DMSA (dimercaptosuccinic acid)

Dimercaptosuccinic Acid (DMSA / Succimer): A Comprehensive Reference

1. Identity and Chemical Characterization

Names and Classification

The chemical name for succimer is meso-2,3-dimercaptosuccinic acid (DMSA), with the empirical formula C₄H₆O₄S₂ and a molecular weight of 182.2. The compound is formally classified as an organosulfur chelating agent. Its CAS registry number is 304-55-2. DMSA is defined as a compound that contains two carboxylic groups and two thiol groups, which participate in metal-ligand reactions. It is a structural analog of dimercaprol (British Anti-Lewisite, BAL), the older chelating agent from which it was derived.

Physical Properties and Form

Succimer is a white crystalline powder with an unpleasant, characteristic mercaptan odor and taste. DMSA is a negatively charged sulfur-containing chelating agent. In its pharmaceutical preparation, each CHEMET (the brand-name oral preparation) opaque white capsule for oral administration contains medicated beads with 100 mg of succimer.

Common Preparations and Forms

The most established pharmaceutical form is the oral capsule (brand name Chemet). DMSA contains two sulfhydryl groups, making it an analog of dimercaprol, and is used for metal chelation. Beyond the oral form, DMSA is also widely employed in nuclear medicine as a radiolabeled diagnostic agent. Technetium-99m–labeled DMSA shows altered organ distribution depending on the method of preparation; at acidic pH (pH 2–3), DMSA chelates with technetium in a lower oxidation state (III) and forms a trivalent complex, Tc-99m (III) DMSA. At alkaline pH (pH 8–9), it chelates with technetium in a higher oxidation state to form a pentavalent complex, Tc-99m (V) DMSA, which resembles the phosphate ion and is rapidly excreted in the urine.

Succimer is on the World Health Organization's List of Essential Medicines.

2. Historical and Traditional Use

Origins and Early Discovery

Dimercaptosuccinic acid was first synthesized by V. L. Nirenburg at the Urals Polytechnic Institute, commissioned by one of the electrical enterprises of Sverdlovsk, Russia, which consumed many tons of mercury and was looking for a medicine to prevent poisoning of personnel. In 1957, Chinese scientists found that dimercaptosuccinic acid can effectively treat antimony poisoning due to overdose of tartar emetic. A pronounced protective effect in animal poisoning with arsenic and mercury was first shown by I. E. Okonishnikova in 1962.

Dimercaptosuccinic acid, known as succimer or DMSA, was developed by Liang and Ding (formerly Ting) and colleagues in Shanghai, China, in the late 1950s. It was developed as a derivative of British anti-Lewisite (BAL) initially intended for the treatment of schistosomiasis. Although ineffective for that parasitic infection, early observations noted its potential chelating properties for heavy metals.

Soviet, Chinese, and Eastern European Use

DMPS (unithiol) and DMSA (succimer), dithiol water-soluble analogs of BAL, were developed in the Soviet Union and China in the late 1950s, and these three agents have remained the mainstay of chelation treatment of arsenic and mercury intoxication for more than half a century. Subsequent research in the Soviet Union and Eastern Europe during the 1960s and 1970s focused on animal models, demonstrating succimer's efficacy in treating poisoning from lead, mercury, and arsenic by enhancing urinary excretion of these metals and reducing tissue burdens.

DMSA was initially studied in China, Japan, and Russia in the 1950s for treating heavy metal toxicity, and in the 1970s gained popularity in Europe and the USA. In China, there is substantial experience with the use of dimercaptosuccinic acid (DMSA, Succimer) in the treatment of Wilson's disease.

Regulatory Milestones

In 1984, the now-defunct Bock Pharmaceutical Company requested the FDA grant approval for orphan drug status under the brand name Chemet, and the FDA approved this in 1991. Developed as a safer alternative to earlier chelators like dimercaprol and EDTA, succimer was granted orphan drug status by the FDA in 1991 for treating mercury intoxication, reflecting its role in addressing rare conditions.

3. Key Constituents and Mechanisms of Action

Structural Basis for Chelation

Succimer is an organo-sulfur compound with two sulfhydryl groups that bind divalent metal ions such as lead, cadmium, mercury, and arsenic. Meso-2,3-dimercaptosuccinic acid binds to "soft" heavy metals such as Hg²⁺ and Pb²⁺, mobilizing these ions for excretion. The geminal dithiol arrangement positions both sulfur atoms to form a stable chelate ring with target metal ions.

