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US Drug Names
Available data are limited and efficacy has not been established. The National Institutes of Health (NIH) COVID-19 treatment guidelines recommend against the use of chloroquine for the treatment of COVID-19 patients. The FDA has revoked the Emergency Use Authorization (EUA) of chloroquine. Previously, the EUA suggested 1,000 mg (600 mg base) PO on day 1 then 500 mg (300 mg base) PO once daily for 4 to 7 days.  The NIH recommends against the use of high-dose, twice daily chloroquine.
16.6 mg (10 mg base)/kg/dose [Max: 1,000 mg/dose (600 mg base/dose)] PO once, then 8.3 mg (5 mg base)/kg/dose [Max: 500 mg/dose (300 mg base/dose)] PO in 6 to 8 hours, then 8.3 mg (5 mg base)/kg/dose [Max: 500 mg/dose (300 mg base/dose)] PO once daily for 2 days. For P. vivax or P. ovale, give in combination with primaquine phosphate or tafenoquine. Guidelines recommend chloroquine for uncomplicated malaria in patients with chloroquine-sensitive P. falciparum or P. vivax or in all patients with P. malariae, P. knowlesi, or P. ovale.
16.6 mg (10 mg base)/kg/dose [Max: 1,000 mg/dose (600 mg base/dose)] PO once, then 8.3 mg (5 mg base)/kg/dose [Max: 500 mg/dose (300 mg base/dose)] PO in 6 to 8 hours, then 8.3 mg (5 mg base)/kg/dose [Max: 500 mg/dose (300 mg base/dose)] PO once daily for 2 days.  For P. vivax or P. ovale, give in combination with primaquine phosphate or tafenoquine. Guidelines recommend chloroquine for uncomplicated malaria in patients with chloroquine-sensitive P. falciparum or P. vivax or in all patients with P. malariae, P. knowlesi, or P. ovale.
500 mg (300 mg base) PO weekly on the same day of each week, starting 2 weeks before entering the endemic area and continuing for 8 weeks after leaving the area. If it is not feasible to begin therapy before entering the endemic area, use 1,000 mg (600 mg base) as initial loading dose given in 2 divided doses 6 hours apart. Alternatively, guidelines suggest a shorter course; start the usual dosage regimen 1 to 2 weeks prior to entry into the endemic area and continue for 4 weeks after leaving the area.
500 mg (300 mg base) PO weekly for duration of pregnancy for P. ovale or P. vivax infections after completing acute treatment. After delivery, subsequent treatment with primaquine phosphate or tafenoquine is needed in patients without G6PD deficiency.
500 mg (300 mg base) PO weekly for duration of pregnancy for P. ovale or P. vivax infections after completing acute treatment. After delivery, subsequent treatment with primaquine phosphate or tafenoquine (16 years and older) is needed in patients without G6PD deficiency.
8.3 mg (5 mg base)/kg/dose [Max: 500 mg/dose (300 mg base/dose)] PO weekly on the same day of each week, starting 2 weeks before entering the endemic area and continuing for 8 weeks after leaving the area. If it is not feasible to begin therapy before entering the endemic area, use 16.6 mg (10 mg base)/kg/dose [Max: 1,000 mg/dose (600 mg base/dose)] as initial loading dose given in 2 divided doses 6 hours apart.  Alternatively, guidelines suggest a shorter course; start the usual dosage regimen 1 to 2 weeks prior to entry into the endemic area and continue for 4 weeks after leaving the area. 
1,000 mg (600 mg base) PO once daily for 2 days, then 500 mg (300 mg base) PO once daily for at least 2 to 3 weeks.
125 to 250 mg (75 to 150 mg base) PO once daily. Do not exceed 3.5 to 4 mg/kg/day to minimize retinal toxicity. Chloroquine is recommended in patients who fail hydroxychloroquine plus quinacrine; quinacrine may be continued with chloroquine.
The following recommendations are for baseline and continuous monitoring when using chloroquine with azithromycin:
1,000 mg/dose (600 mg base/dose) PO for malaria up to a total of 2.5 g (1.5 g base) PO in 48 hours; 500 mg/week (300 mg base/week) PO for malaria prophylaxis; 1,000 mg/day (600 mg base/day) PO for other indications.
16.6 mg/kg/dose (10 mg base/kg/dose) [Max: 1,000 mg (600 mg base)] PO for malaria up to a total of 41.5 mg/kg (25 mg/kg base) [Max: 2.5 g (1.5 g base)] PO in 48 hours; 8.3 mg/kg/week (5 mg base/kg/week) [Max: 500 mg/week (300 mg base/week)] PO for malaria prophylaxis.
16.6 mg/kg/dose (10 mg base/kg/dose) PO for malaria up to a total of 41.5 mg/kg (25 mg/kg base) PO in 48 hours; 8.3 mg/kg/week (5 mg base/kg/week) PO for malaria prophylaxis.
Safety and efficacy have not been established.
