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Skeletal formula and ball and stick model of dimercaprol
Clinical data
Trade namesBAL in Oil
British Anti-Lewisite
British antilewisite
License data
  • US: C (Risk not ruled out)
Routes of
ATC code
Legal status
Legal status
Pharmacokinetic data
CAS Number
PubChem CID
CompTox Dashboard (EPA)
ECHA InfoCard100.000.394 Edit this at Wikidata
Chemical and physical data
Molar mass124.225 g mol−1 g·mol−1
3D model (JSmol)
Density1.239 g cm−3 g/cm3
Boiling point393 °C (739 °F) at 2.0 kPa

Dimercaprol, also called British anti-Lewisite (BAL), is a medication used to treat acute poisoning by arsenic, mercury, gold, and lead.[3] It may also be used for antimony, thallium, or bismuth poisoning, but the evidence for these uses is not very strong.[3][4] It is given by injection into a muscle.[3]

Common side effects include high blood pressure, pain at the site of the injection, vomiting, and fever.[3] It is not recommended in people with peanut allergies.[3] It is unclear if use in pregnancy is safe for the baby.[3] Dimercaprol works by binding with heavy metals.[3]

Dimercaprol was first made during World War II.[5] It is on the World Health Organization's List of Essential Medicines, the most effective and safe medicines needed in a health system.[6] In the United States a course of treatment costs more than US$200.[7]

Medical uses

Dimercaprol has long been the mainstay of chelation therapy for lead or arsenic poisoning,[8] and it remains an essential drug.[9] It is also used as an antidote to the chemical weapon Lewisite. Nonetheless, because it can have serious adverse effects, researchers have also pursued development of less toxic analogues.,[8] such as succimer.

Wilson's disease is a genetic disorder in which copper builds up inside the liver and other tissues. Dimercaprol is a copper chelating agent that has been approved by the FDA to treat Wilson's disease.[10]

Mechanism of action

Arsenic and some other heavy metals act by chemically reacting with adjacent thiol residues on metabolic enzymes, creating a chelate complex that inhibits the affected enzyme's activity.[11] Dimercaprol competes with the thiol groups for binding the metal ion, which is then excreted in the urine.[citation needed]

Dimercaprol is itself toxic, with a narrow therapeutic range and a tendency to concentrate arsenic in some organs. Other drawbacks include the need to administer it by painful intramuscular injection.[12] Serious side effects include nephrotoxicity and hypertension.

Dimercaprol has been found to form stable chelates in vivo with many other metals including inorganic mercury, antimony, bismuth, cadmium, chromium, cobalt, gold, and nickel. However, it is not necessarily the treatment of choice for toxicity to these metals. Dimercaprol has been used as an adjunct in the treatment of the acute encephalopathy of lead toxicity. It is a potentially toxic drug, and its use may be accompanied by multiple side effects. Although treatment with dimercaprol will increase the excretion of cadmium, there is a concomitant increase in renal cadmium concentration, so that its use in case of cadmium toxicity is to be avoided. It does, however, remove inorganic mercury from the kidneys; but is not useful in the treatment of alkylmercury or phenylmercury toxicity. Dimercaprol also enhances the toxicity of selenium and tellurium, so it is not to be used to remove these elements from the body.[citation needed]


Its original name reflects its origins as a compound secretly developed by British biochemists at Oxford University during World War II[13][14] as an antidote for lewisite, a now-obsolete arsenic-based chemical warfare agent.[13]

See also


  1. ^ Poisoning in Children. Jaypee Brothers Publishers. 2013. p. 70. ISBN 9789350257739.
  2. ^ Nomenclature of Organic Chemistry : IUPAC Recommendations and Preferred Names 2013 (Blue Book). Cambridge: The Royal Society of Chemistry. 2014. p. 697. doi:10.1039/9781849733069-FP001. ISBN 978-0-85404-182-4. The prefixes ‘mercapto’ (–SH), and ‘hydroseleno’ or selenyl (–SeH), etc. are no longer recommended.
  3. ^ a b c d e f g "Dimercaprol". The American Society of Health-System Pharmacists. Archived from the original on 21 December 2016. Retrieved 8 December 2016. Cite uses deprecated parameter |deadurl= (help)
  4. ^ WHO Model Formulary 2008 (PDF). World Health Organization. 2009. p. 62. ISBN 9789241547659. Archived (PDF) from the original on 13 December 2016. Retrieved 8 December 2016. Cite uses deprecated parameter |deadurl= (help)
  5. ^ Greenwood, David (2008). Antimicrobial Drugs: Chronicle of a Twentieth Century Medical Triumph. OUP Oxford. p. 281. ISBN 9780199534845. Archived from the original on 2016-12-20. Cite uses deprecated parameter |deadurl= (help)
  6. ^ "WHO Model List of Essential Medicines (19th List)" (PDF). World Health Organization. April 2015. Archived (PDF) from the original on 13 December 2016. Retrieved 8 December 2016. Cite uses deprecated parameter |deadurl= (help)
  7. ^ Hamilton, Richart (2015). Tarascon Pocket Pharmacopoeia 2015 Deluxe Lab-Coat Edition. Jones & Bartlett Learning. p. 470. ISBN 9781284057560.
  8. ^ a b Flora, SJ; Pachauri, V (2010), "Chelation in metal intoxication", International Journal of Environmental Research and Public Health, 7 (7): 2745–2788, doi:10.3390/ijerph7072745, PMC 2922724, PMID 20717537.
  9. ^ "WHO Model List of Essential Medicines" (PDF). World Health Organization. October 2013. Archived (PDF) from the original on 23 April 2014. Retrieved 22 April 2014. Cite uses deprecated parameter |deadurl= (help)
  10. ^ Leggio, L; Addolorato, G; Abenavoli, L; Gasbarrini, G (2005). "Wilson's disease: clinical, genetic and pharmacological findings". International journal of immunopathology and pharmacology. 18 (1): 7–14. doi:10.1177/039463200501800102. PMID 15698506.
  11. ^ Goldman M, Dacre JC. (1989) Lewisite: its chemistry, toxicology, and biological effects. Rev Environ Contam Toxicol 110: 75-115
  12. ^ Mückter H, Liebl B, Reichl FX et al. (1997) Are we ready to replace dimercaprol (BAL) as an arsenic antidote? Human and Experimental Toxicology 16: 460-465
  13. ^ a b Domingo Tabangcura, Jr.; G. Patrick Daubert. "British anti-Lewisite". Archived from the original on 2009-02-02. Cite uses deprecated parameter |deadurl= (help)
  14. ^ Peters, R; Stocken, L; Thompson, R. (1945). "British Anti-Lewisite (BAL)". Nature. 156 (3969): 616–619. doi:10.1038/156616a0. PMID 21006485.