Nifurtimox is a nitrofuran antiprotozoal agent with antitrypanosomal activity.1
Nifurtimox is used for the treatment of Chagas disease (American Trypanosomiasis) caused by Trypanosoma cruzi ( T. cruzi ) in pediatric patients from birth to less than 18 years of age who weigh at least 2.5 kg.1 Nifurtimox has been designated an orphan drug by FDA for the treatment of Chagas disease.2
Safety and efficacy of nifurtimox in pediatric patients (0 to 17 years of age) with Chagas disease are based on results from a prospective, randomized, double-blind, phase 3 study (CHICO) conducted in Argentina, Bolivia, and Colombia.1, 3, 4, 5 The trial consisted of 2 parts; in the first part, patients were treated with nifurtimox and followed for 1 year and the second part included an additional 3 years of follow-up.1, 3, 4, 5 Eligible patients <8 months of age were diagnosed with Chagas disease by direct observation of T. cruzi and patients 8 months to 17 years of age had their diagnosis confirmed by positive results from both recombinant and total purified antigen conventional enzyme-linked immunosorbent assay (ELISA) tests; all patients were asymptomatic.1, 14 Patients were stratified by age into 4 groups (0-27 days, 28 days to less than 8 months, 8 months to less than 2 years, and 2 years to less than 18 years) and then randomized to receive either a 60-day regimen or a 30-day regimen of nifurtimox within each of the age groups.3 Patients were compared to an external historical control group from two placebo-controlled trials of benznidazole, another drug with antitrypanosomal activity, in children with Chagas disease.1 Patients younger than 28 days who were born premature (i.e., gestational age <37 weeks), those weighing <2.5 kg at birth, those with a maximum Apgar score <7 at 5 minutes after birth, and those with known Chagas disease-related cardiac, GI, or neurological disease were excluded from the study.1 Nifurtimox was administered at a dosage of 10-20 mg/kg/day in patients younger than 12 years of age who weighed less than 40 kg and a dosage of 8-10 mg/kg/day in patients 12 years of age or older who weighed 40 kg or more; the total daily dose was administered in 3 divided doses with food.1, 3
A total of 330 patients were randomly assigned to receive nifurtimox for 60 days or 30 days.1 Among these patients, 53.9% were female and 86.7% were 2 years to less than 18 years of age.1, 14 The median weight and height of the study population were 34 kg and 139 cm, respectively.1 The median body mass index (BMI) of study participants was 18.2.1, 3
The primary efficacy outcome was serological response to treatment, which was assessed as either seroreduction (in patients 8 months to 17 years of age), defined as a ≥20% decrease in mean optical density measured using two conventional ELISA tests (lysate ELISA and recombinant ELISA), or negative seroconversion (in all patients), defined as a negative anti- T. cruzi immunoglobulin G concentration on the lysate ELISA and recombinant ELISA tests.1, 3 Secondary outcomes and further exploratory objectives included treatment response at 12-month follow-up. evaluation of indirect hemagglutination and F-29 serology, and quantitative polymerase chain reaction (qPCR) results for both treatment groups at 12-month follow-up.1, 3
Based on conventional serological testing at 1 year, results showed a significantly higher serological response rate with the 60-day nifurtimox regimen compared with the 30-day dosing regimen, as assessed by the lysate ELISA (32 versus 19%) or recombinant ELISA (35 versus 22%) tests.1 At 1 year post-treatment, seroreduction assessed using lysate ELISA occurred in 27% of patients receiving the 60-day dosing regimen and 14% of patients receiving the 30-day dosing regimen of nifurtimox; seroreduction assessed using recombinant ELISA occurred in 30% of patients receiving the 60-day dosing regimen and 15% of patients receiving the 30-day dosing regimen of nifurtimox.1 Negative seroconversion assessed using lysate ELISA was achieved in 5% of patients on the 60-day dosing regimen and 5% of those on the 30-day dosing regimen of nifurtimox; negative seroconversion assessed using recombinant ELISA occurred in 5% of patients receiving the 60-day dosing regimen and 6% of those receiving the 30-day dosing