Succimer does not significantly chelate essential metals such as zinc, copper, or iron, and its specificity, safety, and oral availability make it preferable to other chelating agents for treating lead poisoning such as Ca-EDTA, which must be given intravenously, and dimercaprol (BAL), which requires intramuscular administration. Its effect on elimination of the endogenous minerals calcium, iron, and magnesium is insignificant; minor increases in zinc and copper excretion may occur.

Mechanism of Chelation and Metal Excretion

DMSA binds tenaciously to toxic metal ions such as lead (Pb), mercury (Hg), and arsenic (As), forming a stable, water-soluble complex called a chelate. This complex is biologically inert, preventing the metal from exerting its toxic effects on body tissues. The kidneys then filter this metal–succimer complex from the blood, and it is subsequently excreted from the body in the urine, effectively reducing the overall burden of the toxic metal in the body, particularly from the blood and soft tissues.

Succimer is a lead chelator; it forms water-soluble chelates and, consequently, increases the urinary excretion of lead. Animal experiments and in some instances human data indicate that the dithiol chelators enhance arsenic and mercury excretion.

Distribution Characteristics and Pharmacological Limitation

DMSA has an extracellular distribution that may be responsible for its low toxicity compared to other dithiols. Succimer, although considered safer, shares the limitation of extracellular distribution, which renders the drug less effective in cases of slow, low-dose, chronic metal poisoning (especially lead and arsenic) since the metal reaches cellular compartments behind the physiological barriers, including the blood–brain barrier.

DMSA is compromised with a number of shortcomings, including the inability to treat chronic arsenic poisoning due to its extracellular distribution. DMSA distribution is predominantly extracellular, since it is unable to cross hepatic cell membranes; hence, it is able to chelate arsenic from extracellular sites but not from intracellular sites.

DMPS and DMSA, which have a higher therapeutic index than BAL, do not redistribute arsenic or mercury to the brain, which offers advantages in clinical practice.

Biotransformation and Active Metabolites

Approximately 90% of the absorbed dose is metabolized to mixed succimer–cysteine disulfides. The majority of mixed disulfides consist of succimer in disulfide linkages with two molecules of L-cysteine; the remaining disulfides contain one L-cysteine per succimer molecule. Succimer is eliminated primarily in the urine, where 80–90% appears as mixed disulfides, mainly 2:1 or 1:1 cysteine–succimer adducts. Studies suggest that these adducts, rather than the parent drug, may be responsible for metal-chelating activity in vivo.

Most DMSA in plasma is protein (mainly albumin)-bound through a disulfide bond with cysteine; only a very small amount is present as free drug, which is filtered at the glomerulus and then extensively reabsorbed into proximal tubule cells. Non-filtered protein-bound DMSA in peritubular capillaries is also available for uptake into proximal tubule cells by active anion transport at the basolateral membrane.

Renal elimination of the metal chelates appears to be mediated in part by the multidrug resistance protein 2 (Mrp2).

Reactive Oxygen Species Scavenging

DMSA (meso-2,3-dimercaptosuccinic acid) is also a potent lead chelating agent found to be a scavenger of reactive oxygen species (ROS). This antioxidant-like property may contribute to a reduction in metal-induced oxidative tissue damage beyond the chelation effect itself, though this has been characterized primarily in preclinical settings.

4. Pharmacokinetics

Absorption and Distribution

DMSA is absorbed rapidly but incompletely after oral administration, probably through an active transporter. There is evidence that enterohepatic circulation occurs. After oral administration, peak blood concentrations occur in approximately 3 hours. Distribution is predominantly extracellular, and in the blood, succimer is extensively bound (>90%) to plasma proteins.

Elimination and Half-Life

In a study performed in healthy adult volunteers, after a single dose of ¹⁴C-succimer at 16, 32, or 48 mg/kg, 49% of the radiolabeled dose was excreted on average: 39% in the feces, 9% in the urine, and 1% as carbon dioxide from the lungs. The apparent elimination half-life of the radiolabeled material in the blood was about two days. The elimination half-life of transformed succimer is approximately 2–4 hours. In other studies of healthy adult volunteers receiving a single oral dose of 10 mg/kg, approximately 25% of the administered dose was excreted in the urine, with peak blood level and urinary excretion occurring between two and four hours.

DMSA is biotransformed to a mixed disulfide in humans. By 14 hours after DMSA administration at 10 mg/kg, only 2.5% of the administered DMSA is excreted in the urine as unaltered DMSA, and 18.1% of the dose is found in the urine as altered forms.

Renal clearance may be diminished in the setting of pediatric lead intoxication.

5. Scientific Evidence by Area of Use

5.1 Lead Poisoning (Primary Indication)

DMSA is used to treat lead, mercury, and arsenic toxicity, and is FDA approved for treating lead poisoning in pediatric patients. CHEMET is indicated for the treatment of lead poisoning in pediatric patients aged 1 year and older with blood lead levels above 45 mcg/dL.

