole P (1989). "The pharmacology of dichloroacetate". Metabolism 38 (11): 1124–1144. doi:10.1016/0026-0495(89)90051-6. PMID 2554095. 
  11. ^ Stacpoole P, Lorenz A, Thomas R, Harman E (1988). "Dichloroacetate in the treatment of lactic acidosis". Ann Intern Med 108 (1): 58–63. PMID 3337517. 
  12. ^ a b Stacpoole P, Kerr D, Barnes C, Bunch S, Carney P, Fennell E, Felitsyn N, Gilmore R, Greer M, Henderson G, Hutson A, Neiberger R, O'Brien R, Perkins L, Quisling R, Shroads A, Shuster J, Silverstein J, Theriaque D, Valenstein E (2006). "Controlled clinical trial of dichloroacetate for treatment of congenital lactic acidosis in children". Pediatrics 117 (5): 1519–1531. doi:10.1542/peds.2005-1226. PMID 16651305. 
  13. ^ a b Kaufmann P, Engelstad K, Wei Y, Jhung S, Sano M, Shungu D, Millar W, Hong X, Gooch C, Mao X, Pascual J, Hirano M, Stacpoole P, DiMauro S, De Vivo D (2006). "Dichloroacetate causes toxic neuropathy in MELAS: a randomized, controlled clinical trial". Neurology 66 (3): 324–330. doi:10.1212/01.wnl.0000196641.05913.27. PMID 16476929. 
  14. ^ a b Stacpoole P, Wright E, Baumgartner T, Bersin R, Buchalter S, Curry S, Duncan C, Harman E, Henderson G, Jenkinson S (1992). "A controlled clinical trial of dichloroacetate for treatment of lactic acidosis in adults. The Dichloroacetate-Lactic Acidosis Study Group". N Engl J Med 327 (22): 1564–1569. doi:10.1056/NEJM199211263272204. PMID 1435883. 
  15. ^ Xu R, Pelicano H, Zhou Y, Carew J, Feng L, Bhalla K, Keating M, Huang P (2005). "Inhibition of glycolysis in cancer cells: a novel strategy to overcome drug resistance associated with mitochondrial respiratory defect and hypoxia". Cancer Res 65 (2): 613–21. PMID 15695406. 
  16. ^ Ibid. Bonnet.
  17. ^ a b "Cheap, ‘safe’ drug kills most cancers". New Scientist. 2007-01-17. http://www.newscientist.com/article.ns?id=dn10971. Retrieved 2007-01-17. 
  18. ^ a b c "DCA: Cancer Breakthrough or Urban Legend?" From ABC News, 5 February 2007. Accessed 15 February 2007.
  19. ^ a b "No Wonder Drug", letter to New Scientist from Ralph Moss Lemont. Published February 3, 2007. Accessed 16 February 2007.
  20. ^ T. E. (Thomas Edward) Thorpe. A Dictionary of Applied Chemistry. Vol. 3. Page 9 of 189 at www.ebooksread.com/authors-eng/t-e-thomas-edward-thorpe/a-dictionary-of-applied-chemistry-volume-3-hci/page-9-a-dictionary-of-applied-chemistry-volume-3-hci.shtml
  21. ^ Metabolic disease drug gains popularity among terminally ill cancer patients, Medicor Canter Centres, May 28, 2007
  22. ^ Medicor Cancer Centres – DCA Therapy
  23. ^ [1]
  24. ^ DCA (Dichloroacetate) Therapy
  25. ^ Medicor Cancer Centres' Observational DCA Treatment Data
  26. ^ "Editorial: Gambling with your life", New Scientist, 31 March 2007
  27. ^ a b Shahrzad, Siranoush; Lacombe, Kristen; Adamcic, Una; Minhas, Kanwal; Coomber, Brenda L. (November 2010). "Sodium dichloroacetate (DCA) reduces apoptosis in colorectal tumor hypoxia". Cancer Letters 297 (1): 75–83. doi:10.1016/j.canlet.2010.04.027. PMID 20537792. 
  28. ^ "CTV.ca: Researchers launch website on new cancer research". http://www.ctv.ca/servlet/ArticleNews/story/CTVNews/20070120/DCA_feature_070121/20070122?hub=Health. Retrieved 2007-10-08. 
  29. ^ "Small molecule offers big hope against cancer", by Ryan Smith. From ExpressNews, a University of Alberta publication. Published January 16, 2007. Accessed 15 February 2007.
  30. ^ Official University of Alberta DCA Site
  31. ^ Researchers launch website on new cancer research, CTV.ca, 22 January 2007
  32. ^ A Method of Treating Cancer Using Dichloroacetate, Application to the European Patent Office, 19 October 2006
  33. ^ DCA Update: Health Canada Approves First DCA Clinical Trial in Cancer, 24 September 2007
  34. ^ The Safety and Efficacy of DCA for the Treatment of Brain Cancer, ClinicalTrials.gov identifier: NCT00540176
  35. ^ Outlook 2008, Tufts Center for the Study of Drug Development
  36. ^ Michelakis, ED; Sutendra, G; Dromparis, P; Webster, L; Haromy, A; Niven, E; Maguire, C; Gammer, TL et al. (2010). "Metabolic modulation of glioblastoma with dichloroacetate". Science translational medicine 2 (31): 31ra34–31ra34. doi:10.1126/scitranslmed.3000677. PMID 20463368. 