regimen of nifurtimox.1 Serological response varied by age with the higher dose being more effective in older patients.1 The dose response effect between the 60-day and 30-day regimens was driven largely by the group of patients in the 6 to 17 year age range, which comprised the majority of the study population (77%).14 In the younger age groups, serological response rate was high, but not significantly different between the 60- and 30-day treatment groups; however, efficacy of the drug can be extrapolated from patients 6 to 17 years of age to patients younger than 6 years of age based on the high response rates and seroconversion observed in the younger age group. 1, 3
In addition to conventional serological testing, the use of F-29 ELISA was also employed in the CHICO study.1, 5 The F-29 ELISA detects antibodies to recombinant antigens obtained from the flagellar protein F29 on T. cruzi and was used as an early biomarker of response to treatment with trypanocidal therapy (i.e. nifurtimox or benznidazole).5 Among the subpopulation of patients with a positive F-29 ELISA response at baseline, 32.4% of those who received the 60-day nifurtimox regimen compared with 27.8% of those who received the 30-day regimen seroconverted to negative after 1 year of post-treatment follow-up.1, 1, 3
A total of 295 pediatric patients from the CHICO study were followed for an additional 3 years in the CHICO SECURE study to determine seroconversion rates at 4 years.1, 4 Among these patients, 197 pediatric patients received the 60-day regimen of nifurtimox and 98 pediatric patients received the 30-day regimen.1 Seroconversion to negative was confirmed using three assays (lysate ELISA, recombinant ELISA, and IHA).1 Seronegative conversion at 4 years post-treatment occurred only in those who were younger than 2 years at baseline.1, 4 Increasing age was associated with lower seroconversion rates; the seroconversion rate to negative in patients treated with the 60-day nifurtimox regimen was 81.8% at 4 years post-treatment in children 0 to less than 8 months of age, 20% in those 8 months to less than 2 years of age, and 0% in those 2-17 years of age.1 However, the manufacturer states that efficacy in the older pediatric population (5 to less than 19 years of age) can be extrapolated from the efficacy established in younger pediatric patients (0 to 4 years of age) given that a similar disease pathogenesis has been observed across the pediatric population.1 In addition, the longer duration of infection in older patients may prolong the time to seroconversion. 1, 4 When the F-29 ELISA test was used to evaluate serological response to nifurtimox treatment at 4 years, the number of patients with negative ELISA F29 values increased over the period of observation and was higher in both the 60-day and 30-day treatment groups compared with the rate measured by conventional serological assays.5 Therefore, the F-29 ELISA was found to be a reliable and appropriate biomarker to assess the response to antitrypanosomal therapy.5 The earlier disappearance of the antibodies against F-29 as seen with the F-29 ELISA compared with the conventional ELISA test indicates differences in the overall serological response to antitrypanosomal treatment.1, 5
Chagas disease is caused by T. cruzi , a protozoan parasite that is usually transmitted to humans by the bite of infected triatomine insects.26, 27, 28 Vector-borne transmission of T. cruzi primarily occurs in rural areas of Latin America where the disease is endemic.27, 28 The disease can also be transmitted via blood (e.g., blood transfusions) or organ transplants, perinatally from mother to infant, by ingestion of contaminated drink or food, and via accidental laboratory exposure.26, 27, 28 Chagas disease has been reported with increasing frequency in the US, most frequently in immigrants from endemic areas.28, 29, 30 However, triatomine vectors that can transmit T. cruzi and mammalian reservoir hosts of the organism (e.g., raccoons, opossums, domestic dogs) are found in the US and cases of autochthonous transmission have been documented in the US, especially in the southern states.27, 28, 29, 30