Dose-Ranging Clinical Studies

Dose-ranging studies were performed in 18 men with blood lead levels of 44–96 mcg/dL. Three groups of 6 patients received either 10.0, 6.7, or 3.3 mg/kg succimer orally every 8 hours for 5 days. After five days the mean blood levels of the three groups decreased 72.5%, 58.3%, and 35.5%, respectively. The mean urinary lead excretions in the initial 24 hours were 28.6, 18.6, and 12.3 times the pretreatment 24-hour urinary lead excretion.

Adult Lead Poisoning

Oral DMSA at 30 mg/kg/day was administered to adults with blood lead concentrations ≥50 µg/dL, and the impact of DMSA on urine lead excretion, on blood lead concentrations, and on symptoms was observed. Thirty-five courses were given to 17 patients. DMSA significantly (P < 0.0001) increased urine lead excretion and significantly (P < 0.0001) reduced blood lead concentrations. Mean daily urine lead excretion exceeded the pre-treatment value by a median of 12-fold.

The Treatment of Lead-Exposed Children (TLC) Trial

The Treatment of Lead-Exposed Children (TLC) clinical trial was a randomized, double-blind, placebo-controlled clinical trial comparing the effect of lead chelation with succimer to placebo therapy, with sites in Cincinnati and Columbus, Ohio; Philadelphia, Pennsylvania; Baltimore, Maryland; and Newark, New Jersey. The study was designed to test outcomes in IQ, neuropsychological function, behavior, physical growth, and blood pressure three years after initiation of treatment. Enrollment was conducted between 1994 and 1997, with completion of the initial three-year follow-up in 2000.

The trial enrolled 780 children in a placebo-controlled, randomized design of up to three courses of succimer in children with blood lead levels of 20–44 µg/dL (1.0–2.1 µM). Children were aged 12–33 months, 77% were African-American, and 7% were Hispanic; they lived in deteriorating inner-city housing. Placebo-treated children had a gradual decrease in blood lead level. Succimer-treated children had an abrupt drop in blood lead level, followed by rebound. The mean blood lead level of the succimer-treated children during the 6 months after initiation of treatment was 4.5 µg/dL lower than that of placebo-treated children. However, this large randomized, double-blind, placebo-controlled trial of succimer in children with blood lead concentrations between 25 and 44 mcg/dL found no evidence of benefit in clinical outcome or long-term blood lead reduction. Although succimer treatment has been associated with subjective clinical improvement, controlled clinical trials demonstrating therapeutic efficacy in neurodevelopmental outcomes have not been conclusively reported.

Pediatric Blood Lead Reduction: Retrospective Evidence

In a retrospective study from Nigeria, chelation therapy using DMSA lowered blood lead levels in children with severe lead poisoning. Each course of oral DMSA was associated with an average reduction to 75% of the pre-course blood lead level, with slightly better improvement when the pre-course level was higher.

Chisolm (2000), studying 59 children given 116 four-week courses of succimer for lead toxicity, found that lead levels fell rapidly on treatment but rebounded to 58% of pretreatment values thereafter; there were no adverse reactions. This rebound phenomenon underscores that DMSA reduces blood lead but does not necessarily address deeper tissue or bone stores of lead in a sustained way.

Comparison with Other Chelators

At moderately elevated blood lead concentrations, oral succimer is comparable with parenteral calcium EDTA in decreasing blood lead concentrations. The efficiency of succimer in eliminating lead from the blood and tissues may somewhat decline at very high blood concentrations of lead (e.g., >100 mcg/dL).

5.2 Mercury Poisoning

Dimercaptosuccinic acid (DMSA or succimer – Chemet®) is currently considered to be the chelator of choice to reduce the body burden of mercury. It is used off-label to treat adults with lead poisoning and for therapy of arsenic and mercury intoxication. Succimer (DMSA) is now recommended as an antidote in clinical cases of lead and organic mercury poisonings.

There is no specific antidote for mercury poisoning. While DMSA is the most commonly used agent, the overall clinical evidence base for mercury chelation remains less robust than for lead. Dimercaptosuccinic acid can cross the blood–brain barrier of mice, but it is not known if this is also the case in humans. Even if dimercaptosuccinic acid cannot reverse the damages done to the central nervous system, it might prevent further deterioration.

5.3 Arsenic Poisoning

Meso-2,3-dimercaptosuccinic acid (DMSA) has been recognized as one of the most effective chelating drugs to treat arsenic poisoning. Dimercaptosuccinic acid increased the rate of excretion of radioactive arsenic by poisoned rats and increased their survival compared with controls.

