Dimercaprol (BAL)

Why this drug is interesting

Dimercaprol is where chelation therapy began. "Chelation for heavy metal intoxication began more than 70 years ago with the development of British anti-lewisite (BAL; dimercaprol) in wartime Britain as a potential antidote [sic] the arsenical warfare agent lewisite."¹ The name is a wartime acronym that stuck.

Its successors were designed specifically to be better versions of it: "DMPS (unithiol) and DMSA (succimer), dithiol water-soluble analogs of BAL, were developed in the Soviet Union and China in the late 1950s. These three agents have remained the mainstay of chelation treatment of arsenic and mercury intoxication for more than half a century."¹ Reading dimercaprol's limitations is therefore the clearest way to understand why the other two exist.

Pharmacology

Mechanism

Dimercaprol is a dithiol: two adjacent sulfhydryl groups that bind trivalent arsenic and divalent mercury, competing with the sulfhydryl groups on enzymes that these metals poison. Lewisite works by attacking those same enzyme thiols, which is exactly why an agent with two spare thiols was designed against it.

It is lipophilic and formulated in peanut oil for deep intramuscular injection. That solves the delivery problem for a lipid-soluble drug, and creates two others: the injections are notoriously painful, and the vehicle is a consideration in peanut allergy.

Timing

Where it is and is not used

Reasonable uses

• Acute arsenic poisoning — the original indication, though DMPS and DMSA are now generally preferred where available.¹
• Acute inorganic mercury salt poisoning — same caveat.¹
• Severe lead poisoning, especially with encephalopathy — where it is classically given before sodium calcium edetate, on the reasoning that starting the extracellular chelator first risks redistributing lead. That sequencing is long-standing practice rather than a conclusion of the modern comparative literature.

Where it is contraindicated or useless

It is also not the agent for iron (desferrioxamine) or for the metals where a specific binder exists. As a general rule, the era of "a chelator for any metal" is over — each metal now has a preferred agent, and using the wrong one is not merely ineffective.

Dosing

What is useful to know in advance is the shape of treatment: deep intramuscular injection, repeated at short intervals over the first days, with the interval lengthening as the patient improves; and, in severe lead poisoning, started before the intravenous chelator rather than alongside it.

Safety

Dimercaprol is the least well tolerated of the three dithiols, which is what "lower therapeutic index" means in practice.¹ The reactions most often described are dose-related and begin soon after injection: hypertension and tachycardia, a burning sensation in the mouth and throat, lacrimation and rhinorrhoea, nausea and vomiting, headache, and painful sterile abscesses at injection sites.

Because the toxicity is largely dose-related and the drug is given for days, the practical management is the same as for its rivals: the shortest effective course, guided by a poisons unit, with the exposure source removed so that repeated courses are not needed.

Critical appraisal

The case for dimercaprol is now largely historical and logistical. Where DMPS or DMSA can be obtained, the comparative argument favours them on two counts that are not close: a higher therapeutic index and no redistribution of arsenic or mercury to the brain.¹ Dimercaprol's remaining niches are severe lead poisoning with encephalopathy, where sequencing convention still places it first, and the situation every UK department should plan for — the one where it is the only chelator anybody can actually get hold of tonight.

That distinction — acute poisoning treated within hours, where the animal evidence is reasonable, versus chronic exposure, where accelerating excretion has not been shown to change outcomes — is the most useful thing to carry away from this page. It applies equally to dimercaprol, DMPS and succimer, and it is the reason chelation for vague chronic "heavy metal toxicity" outside a poisons-unit indication is not supportable.

References

1. 1
   Kosnett MJ. The role of chelation in the treatment of arsenic and mercury poisoning. Journal of Medical Toxicology 2013;9(4):347–354. PubMed 24178900. The backbone of this page. Source of the wartime lewisite origin, the development of DMPS and DMSA as water-soluble analogues in the Soviet Union and China in the late 1950s, the higher therapeutic index of DMPS and DMSA and their lack of brain redistribution, the within-minutes-to-hours timing requirement and declining efficacy with delay, and the statement that efficacy in chronic intoxication in terms of morbidity and mortality is largely unestablished. Abstract read 6 September 2026.
2. 2
   Hoffman RS. Thallium toxicity and the role of Prussian blue in therapy. Toxicological Reviews 2003;22(1):29–40. PubMed 14579545. Source of the evidence against dimercaprol and penicillamine in thallium poisoning. Abstract read 6 September 2026.
3. 3
   electronic Medicines Compendium. medicines.org.uk/emc. Searched 6 September 2026 for dimercaprol: returns a "No search results" page. BAL was searched as a synonym and matched only unrelated products (Anusol preparations), which confirms the search resolves substrings rather than failing silently. No SmPC is published for dimercaprol in the UK. The emc is an industry-hosted compendium of published SmPCs and PILs, not the MHRA register — this establishes that no SmPC is published, rather than that no marketing authorisation exists anywhere.
4. 4
   National Poisons Information Service. TOXBASE · NPIS 0344 892 0111. Required, and this page deliberately gives no dose. NPIS also advises on whether dimercaprol or one of its analogues is the appropriate agent, and on sequencing with sodium calcium edetate in severe lead poisoning.