Following infection with T. cruzi , Chagas disease includes an acute and chronic phase.28 The acute phase occurs within weeks of infection and usually lasts 4 to 8 weeks; although parasitemia is present and trypomastigotes are usually detectable in blood by microscopy, patients are typically asymptomatic or have symptoms that are mild or nonspecific.28 Rarely, severe, potentially life-threatening disease (e.g., myocarditis, meningoencephalitis) occurs during the acute phase.28 If untreated, the acute phase is followed by a prolonged asymptomatic chronic phase (“chronic indeterminate”) that may last for decades or for life and, although parasitemia levels become low or undetectable, the infection can be transmitted to others (e.g., congenitally, through blood or organ donation).28 Reactivation of chronic T. cruzi infection can occur in those who become immunocompromised because of other disease or drug therapy.28
The Centers for Disease Control and Prevention (CDC) and other experts provide guidelines for the treatment of Chagas disease.25, 26 Antiparasitic treatment is indicated for all cases of acute or reactivated Chagas disease and also for chronic T. cruzi infection in children up to 18 years of age.25, 26 Currently available antiparasitic drugs for the treatment of Chagas disease include benznidazole and nifurtimox.25 Both drugs are FDA-labeled for use in pediatric patients; however, the indicated age range differs between these drugs.25 Although these drugs are not FDA-labeled for use in the adult population, CDC states that antitrypanosomal treatment is strongly recommended in adults 18-50 years of age with chronic Chagas disease if they do not already have advanced disease (Chagas cardiomyopathy).25 When considering antitrypanosomal treatment in adults older than 50 years of age, CDC and other experts recommend that the risks versus benefits of such therapy be considered for each individual patient based on the patient's age, clinical status, preference, and overall health.25, 26
Between 2001 and 2021, the U.S. Centers for Disease Control and Prevention (CDC) was the sole provider of nifurtimox (under an investigational new drug [IND] protocol) before the drug became commercially available in the US.27 Most of the patients who received the drug under the IND were adults.27 While the CDC no longer distributes nifurtimox for the treatment of Chagas disease, the agency provides reference diagnostic testing for T. cruzi infection and teleconsulting services regarding Chagas disease.25 For assistance with diagnosis or treatment of Chagas disease in the US, clinicians can contact the CDC at the Parasitic Diseases Hotline at 404-718-4745 or by email at [email protected].25
Nifurtimox is administered orally, 3 times daily with food.1
Nifurtimox is commercially available as scored 30 mg or 120 mg tablets.1 The tablets can be administered whole or split at the score line; do not use a mechanical tablet splitter.1
For patients who are unable to swallow tablets, a tablet and water mixture (slurry) can be prepared.1 To make the slurry, place the prescribed dose in approximately 2.5 mL of water on a spoon and allow the tablet to disintegrate, which should take less than 30 seconds.1 Consume the slurry mixture immediately with food.1
Do not consume alcohol while taking nifurtimox.1
If a dose of nifurtimox is missed within 3 hours of the next scheduled dose, skip the missed dose and take the next dose at the regularly scheduled time.1
Store nifurtimox tablets at controlled room temperature at 20-25°C (excursions between 15-30°C permitted).1 The tablets should be stored in the original bottle with child-resistant closures; keep the bottle tightly closed, protect from moisture, and do not remove the desiccant.1
For the treatment of Chagas disease in pediatric patients from birth to less than 18 years of age, the recommended dosage of nifurtimox is based on body weight.1 In patients who weigh 41 kg or more, the total daily dose of nifurtimox is 8-10 mg/kg; in patients who weigh less than 41 kg, the total daily dose of nifurtimox is 10-20 mg/kg.1 The total daily dose should be given in 3 divided doses.1 See Table 1 for individual dosages based on body weight.1 Complete the full 60-day course of therapy to prevent recurrence of infection.1
Because the dosing of nifurtimox is based on body weight, the dose may need to be adjusted during therapy based on changes in weight.1