Despite this preclinical promise, the clinical evidence for chronic arsenicosis is less clear. Guha Mazumder et al. conducted a randomized, placebo-controlled trial of 2,3-dimercaptosuccinic acid in 21 patients with chronic arsenic toxicity due to drinking water contamination in West Bengal (Journal of Toxicology and Clinical Toxicology, 1998). There were no differences between succimer and placebo therapy in changes in symptoms or arsenic levels after two two-week courses. This negative finding highlights that DMSA's limitation of extracellular-only distribution makes it insufficient for chronic arsenic poisoning where metal has accumulated in intracellular compartments.

5.4 Wilson's Disease (Copper Overload)

In China, there is substantial experience with the use of DMSA in the treatment of Wilson's disease. Comparing long-term therapeutic effects, it has been claimed that DMSA is superior to penicillamine because the side-effect incidence of DMSA was lower. DMSA appeared to have comparable short- and long-term therapeutic efficacy as penicillamine, implicating that DMSA might be recommended as initial therapy and in reduced dosage as maintenance therapy. The introduction of DMSA in the treatment of Wilson's disease may represent an important development. Most of this experience derives from Chinese clinical series rather than large multicenter randomized controlled trials; the evidence is promising but not yet conclusive by Western regulatory standards.

5.5 Autism Spectrum Disorder (ASD) — Evidence Negative

DMSA has been used off-label in some alternative medical circles based on the hypothesis that heavy metal burden contributes to ASD symptoms. The Cochrane Collaboration conducted a systematic review of this question. The review searched multiple databases to find studies that examined pharmaceutical chelating agents as treatment for ASD symptoms and found only one randomised controlled trial that evaluated oral DMSA for ASD, but this trial did not use ideal methods for answering the question.

During the first phase of the study, 77 children with ASD were randomly assigned to receive seven days of glutathione lotion or placebo lotion, followed by three days of oral DMSA. Forty-nine children who were found to be high excreters of heavy metals continued on to phase two to receive three days of oral DMSA or placebo, followed by 11 days off, with the cycle repeated up to six times. Overall, no evidence suggests that multiple rounds of oral DMSA had an effect on ASD symptoms.

No clinical trial evidence was found to suggest that pharmaceutical chelation is an effective intervention for ASD. No evidence suggests that multiple rounds of oral DMSA had an effect on ASD symptoms. Given prior reports of serious adverse events such as hypocalcemia, renal impairment, and reported death, the risks of using chelation for ASD currently outweigh proven benefits. Before further trials are conducted, evidence that supports a causal link between heavy metals and autism and methods that ensure the safety of participants are needed.

5.6 Tc-99m DMSA in Nuclear Medicine and Renal Imaging

Tc-99m DMSA accumulates in the proximal tubular cells of kidneys and is used for renal cortical imaging. Roughly 40% of the injected dose localizes in the cortex, predominantly in the proximal tubules. Imaging is generally done after a 2- to 3-hour delay to allow time for uptake and slow background clearance. Tc-99m DMSA is the preferred cortical imaging agent because its cortical binding is much higher than that of Tc-99m GH.

Dimercaptosuccinic acid is a very useful radiopharmaceutical used for the detection of many diseases such as renal disorder, medullary thyroid cancer (MTC), and brain tumors. Diseases affecting the proximal tubules, such as renal tubular acidosis and Fanconi's syndrome, inhibit Tc-99m DMSA uptake.

The pentavalent form has separate oncological applications: pentavalent Re-188/Re-186 DMSA is a suitable candidate for internal radiation therapy.

6. Dosage Forms and Reported Dosages

Oral Pharmaceutical Form

DMSA is administered orally in divided doses based on the size of the patient, making administration easier and not requiring hospitalization. The standard FDA-approved pediatric dosing regimen for lead poisoning is as follows, based on prescribing information: typical course: 10 mg/kg every 8 hours for 5 days, then every 12 hours for 14 days (oral).

DMSA at 30 mg/kg/day is more effective than either 10 or 20 mg/kg/day in enhancing urinary lead excretion. In dose-ranging studies, three groups of 6 patients received either 10.0, 6.7, or 3.3 mg/kg succimer orally every 8 hours for 5 days; after five days the mean blood lead levels of the three groups decreased 72.5%, 58.3%, and 35.5%, respectively.

For adults with inorganic lead poisoning, oral DMSA at 30 mg/kg/day was administered to adults with blood lead concentrations ≥50 µg/dL.