  37. ^ The Cure for Cancer Has Been Found and is Purposely Being Ignored - Technorati blog (accessed 16/05/2011)
  38. ^ DCA Research Team publishes results of Clinical Trials - University of Alberta website
  39. ^ Potential cancer drug DCA tested in early trials - Cancer Research UK science blog
  40. ^ @CR_UK tweet - tweeted 16/05/11
  41. ^ Cancer drug resurfaces and threatens false optimism - New Scientist, 16 May 2011
  42. ^ a b Picard, André (2007-01-17). "Long-used drug shows new promise for cancer". Toronto: The Globe and Mail. http://www.theglobeandmail.com/servlet/story/RTGAM.20070117.wxhcancer17/BNStory/specialScienceandHealth/home. Retrieved 2007-01-17. 
  43. ^ Pearson H; Kurtz, TL; Han, Z; Langaee, T (2008). "Role of dichloroacetate in the treatment of genetic mitochondrial diseases". Adv Drug Deliv Rev. 60 (13,14): 1478–1487. doi:10.1016/j.addr.2008.02.014. PMID 18647626. 
  44. ^ Agbenyega T, Planche T, Bedu-Addo G, Ansong D, Owusu-Ofori A, Bhattaram VA, Nagaraja NV, Shroads AL, Henderson GN, Hutson AD, Derendorf H, Krishna S, Stacpoole PW (2003). "Population kinetics, efficacy, and safety of dichloroacetate for lactic acidosis due to severe malaria in children". J Clin Pharmacol. 43 (4): 386–396. doi:10.1177/0091270003251392. PMID 12723459. 
  45. ^ Medicor Cancer Centre (July, 2009). "Medicor Cancer Centre’s Observational DCA Treatment Data". http://www.medicorcancer.com/dca-data.html. Retrieved 10 November 2010. 
  46. ^ Stacpoole PW (1989). "The pharmacology of dichloroacetate". Metabolism 38 (11): 1124–1144. doi:10.1016/0026-0495(89)90051-6. PMID 2554095. 
  47. ^ a b DeAngelo AB, Daniel FB, Stober JA, Olson GR (1991). "The carcinogenicity of dichloroacetic acid in the male B6C3F1 mouse". Fundam Appl Toxicol. 16 (2): 337–347. doi:10.1016/0272-0590(91)90118-N. PMID 2055364. 
  48. ^ Kaufmann P, Engelstad K, Wei Y et al. (2006). "Dichloroacetate causes toxic neuropathy in MELAS: a randomized, controlled clinical trial". Neurology 66 (3): 324–330. doi:10.1212/01.wnl.0000196641.05913.27. PMID 16476929. 
  49. ^ Stacpoole P, Harwood H, Cameron D, Curry S, Samuelson D, Cornwell P, Sauberlich H (1990). "Chronic toxicity of dichloroacetate: possible relation to thiamine deficiency in rats". Fundam Appl Toxicol 14 (2): 327–37. doi:10.1016/0272-0590(90)90212-3. PMID 2318357. 
  50. ^ Kurlemann G, Paetzke I, Moller H, Masur H, Schuierer G, Weglage J, Koch HG (1995). "Therapy of complex I deficiency: peripheral neuropathy during dichloroacetate therapy". Eur J Pediatr 154 (11): 928–32. doi:10.1007/BF01957508. PMID 8582409. 
  51. ^ Spruijt L, Naviaux RK, McGowan KA, Nyhan WL, Sheean G, Haas RH, Barshop BA (2001). "Nerve conduction changes in patients with mitochondrial diseases treated with dichloroacetate". Muscle Nerve 24 (7): 916–24. doi:10.1002/mus.1089. PMID 11410919. 
  52. ^ Oishi K, Yoshioka M, Ozawa R, Yamamoto T, Oya Y, Ogawa M, Kawai M (2003). "Dichloroacetate treatment for adult patients with mitochondrial disease". Rinsho Shinkeigaku 43 (4): 154–61. PMID 12892050. 
  53. ^ Felitsyn N, McLeod C, Shroads AL, Stacpoole PW, Notterpek L (2008). "The heme precursor delta-aminolevulinate blocks peripheral myelin formation". J Neurochem. 106 (5): 2068–79. doi:10.1111/j.1471-4159.2008.05552.x. PMC 2574579. PMID 18665889. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2574579. 
  54. ^ Felitsyn, N; McLeod, C; Shroads, AL; Stacpoole, PW; Notterpek, L (2008). "The heme precursor delta-aminolevulinate blocks peripheral myelin formation". Journal of neurochemistry 106 (5): 2068–79. doi:10.1111/j.1471-4159.2008.05552.x. PMC 2574579. PMID 18665889. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2574579. 
  55. ^ Environ Health Perspect. 2006 Sep;114(9):1457-63 PMID 16966105 (free full text)
  56. ^ Pearson, Helen (2007). "Cancer patients opt for unapproved drug". Nature 446 (7135): 474–475. doi:10.1038/446474a. PMID 17392750. 
  57. ^ Interview: Would you try an untested cancer drug?, New Scientist, August 15, 2007
  58. ^ Andrea Sands (March 18, 2007). "Experts caution against patients compiling own data on unapproved cancer drug". Edmonton Journal. http://www.canada.com/topics/news/national/story.html?id=80b15f9d-cb4a-46a0-a4bc-f1a4ddea60d3&k=56245. 