Body Weight (kg) | Dose | Number of Nifurtimox 30 mg tablets per dose (3 times daily) | Number of Nifurtimox 120 mg tablets per dose (3 times daily) |
|---|---|---|---|
2.5 to 4.5 | 15 mg | 1/2 tablet | N/A |
4.6 to <9 | 30 mg | 1 tablet | N/A |
9 to <13 | 45 mg | 1-1/2 tablets | N/A |
13 to <18 | 60 mg | 2 tablets | 1/2 tablet |
18 to <22 | 75 mg | 2-1/2 tablets | N/A |
22 to <27 | 90 mg | 3 tablets | N/A |
27 to <35 | 120 mg | 4 tablets | 1 tablet |
35 to <41 | 180 mg | N/A | 1-1/2 tablets |
41 to <51 | 120 mg | N/A | 1 tablet |
51 to <71 | 180 mg | N/A | 1-1/2 tablets |
71 to <91 | 240 mg | N/A | 2 tablets |
≥91 | 300 mg | N/A | 2-1/2 tablets |
No dosage adjustment is recommended for patients with hepatic impairment.1 Administer nifurtimox under close supervision.1
No dosage adjustment is recommended for patients with renal impairment.1 Blood concentrations of nifurtimox are increased in patients with end-stage renal disease requiring hemodialysis.1 Administer nifurtimox under close supervision.1
There are no specific dosage recommendations for geriatric patients.1 Nifurtimox is only approved for pediatric patients.1
Potential for Genotoxicity and Carcinogenicity
Nifurtimox has been found to be genotoxic in vitro in several bacterial species (including S. typhimurium), in mammalian cell systems, and in vivo in rodents and in humans (i.e., human lymphocytes).1 Nifurtimox was associated with a 13-fold increase in chromosomal aberrations in a study evaulating the cytogenetic effect of the drug in pediatric patients 7 months to 14 years of age.1 Although nifurtimox has been found to be genotoxic in mice and in a human chromosome aberration assay, oral nifurtimox has not been found to cause a significant increase in the sister-chromatid exchange in blood lymphocytes.1
It is not known if nifurtimox is carcinogenic in humans, but structurally similar compounds have been found to be carcinogenic in mice and rats.1 There is a lack of long-term carcinogenicity data for nifurtimox.1
Fetal/Neonatal Morbidity and Mortality
Based on animal data, nifurtimox may cause fetal harm when administered during pregnancy.1 Structural fetal abnormalities (i.e., skeletal variations), reduction in maternal and fetal weight, reduced live births, and small testes in male offspring have been observed in animal reproductive studies in doses ranging from 0.2 to 2-times the maximum recommended human dose.1
Verify pregnancy status in females of reproductive potential prior to initiation of therapy.1
Pregnant females should be apprised of the potential risk to a fetus.1 Females of reproductive potential should use effective contraception during treatment with nifurtimox and for 6 months after discontinuing treatment.1
Males with female partners of reproductive potential should also use effective contraception during treatment with nifurtimox and for 3 months after discontinuing treatment.1
Worsening of Neurological and Psychiatric Conditions
Patients receiving nifurtimox who have a history of brain injury, seizures, psychiatric disease, or serious behavioral alterations may have worsening of their conditions.1 Close medical supervision is advised for patients with these medical conditions and in those who develop neurological disturbances or psychiatric reactions while receiving nifurtimox.1
Hypersensitivity reactions during nifurtimox therapy may be drug-induced or may be caused by an immune response triggered by Chagas disease.1 Hypersensitivity reactions may manifest as hypotension, angioedema (including laryngeal and facial edema), dyspnea, itching, rash, or other severe skin reactions.1 Nifurtimox should be discontinued at the first signs of a hypersensitivity reaction.1
Decreased Appetite and Weight Loss
Both decreased appetite and weight loss, secondary to loss of appetite and/or nausea/vomiting have been reported with nifurtimox.1 Body weight should be monitored every 14 days and the dose of nifurtimox adjusted accordingly.1
As with other nitrofuran derivatives, nifurtimox may precipitate acute attacks of porphyria.1 Nifurtimox should be administered under close supervision in patients with porphyria.1
Based on animal data, nifurtimox may cause fetal harm when administered during pregnancy.1 (See Fetal/Neonatal Morbidity and Mortality under Cautions.)
