|CAS number||, (2R)-2-sulfanyl , (2S)-2-sulfanyl|
|PubChem||, (2R)-2-sulfanyl, (2S)-2-sulfanyl|
|ChemSpider||, (2R)-2-sulfanyl , (2S)-2-sulfanyl|
|Jmol-3D images||Image 1|
|Molar mass||124.225 g mol-1|
|Density||1.239 g cm-3|
|Boiling point||120 °C; 248 °F; 393 K at 2.0 kPa|
Refractive index (nD)
|GHS signal word||DANGER|
|H301, H315, H319, H335|
|P261, P301+310, P305+351+338|
|Flash point||112 °C (234 °F; 385 K)|
|Except where noted otherwise, data are given for materials in their standard state (at 25 °C (77 °F), 100 kPa)|
Dimercaprol (INN) or British anti-Lewisite (abbreviated BAL), is a compound developed by British biochemists at Oxford University during World War II. It was developed secretly as an antidote for lewisite, the now-obsolete arsenic-based chemical warfare agent. Today, it is used medically in treatment of arsenic, mercury, gold, lead, antimony, and other toxic metal poisoning. In addition, it has in the past been used for the treatment of Wilson's disease, a genetic disorder in which the body tends to retain copper.
It is on the World Health Organization's List of Essential Medicines, a list of the most important medication needed in a basic health system.
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. Dimercaprol competes with the thiol groups for binding the metal ion, which is then excreted in the urine.
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. Serious side effects include nephrotoxicity and hypertension.
Dimercaprol has been found to form stable chelates in vivo with many other toxic 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 phenyl mercury toxicity. Dimercaprol also enhances the toxicity of selenium and tellurium, so it is not to be used to remove these elements from the body.
- Domingo Tabangcura, Jr., G. Patrick Daubert. "British anti-Lewisite".
- Peters, R; Stocken, L; Thompson, R. (1945). "British Anti-Lewisite (BAL)". Nature 156 (3969): 616–619. doi:10.1038/156616a0. PMID 21006485.
- Denny-Brown D, PORTER H (December 1951). "The effect of BAL (2,3-dimercaptopropanol) on hepatolenticular degeneration (Wilson's disease)". N. Engl. J. Med. 245 (24): 917–25. doi:10.1056/NEJM195112132452401. PMID 14882450.
- "WHO Model List of EssentialMedicines". World Health Organization. October 2013. Retrieved 22 April 2014.
- Goldman M, Dacre JC. (1989) Lewisite: its chemistry, toxicology, and biological effects. Rev Environ Contam Toxicol 110: 75-115
- 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