Head-to-head clinical analysis & difference comparison: details on mechanism of action, dosing, half-life, interactions, and maternal-fetal safety.
DESFERAL vs CHEMET
Clinician-reviewed, head-to-head comparison of mechanism, dosing, pharmacokinetics, and safety profiles.
Last clinically reviewed: July 2026 · OpiCalc Medical Review Team
Deferoxamine is an iron-chelating agent that binds ferric iron forming ferrioxamine, a stable complex that is excreted renally, reducing iron accumulation in tissues.
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.
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)
Treatment of acute and chronic lead poisoning,Treatment of mercury poisoning,Treatment of arsenic poisoning,Diagnostic chelation challenge test
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.
10-20 mg/kg orally every 8 hours for 5 days; maximum single dose 1250 mg.
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).
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).
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.
Metabolized in liver to disulfide dimers; undergoes enterohepatic circulation; primarily excreted renally as metabolites and unchanged drug.
Renal: approximately 40-60% of absorbed dose excreted in urine as unchanged drug and iron complex; biliary/fecal: minor route, <5%.
Renal: 80–90% as unchanged drug and metabolites (primarily as chelated complexes); biliary/fecal: <10%.
~10-20% bound to plasma proteins; primarily albumin and transferrin (minimal due to low affinity).
Approximately 80% bound to plasma proteins, primarily albumin.
Dry weight: 1.5-2.0 L/kg (indicates extensive distribution into extracellular fluid and tissues; increased in iron overload due to iron stores).
0.5–0.8 L/kg, indicating distribution mainly in extracellular fluid; limited intracellular penetration.
Subcutaneous: ~80-90% (injectable only; oral bioavailability negligible, <5%).
20–40% after oral administration due to first-pass metabolism and limited absorption.
GFR >60 m L/min: no adjustment; GFR 10-60: reduce dose by 50%; GFR <10: avoid use or use with extreme caution.
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.
Child-Pugh A: no adjustment; Child-Pugh B: reduce dose by 25-50%; Child-Pugh C: avoid use.
No specific recommendations; caution in severe hepatic impairment (Child-Pugh C) due to potential toxicity.
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.
Children >1 year: 10-20 mg/kg/dose orally every 8 hours for 5 days; maximum 1250 mg/dose.
Start at lower end of dosing range due to potential renal impairment; monitor renal function and iron levels.
Consider starting at lower end of dosing range (10 mg/kg) due to potential renal impairment; adjust per renal function.
None
None
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
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
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)
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)
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.
No specific food interactions reported. However, due to gastrointestinal side effects (nausea, vomiting), it is advisable to maintain small, frequent meals. Avoid alcohol.
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.
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.
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 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.
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.
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.
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.
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).
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.
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.
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 DESFERAL vs CHEMET, answered by our medical review team.
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.. 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.. They differ in pharmacokinetic profiles, FDA-approved indications, and side effect profiles.
Potency comparisons between DESFERAL and CHEMET 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 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.. The standard adult dose of CHEMET is: 10-20 mg/kg orally every 8 hours for 5 days; maximum single dose 1250 mg.. 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 DESFERAL and CHEMET 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. 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. 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. Always consult a maternal-fetal medicine specialist before taking either drug during pregnancy or lactation.