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Reference material for UK healthcare professionals. Doses and licensing change — verify against the current SmPC and local policy before use.

Drug monographs / Succimer (DMSA)

Succimer (DMSA)

An antidote UK poisons units recommend, UK hospitals struggle to stock, and the UK regulator has never licensed.

AntidoteLeadPoisoningToxicologyHeavy metalsUnlicensed

At a glance

ClassOral dithiol chelator (meso-2,3-dimercaptosuccinic acid)
UK licenceNone. No succimer product on the emc (checked 6 Sep 2026)
Dose in a UK series30 mg/kg/day orally — one West Midlands series
Main useInorganic lead poisoning; also used in arsenic and mercury
Vs sodium calcium edetateInsufficient data to call either superior
Probably acts in theKidney — if mixed cysteine disulfides are the active moiety
CNS penetrationNot to any major extent — as for edetate
Stop forSevere mucocutaneous reaction; watch transaminases
Practical catchStock. UK hospitals may not hold it
Who decidesNPIS 0344 892 0111 — not this page

Why this drug is interesting

Succimer is the drug that made outpatient lead chelation conceivable. It is taken by mouth, it is comparatively well tolerated, and in the best available comparison no difference in efficacy against intravenous sodium calcium edetate could be demonstrated either way. For a poisoning that often needs repeated courses in children, that combination is genuinely valuable.

The consequence is practical and it has bitten. In a 2024 UK outbreak, the choice between succimer and sodium calcium edetate for the fifteen patients who were chelated was made "dependent on stock availability", and the authors explicitly flag "potential issues surrounding stock availability of rarely used antidotes for uncommon presentations in the event of an outbreak of poisoning".2

Pharmacology

Mechanism

Succimer is a dithiol — two sulfhydryl groups on a succinic acid backbone. The nature of the succimer–lead chelate is, unusually for a drug in routine use, less clearly defined than that of its intravenous rival. There is evidence that the mixed disulfides of cysteine formed by extensive metabolism are the active chelating moiety in humans; if so, chelation occurs principally, if not exclusively, in the kidney.1

Absorption and elimination

Oral absorption of succimer is more complete than that of sodium calcium edetate, which is why the latter has to be given parenterally at all. Both are distributed predominantly extracellularly and both have elimination half-lives of less than 60 minutes. Succimer is extensively metabolised; edetate is not metabolised at all.1

Dosing

In the West Midlands Poisons Unit series of a lead outbreak at a UK indoor firing range, patients were chelated with oral succimer 30 mg/kg/day, or with intravenous sodium calcium edetate 75 mg/kg/day, according to what was in stock.2 Fifteen of the sixty-three patients tested were chelated.

For mercury-vapour poisoning, the closely related thiol DMPS has been used at the same figure — 30 mg/kg/day orally, given as four five-day courses — in a UK case with objective neurological recovery.3 The coincidence of dose between two different drugs is worth noticing but is not a reason to substitute one for the other; see DMPS.

Duration and endpoint

Courses are conventionally given over days rather than as a single dose, repeated according to blood lead concentration and symptoms, with the source of exposure removed in between. The endpoint is a clinical and biochemical judgement made with the poisons service — this page deliberately does not offer a stopping rule, because no UK label defines one and the published sources describe practice rather than prescribe it.

Safety

Compared with sodium calcium edetate

The comparison is the most useful safety information available, because the two drugs are the realistic alternatives to each other:1

Nephrotoxicity
Sodium calcium edetate causes dose-related nephrotoxicity. This is the clearest safety difference between the two and it favours succimer.
Zinc and copper
Both deplete zinc and copper, but the effect on zinc is significantly greater with sodium calcium edetate.
Transaminases
A transient rise has been reported with both and "appears to be more common with DMSA" — but neither has been associated with clinically significant hepatic toxicity.
Skin
Skin lesions on edetate are unusual and have been attributed to zinc deficiency. Succimer "has occasionally been associated with a severe mucocutaneous reaction necessitating discontinuation of therapy."

In pregnancy and childhood

Lead poisoning disproportionately affects children, and the UK outbreak included patients from 6 months of age.2 Neither the paediatric dose nor the pregnancy position can be taken from a UK label because there is none. Both are NPIS conversations, and in pregnancy the competing risks — fetal exposure to mobilised maternal lead against continued maternal poisoning — are the substance of that conversation.