Available human data do not establish the presence or absence of major birth defects or miscarriage related to the use of nifurtimox.1
Nifurtimox crosses the placental barrier.1
Verify pregnancy status in females of reproductive potential prior to the initiation of nifurtimox.1 (See Females and Males of Reproductive Potential under Cautions.)
Data based on case-control and observational studies are conflicting regarding the risk of chronic Chagas disease during pregnancy with some but not all, showing an increased risk of pregnancy loss, prematurity, and neonatal mortality.1 While acute symptomatic Chagas disease is uncommon in pregnant women, a risk versus benefit assessment for both mother and fetus prior to administering nifurtimox should be conducted on a case-by-case basis.1
If nifurtimox is administered during pregnancy, or if a patient becomes pregnant while receiving nifurtimox or within 6 months following the last dose, report exposure by calling 1-888-842-2937.1
Nifurtimox is present in human breastmilk with the amount observed in infants estimated to be <15% of the recommended dose for pediatric patients with Chagas disease.1 Based on a small number of infants who were breastfed by mothers receiving nifurtimox, no adverse events have been reported with therapy.1 The effects of nifurtimox on the production of milk are unknown.1 Monitor infants exposed to nifurtimox through breast milk for vomiting, rash, decreased appetite, fever, and irritability.1 Consider the developmental and health benefits of breastfeeding along with the mother's clinical need for nifurtimox and any potential adverse effects on the breastfed infant from the drug or underlying maternal condition.1
Females and Males of Reproductive Potential
Verify pregnancy status in females of reproductive potential prior to the initiation of nifurtimox.1
Advise females of reproductive potential to use effective contraception during treatment with nifurtimox and for 6 months after the final dose.1 Advise male patients with female partners of reproductive potential to use condoms during treatment with nifurtimox and for 3 months after the final dose.1
Results of animal studies suggest that nifurtimox may impair male fertility.1
Safety and effectiveness of nifurtimox have been established for pediatric patients from birth to less than 18 years of age who weigh at least 2.5 kg.1 Safety and efficacy have not been established in pediatric patients who weigh less than 2.5 kg.1
Safety and efficacy of nifurtimox have not been established in patients 65 years of age or older.1 Nifurtimox is only approved for pediatric patients (newborn to less than 18 years of age).1
Nifurtimox has not been studied in patients with hepatic impairment.1 Administer nifurtimox under close medical supervision.1
Nifurtimox plasma concentrations are increased in patients with end-stage renal disease requiring hemodialysis.1 Administer nifurtimox under close medical supervision.1
The most common (≥5%) adverse effects of nifurtimox in clinical studies were vomiting, abdominal pain, headache, decreased appetite, nausea, fever, and rash.1
The potential for drug interactions with nifurtimox has not been studied.1
Cytochrome P-450 (CYP) isoenzymes do not appear to play a major role in the metabolism of nifurtimox.1 In vitro studies indicate that nifurtimox is not a substrate of CYP isoenzymes.1 Neither nifurtimox nor its metabolites (M-4 or M-6) inhibit or induce CYP isoenzymes.1
Nifurtimox is not a substrate of P-glycoprotein (P-gp) or breast cancer resistance protein (BCRP).1 Neither nifurtimox nor its major metabolites (M-4 or M-6z) are inhibitors of P-gp, BCRP, organic anion transporting polypeptide (OATP), multidrug and toxin extrusion (MATE) proteins (MATE1/MATE2-K), organic anion transporter 1/3 (OAT1/OAT3), or organic cation transporter 2 (OCT2).1, 1
Nifurtimox is a nitrofuran antiprotozoal agent that is active against T. cruzi .1 While the exact mechanism of action is not clearly understood, the drug is metabolized/activated by Type I (oxygen insensitive) and Type II (oxygen sensitive) nitroreductases, resulting in DNA damage and cell death of both intracellular and extracellular forms of T. cruzi due to the production of toxic intermediate metabolites and/or reactive oxygen species.1
