Head-to-head clinical analysis & difference comparison: details on mechanism of action, dosing, half-life, interactions, and maternal-fetal safety.
CHEMET vs DESFERAL
Clinician-reviewed, head-to-head comparison of mechanism, dosing, pharmacokinetics, and safety profiles.
Last clinically reviewed: July 2026 · OpiCalc Medical Review Team
Chelates heavy metals, particularly lead, mercury, and arsenic, by forming soluble complexes that are excreted renally. Acts as an antidote by binding to toxic metals and reducing their tissue concentrations.
Deferoxamine is an iron-chelating agent that binds ferric iron forming ferrioxamine, a stable complex that is excreted renally, reducing iron accumulation in tissues.
Treatment of acute and chronic lead poisoning,Treatment of mercury poisoning,Treatment of arsenic poisoning,Diagnostic chelation challenge test
Acute iron intoxication,Chronic iron overload due to transfusion-dependent anemias (e.g., thalassemia major),Chronic iron overload due to hereditary hemochromatosis with contraindications to phlebotomy,Chelation therapy in patients with secondary iron overload from myelodysplastic syndromes or sickle cell disease (off-label)
10-20 mg/kg orally every 8 hours for 5 days; maximum single dose 1250 mg.
Acute iron poisoning: 1 g IM, then 0.5 g IM every 4-12 hours; max 6 g/day. Chronic iron overload: 0.5-1 g IM daily; also IV/SC 20-40 mg/kg/day over 8-24 hours.
Terminal elimination half-life: 1.6–3.5 hours (mean 2.1 h) in adults with normal renal function; prolonged in renal impairment (up to 20 h).
Terminal elimination half-life: 6-12 hours (prolonged in iron overload, up to 20-30 hours with large doses; clinical context: supports subcutaneous infusion over 8-12 hours for chronic chelation).
Metabolized in liver to disulfide dimers; undergoes enterohepatic circulation; primarily excreted renally as metabolites and unchanged drug.
Deferoxamine is metabolized primarily in the liver via oxidative deamination to two major metabolites: an acid-degradation product and a neutral compound. The exact enzymes are not well-defined but likely involve hepatic oxidases.
Renal: 80–90% as unchanged drug and metabolites (primarily as chelated complexes); biliary/fecal: <10%.
Renal: approximately 40-60% of absorbed dose excreted in urine as unchanged drug and iron complex; biliary/fecal: minor route, <5%.
Approximately 80% bound to plasma proteins, primarily albumin.
~10-20% bound to plasma proteins; primarily albumin and transferrin (minimal due to low affinity).
0.5–0.8 L/kg, indicating distribution mainly in extracellular fluid; limited intracellular penetration.
Dry weight: 1.5-2.0 L/kg (indicates extensive distribution into extracellular fluid and tissues; increased in iron overload due to iron stores).
20–40% after oral administration due to first-pass metabolism and limited absorption.
Subcutaneous: ~80-90% (injectable only; oral bioavailability negligible, <5%).
GFR 50-80 m L/min: same dose every 12 hours. GFR 10-49 m L/min: same dose every 24 hours. GFR <10 m L/min: same dose every 48 hours.
GFR >60 m L/min: no adjustment; GFR 10-60: reduce dose by 50%; GFR <10: avoid use or use with extreme caution.
No specific recommendations; caution in severe hepatic impairment (Child-Pugh C) due to potential toxicity.
Child-Pugh A: no adjustment; Child-Pugh B: reduce dose by 25-50%; Child-Pugh C: avoid use.
Children >1 year: 10-20 mg/kg/dose orally every 8 hours for 5 days; maximum 1250 mg/dose.
Acute poisoning: 15 mg/kg/h IV initially, max 6 g/24h; acute chronic overload: 20-40 mg/kg/day SC/IV over 8-24h.
Consider starting at lower end of dosing range (10 mg/kg) due to potential renal impairment; adjust per renal function.
Start at lower end of dosing range due to potential renal impairment; monitor renal function and iron levels.
None
None
May cause nephrotoxicity; monitor renal function,May cause hypersensitivity reactions, including fever, rash, and anaphylaxis,Monitor for neutropenia; obtain CBC before and during therapy,Use caution in patients with hepatic impairment or glucose-6-phosphate dehydrogenase (G6PD) deficiency,May chelate essential minerals (e.g., zinc, copper); monitor levels with prolonged use,Not recommended for routine use in asymptomatic lead poisoning with low blood lead levels
Hypersensitivity reactions including anaphylaxis, urticaria, and angioedema,Ocular toxicity (cataracts, decreased visual acuity, retinal damage) with high doses or prolonged therapy,Auditory toxicity (tinnitus, sensorineural hearing loss) especially at high doses,Renal impairment may reduce drug clearance; monitor renal function,Growth retardation in children with long-term use,Increased risk of infections, particularly Yersinia enterocolitica and Mucorales fungi,Severe neurotoxicity including seizures, coma, and encephalopathy, especially with rapid intravenous administration,Acute respiratory distress syndrome (ARDS) reported with rapid IV infusion
Hypersensitivity to dimercaprol or any component of the formulation,Hepatic failure (except severe heavy metal poisoning),Concurrent use with iron (increases nephrotoxicity); avoid iron therapy within 24 hours,Pregnancy (if not life-saving indication due to risk of teratogenicity),Peanut allergy (formulation contains peanut oil)
Severe renal disease or anuria (as drug is excreted renally),Hypersensitivity to deferoxamine or any component of the formulation,Primary hemochromatosis with mild iron overload (prefer phlebotomy)
No specific food interactions reported. However, due to gastrointestinal side effects (nausea, vomiting), it is advisable to maintain small, frequent meals. Avoid alcohol.