Practical use in the ED

  1. Confirm with a blood lead concentration and check the units your laboratory uses — µg/dL and µmol/L are both current in the UK (1 µg/dL ≈ 0.048 µmol/L).
  2. Call NPIS on 0344 892 0111. Whether to chelate, with what, and for how long are all decisions for the poisons service.
  3. Ask pharmacy what you actually have, early. Succimer is unlicensed and may not be stocked; the published UK experience is of the agent being chosen by availability.2
  4. Remove the source before anything else. Chelating a patient who is still being exposed treats a number rather than a person — the UK outbreak was, at root, an occupational hygiene failure.
  5. Do not expect chelation to fix encephalopathy directly. Neither succimer nor edetate meaningfully enters the brain.1 Severe neurological presentations need critical care and expert toxicology, not a larger oral dose.
  6. Think about the contacts. In the UK outbreak, exposure reached household contacts as well as staff, and 87 people were identified as potentially exposed.2

Critical appraisal

The honest position on succimer versus sodium calcium edetate is that nobody knows which is better. The 2009 systematic comparison searched Medline, Toxline and Embase to June 2009 and found that comparison between the experimental studies was "complicated by substantial variations in study design" — antidote dose, route, duration, the amount and duration of lead dosing, and a lack of direct comparison between antidotes, most studies having compared against control rather than each other.1

So the choice in practice is made on route, toxicity and supply rather than on efficacy: oral where oral will do, edetate where there is more experience in the sickest patients, and in the UK, frequently, whichever one the pharmacy can obtain. That is an uncomfortable basis for an antidote decision, and it is the actual one.

References

  1. 1
    Bradberry S, Vale A. A comparison of sodium calcium edetate (edetate calcium disodium) and succimer (DMSA) in the treatment of inorganic lead poisoning. Clinical Toxicology (Philadelphia) 2009;47(9):841–858. PubMed 19852620. The backbone of this page. Source of the pharmacokinetic comparison (oral absorption, extracellular distribution, <60 min half-lives, metabolism to mixed disulfides of cysteine), the compartment findings (bone vs kidney), the blood–brain barrier statement, the adverse-effect comparison (edetate nephrotoxicity and greater zinc depletion; DMSA transaminase rise and severe mucocutaneous reaction) and the quoted conclusion. Abstract read 6 September 2026.
  2. 2
    Warsi A, Pucci MR, Bradberry SM, et al. Outbreak of lead poisoning from a civilian indoor firing range in the UK. Occupational and Environmental Medicine 2024;81(3):159–162. PubMed 38302418. West Midlands Poisons Unit. Source of the UK doses (oral succimer 30 mg/kg/day, IV sodium calcium edetate 75 mg/kg/day), the stock-availability finding, the 87 exposed / 63 tested / 15 chelated / 9 symptomatic figures, the 6-months-to-78-years age range and the 242 µg/dL (11.7 µmol/L) peak. Abstract read 6 September 2026.
  3. 3
    Bradberry SM, Sheehan TM, Barraclough CR, Vale JA. DMPS can reverse the features of severe mercury vapor-induced neurological damage. Clinical Toxicology (Philadelphia) 2009;47(9):894–898. PubMed 19852623. Cited only for the DMPS dose and course structure referred to on this page. Abstract read 6 September 2026.
  4. 4
    Varma A, Bradberry SM, Vale JA. Rash and pyrexia after succimer (dimercaptosuccinic acid; DMSA). Clinical Toxicology (Philadelphia) 2017;55(7):680. PubMed 28349748. A single-page correspondence with no abstract in PubMed (confirmed 6 September 2026). Cited solely for the event its title reports; no clinical detail beyond that has been attributed to it.
  5. 5
    electronic Medicines Compendium. medicines.org.uk/emc. Searched 6 September 2026 for succimer, DMSA, Chemet and Succicaptal: all four return a "No search results" page. No SmPC is published for succimer in the UK, so none can be cited and all UK use is of an unlicensed medicine. 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.
  6. 6
    National Poisons Information Service. TOXBASE · NPIS 0344 892 0111. Required. Succimer is unlicensed in the UK; the indication for chelation, the agent, the dose and the endpoint are all NPIS decisions.

Last reviewed 2026-09-07 · Author: Dr Nirmalya Hore