Nifurtimox is active against all 3 stages of T. cruzi , which include tryptomastigotes, the flagellated stage of trypanosomes that is found in the blood of infected persons; amastigotes, a non-flagellated, intracellular replicative form of trypanosomes; and epimastigotes, a form of trypanosomes that multiplies and differentiates in the midgut.1, 12 T. cruzi sensitivity varies based on geographic region.1 The mechanism of resistance to antitrypanosomal therapy is multifactorial.13 There is evidence of multi-drug resistance to benznidazole with a demonstrated risk for cross-resistance to nifurtimox.13
Administration of nifurtimox with a high-fat meal containing 800-1000 calories increases the peak plasma concentration of the drug by 68%, AUC by 71%, and time to peak plasma concentration by 1 hour compared to the fasted state.1 The median time to reach peak plasma concentration of nifurtimox under fed conditions was 4 hours (range: 2 to 8 hours).1 Nifurtimox crosses both the blood brain barrier and the placental barrier.1 Nifurtimox is 42% bound to plasma proteins.1 Nifurtimox is primarily metabolized via nitroreductases into two major pharmacologically inactive metabolites, M-4 and M-6, and several minor metabolites; the half-life of M-4 is approximately 28 hours and the half-life of M-6 is about 10 hours.1 The mean coefficient of variation of the elimination half-life ranged from 2.4-3.6 hours (12-37%).1 Approximately 44% and 27% of a nifurtimox dose is recovered in the urine as metabolites under fed and fasted conditions, respectively.1 There is no information about the elimination of nifurtimox via the biliary or fecal routes.1 While the effect of renal and/or hepatic impairment on the pharmacokinetics of nifurtimox is unknown, plasma concentrations of the drug are elevated in patients with end-stage renal disease.1
Additional Information
The American Society of Health-System Pharmacists, Inc. represents that the information provided in the accompanying monograph was formulated with a reasonable standard of care, and in conformity with professional standards in the field. Readers are advised that decisions regarding use of drugs are complex medical decisions requiring the independent, informed decision of an appropriate health care professional, and that the information contained in the monograph is provided for informational purposes only. The manufacturer's labeling should be consulted for more detailed information. The American Society of Health-System Pharmacists, Inc. does not endorse or recommend the use of any drug. The information contained in the monograph is not a substitute for medical care
Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.
Please refer to the ASHP Drug Shortages Resource Center for information on shortages of one or more of these preparations.
AHFS® Drug Information. © Copyright, 1959-2025, Selected Revisions November 10, 2025. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, MD 20814.
Only references cited for selected revisions after 1984 are available electronically.
1. Bayer Healthcare Pharmaceuticals. LAMPIT® (nifurtimox) ORAL prescribing information. Whippany, NJ; 2024 Dec
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5. Rivero R, Esteva MI, Huang E, Colmegna L, Altcheh J, Grossmann U, Ruiz AM; CHICO and CHICO SECURE Study Groups. ELISA F29 -A therapeutic efficacy biomarker in Chagas disease: Evaluation in pediatric patients treated with nifurtimox and followed for 4 years post-treatment. PLoS Negl Trop Dis. 2023 Jun 23;17(6):e0011440. doi: 10.1371/journal.pntd.0011440. PMID: 37352322; PMCID: PMC10325040. http://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0011440
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28. Bern C, Montgomery SP, Herwaldt BL, Rassi A Jr, Marin-Neto JA, Dantas RO, Maguire JH, Acquatella H, Morillo C, Kirchhoff LV, Gilman RH, Reyes PA, Salvatella R, Moore AC. Evaluation and treatment of chagas disease in the United States: a systematic review. JAMA. 2007 Nov 14;298(18):2171-81. doi: 10.1001/jama.298.18.2171. PMID: 18000201. http://jamanetwork.com/journals/jama/fullarticle/209410
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