Avoid high-iron foods (e.g., red meat, liver, fortified cereals) during therapy. Do not take with vitamin C supplements as they may increase iron absorption and toxicity. No significant food interaction except iron-containing foods/supplements.
FDA Pregnancy Category C. First trimester: No adequate studies, but animal studies show fetal resorption at maternally toxic doses, risk cannot be excluded. Second and third trimesters: No specific teratogenicity, but may cause anemia in fetus due to maternal chelation of essential metals. Avoid use unless clearly needed.
FDA Category C. First trimester: Animal studies show fetal abnormalities, but no adequate human studies. Second/Third trimesters: Avoid unless essential; deferoxamine crosses placenta and may cause fetal skeletal anomalies, anemia, and growth restriction at high doses.
No human data on excretion in breast milk. M/P ratio unknown. Caution due to potential for infant exposure and chelation of trace elements; consider benefit-risk. Avoid breastfeeding during therapy and for 2 weeks after last dose.
Excreted into breast milk in low levels; M/P ratio unknown. Use with caution, especially in infants with iron overload; consider risk of maternal iron deficiency. Monitor infant for gastrointestinal effects.
No specific dose adjustments recommended for pregnancy. Increased plasma volume in pregnancy may alter pharmacokinetics, but studies not performed. Use lowest effective dose; monitor therapeutic response and toxicity closely.
No standard dose adjustment; lower doses may be required due to increased plasma volume and renal clearance. Monitor iron levels closely; avoid high doses to minimize fetal toxicity.
Chelation therapy with dimercaprol (CHEMET) should be initiated within 4 hours of arsenic or mercury exposure for maximal efficacy. Administer only via deep intramuscular injection, never intravenously. Monitor renal function and urine output closely, as dimercaprol can cause nephrotoxicity. Alkalinize urine to p H 7.5-8.5 to decrease renal precipitation of metal-drug complexes. Use with caution in patients with glucose-6-phosphate dehydrogenase deficiency due to risk of hemolysis. Contraindicated in patients with peanut allergy (vehicle is peanut oil).
Administer IM or IV, but avoid rapid IV infusion to prevent hypotension. Monitor urine color for reddish hue indicating iron excretion. For acute iron poisoning, check serum iron and total iron-binding capacity (TIBC); chelation is indicated if serum iron exceeds TIBC or >350 mcg/d L. Use test dose (50 mg/kg) if uncertain of iron overload. Avoid in severe renal failure unless dialysis is available due to desferrioxamine-iron complex excretion. Can cause Yersinia enterocolitica infection; discontinue if fever or diarrhea develops.
This medication is given as a shot into a muscle, usually in the buttock. It may cause pain at the injection site.,You may experience a metallic taste, nausea, vomiting, headache, or burning sensation in the mouth or throat.,Drink plenty of fluids unless otherwise instructed to help flush metals from your body.,Avoid alcohol during treatment and for at least 48 hours after the last dose.,Report any signs of allergic reaction (rash, itching, difficulty breathing) or dark urine immediately.
Take this medication exactly as prescribed; it is given by injection under the skin, into a muscle, or into a vein.,Your urine may turn a reddish-brown color during treatment; this is normal and indicates iron excretion.,Report any signs of infection such as fever, sore throat, or diarrhea immediately.,Avoid alcohol and large amounts of vitamin C unless approved by your doctor, as they can affect iron removal.,Stay hydrated; drink plenty of fluids unless instructed otherwise.,Do not take any iron supplements or multivitamins containing iron without consulting your healthcare provider.,If you miss a dose, contact your doctor for instructions; do not double the dose.
No interactions on record
No interactions on record
Explore head-to-head clinical comparisons of other medications in the same therapeutic classes.
Common clinical questions about CHEMET vs DESFERAL, answered by our medical review team.
CHEMET is a Chelating agent that works by Chelates heavy metals, particularly lead, mercury, and arsenic, by forming soluble complexes that are excreted renally. Acts as an antidote by binding to toxic metals and reducing their tissue concentrations.. DESFERAL is a Iron Chelating Agent that works by Deferoxamine is an iron-chelating agent that binds ferric iron forming ferrioxamine, a stable complex that is excreted renally, reducing iron accumulation in tissues.. They differ in pharmacokinetic profiles, FDA-approved indications, and side effect profiles.
Potency comparisons between CHEMET and DESFERAL depend on the specific clinical indication. These are agents from distinct pharmacological classes and are not directly interchangeable by dose. A physician or clinical pharmacist should guide any therapeutic switching decisions.
The standard adult dose of CHEMET is: 10-20 mg/kg orally every 8 hours for 5 days; maximum single dose 1250 mg.. The standard adult dose of DESFERAL is: Acute iron poisoning: 1 g IM, then 0.5 g IM every 4-12 hours; max 6 g/day. Chronic iron overload: 0.5-1 g IM daily; also IV/SC 20-40 mg/kg/day over 8-24 hours.. Dosing should always be individualized based on indication, renal and hepatic function, age, and other patient factors.
No direct drug-drug interaction has been formally documented between CHEMET and DESFERAL in current clinical databases. However, individual patient risk factors including other medications, organ function, and comorbidities should always be evaluated by a qualified healthcare provider.
The maternal-fetal safety profiles differ. CHEMET is classified as Category C. FDA Pregnancy Category C. First trimester: No adequate studies, but animal studies show fetal resorption at maternally toxic doses, risk cannot be excluded. Second and third trimes. DESFERAL is classified as Category C. FDA Category C. First trimester: Animal studies show fetal abnormalities, but no adequate human studies. Second/Third trimesters: Avoid unless essential; deferoxamine crosses place. Always consult a maternal-fetal medicine specialist before taking either drug during pregnancy or lactation.