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  • dichloroacetic acid — di·chlo·ro·ace·tic ac·id (di klor″o ə seґtik) acetic acid with two of its three hydrogen ions exchanged for chlorine atoms; it is a strong organic acid and is used as a protein precipitant in clinical chemistry …   Medical dictionary

  • dichloroacetic acid — (|)dī|klōrō+... noun Etymology: International Scientific Vocabulary dichlor + acetic : a strong high boiling liquid acid CHCl2COOH obtained especially by chlorination of acetic acid …   Useful english dictionary

  • dichloroacetic acid — noun An analogue of acetic acid in which two of the three hydrogen atoms of the methyl group are replaced by chlorine. Syn: DCA …   Wiktionary

  • Trichloroacetic acid — Chembox new Name = Trichloroacetic acid ImageFileL1 = Trichloroacetic acid 2D skeletal.png ImageSizeL1 =100px ImageFileR1 = Trichloroacetic acid 3D vdW.png ImageSizeR1 =120px ImageFile2 = Trichloroacetic acid elpot.png ImageSize2 =150px IUPACName …   Wikipedia

  • Carboxylic acid — Structure of a carboxylic acid Carboxylate ion …   Wikipedia

  • Acetic acid — Acetic redirects here. It is not to be confused with Ascetic. Acetic acid …   Wikipedia

  • Chloroacetic acid — Chloroacetic acid …   Wikipedia

  • Chloroformic acid — IUPAC name …   Wikipedia

  • chloroacetic acid — /ˌklɔroʊəsitɪk ˈæsəd/ (say .klawrohuhseetik asuhd) noun any of three acetic acids monochloroacetic acid, CH2Cl.COOH, which forms rhombic crystals; dichloroacetic acid, CHCl2.COOH, which is a colourless liquid; and trichloroacetic acid, CCl3.COOH …  

  • chloroacetic acid — An acetic acid in which one or more of the hydrogen atoms are replaced by chlorine. According to the number of atoms so displaced the acid is called monochloroacetic (chloroacetic), dichloroacetic, or trichloroacetic. SYN: chloracetic acid. * * * …   Medical dictionary

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