One commonly described off-label dosing schedule for chelation use, as reported in the literature, is 10 mg/kg/day every eight hours for three days, followed by eleven days with no DMSA. These two-weekly cycles are repeated up to six times, totaling approximately three months of treatment.

For Wilson's disease, a usual initial oral dose in adults is 100 mg three times daily.

Radiopharmaceutical Form

Renal scintigraphy is performed three to four hours after intravenous administration of a mean dose of 188.7 MBq (5.1 mCi) of Tc-99m DMSA, typically six to twenty-four hours before surgery.

7. Body Systems and Health Areas

• Hematological/Toxicological System: Primary area of use; DMSA binds divalent heavy metals (lead, mercury, arsenic, cadmium, antimony) to form water-soluble chelates excreted in urine.
• Renal System: DMSA accumulates in the kidney where it is extensively metabolized in humans to mixed disulfides of cysteine; some 10–25% of an orally administered dose is excreted in urine, the majority within 24 hours and most (>90%) as DMSA–cysteine disulfide conjugates.
• Central Nervous System: Dimercaptosuccinic acid can cross the blood–brain barrier of mice, but it is not known if this is also the case in humans. Even if it cannot reverse damages to the CNS, it might prevent further deterioration.
• Hepatic System: Succimer has been linked to a low rate of transient serum aminotransferase elevations during therapy, but its use has not been linked to cases of clinically apparent liver injury with jaundice.
• Cardiovascular System: Preliminary and primarily preclinical; murine experiments have shown that this compound also lowers blood pressure in rat arterial hypertension.
• Nuclear Medicine/Diagnostic Imaging: Tc-99m DMSA is a well-established renal cortical imaging agent used diagnostically to detect renal scarring, assess split renal function, and identify proximal tubular dysfunction.

8. Safety Considerations and Drug Interactions

Adverse Effects Profile

Systemic adverse events known with succimer administration include nausea, vomiting, diarrhea, anorexia, loose stools, and metallic taste, which occur singly or in combination in up to 12% of children and 21% of adults. In addition, back pain, abdominal cramps, chills, and flu-like symptoms have been reported in 5% of children and 16% of adults.

Mild, reversible increases in liver transaminases have been observed in 6–10% of patients. Rashes, some requiring discontinuation of treatment, have been reported in less than 5% of patients.

Mild to moderate neutropenia and episodes of granulocytopenia, possibly related to succimer, have been reported. A 45-year-old man with glucose-6-phosphate dehydrogenase deficiency and a 17-year history of occupational lead exposure developed hemolysis during treatment with succimer for symptomatic lead intoxication. This case illustrates a specific pharmacogenomic risk.

Renal and Hepatic Concerns

Because succimer and its transformation products undergo renal elimination, safety and efficacy in patients with severe renal insufficiency are uncertain. There is no available evidence that succimer increases hemodialysis clearance of toxic metals in anuric patients.

Precautions are required in individuals with renal or hepatic impairment, neutropenia, or glucose-6-phosphate dehydrogenase deficiency.

Embryo/Fetal Toxicity

Some evidence of embryo toxicity/fetal toxicity due to DMSA administration has been reported. DMSA is not categorically contraindicated in pregnancy under all circumstances—its use may be necessary in cases of severe acute lead poisoning—but this evidence warrants caution.

Blood Lead Rebound

A clinically important phenomenon observed in multiple studies is blood lead rebound after cessation of DMSA therapy. Among 59 children given 116 four-week courses of succimer for lead toxicity, lead levels fell rapidly on treatment but rebounded to 58% of pretreatment values thereafter. This rebound is attributed to redistribution of lead from bone depots back into blood after chelation. Environmental source removal is therefore a necessary adjunct.

Laboratory Interference

Succimer is known to interact with various laboratory tests, resulting in incorrect values for urine ketones, uric acid, and creatine phosphokinase activity. Clinicians should be aware of this potential interference when interpreting laboratory results during therapy.

Specificity Compared to Older Chelators

A key distinguishing safety advantage of DMSA is its relative selectivity for toxic metals. Succimer is an organo-sulfur compound with two sulfhydryl groups that bind divalent metal ions such as lead, cadmium, mercury, and arsenic. It does not significantly chelate essential metals such as zinc, copper, or iron, and its specificity, safety, and oral availability make it preferable to Ca-EDTA (which must be given intravenously) and dimercaprol (BAL, which requires intramuscular administration).

Off-Label and Unorthodox Use

Succimer is also used in naturopathic medicine administered orally as well as intravenously as part of chelation therapy for various conditions. Such uses extend beyond the established FDA label and lack robust clinical evidence. CHEMET is not indicated for prophylaxis of lead poisoning in a lead-containing environment.

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