Chloroquine concentrates in the liver. However, no specific dosage adjustment guidelines are available for patients with hepatic impairment.
CrCl 10 mL/minute or more: No dosage adjustment necessary.
CrCl less than 10 mL/minute: Decrease dose by 50%.
Decrease dose by 50%.
Continuous renal replacement therapy:
No dosage adjustment necessary.
Chloroquine is a 4-aminoquinoline anti-protozoal agent indicated for the treatment and prophylaxis of susceptible malaria strains and for the treatment of extraintestinal amebiasis. Chloroquine is not active against gametocytes and the exoerythrocytic forms including the hypnozoite stage of the Plasmodium parasites. Resistance to chloroquine is widespread. Irreversible retinal damage has been observed with use, and postmarketing cases of life-threatening and fatal cardiomyopathy, including ventricular arrhythmias and torsade de pointes (TdP), have been reported.
Updates for coronavirus disease 2019 (COVID-19):
Available data are limited. The National Institutes of Health (NIH) COVID-19 treatment guidelines recommend against the use of chloroquine for the treatment of COVID-19 patients. On June 15, 2020, the FDA revoked the Emergency Use Authorization (EUA) for chloroquine stating that it is unlikely to be effective in treating COVID-19. Also, in light of ongoing serious cardiac adverse events and other serious side effects, the known and potential benefits of chloroquine no longer outweigh the known and potential risks for the authorized use. The FDA had previously issued the EUA for the use of chloroquine to treat hospitalized COVID-19 patients for whom clinical trial participation is not feasible. Use in COVID-19 patients outside of clinical trials or in a nonhospital setting is not recommended due to the potential for serious adverse events and drug interactions. The NIH recommends against the use of high-dose, twice daily chloroquine.
There have been reports of potential benefit in inhibiting the exacerbation of pneumonia patients with SARS-CoV-2 infection; however, specific data are not available.
In a parallel, double-masked, randomized clinical trial (n = 81), two doses of chloroquine were analyzed. The high-dose group had a higher incidence of QT interval greater than 500 milliseconds (18.9%) compared with the low-dose group (11.1%); therefore, the study was unmasked and all patients were reverted to the low-dose group. Respiratory secretions on day 4 were negative in 22.2% of patients (6 of 27 patients analyzed).
An observational, multicenter, cohort study assessed death on the COVID-19 ward and transfer to the ICU in hospitalized patients with moderate to severe COVID-19 receiving chloroquine (n = 377) compared to no treatment (n = 498). There was no significant difference between groups in regard to mortality (HR 0.99; 95% CI, 0.7 to 1.43). There was no significant difference between groups in regard to transfer to the ICU (HR 0.8; 95% CI, 0.55 to 1.15, p = 0.207) compared to controls.
Additional data regarding clinical efficacy for COVID-19 are being evaluated.
For storage information, see the specific product information within the How Supplied section.
NOTE: Chloroquine extemporaneous suspension is not FDA-approved.
Extemporaneous chloroquine suspension has been compounded using the following formulations:
Irreversible maculopathy and macular degeneration have been reported with chloroquine or other 4-aminoquinoline compounds during postmarketing use. Irreversible retinopathy with retinal pigment changes (bull's eye appearance) and visual field defects (paracentral scotomas) have been reported in patients receiving long-term or high-dose 4-aminoquinoline therapy. Visual impairment (i.e., blurred vision and difficulty in focusing or accommodation), nyctalopia (night blindness), scotomatous vision with field defects of paracentral, pericentral ring types, and typically temporal scotomata (e.g., difficulty in reading with words tending to disappear, seeing half an object, misty vision, and fog before the eyes), and reversible corneal opacification (corneal deposits) have been reported. For patients with significant risk factors, monitoring should include annual examinations which include best corrected distance visual acuity (BCVA), automated threshold visual field (VF), and spectral domain optical coherence tomography (SD-OCT). For individuals without significant risk factors, annual exams can usually be deferred until 5 years of treatment. Discontinue chloroquine if ocular toxicity is suspected, and monitor the patient closely as retinal changes and visual disturbances may progress after cessation of therapy.
Erythema multiforme, Stevens-Johnson syndrome, toxic epidermal necrolysis, exfoliative dermatitis, pleomorphic skin eruptions, skin and mucosal pigmentary changes (skin discoloration), lichen planus-like eruptions, pruritus, drug reaction with eosinophilia and systemic symptoms (DRESS), photosensitivity, hair loss (alopecia), bleaching of hair pigment (hair discoloration), urticaria, anaphylactoid reactions or anaphylactic shock, and angioedema have been reported during postmarketing use of chloroquine or other 4-aminoquinoline compounds. An acute attack of psoriasis can be precipitated by chloroquine in predisposed patients.
Chloroquine has been associated with acute generalized exanthematous pustulosis (AGEP). The non-follicular, pustular, erythematous rash starts suddenly and is associated with fever above 38 degrees C. Drugs are the main cause of AGEP. A period of 2 to 3 weeks after an inciting drug exposure appears necessary for a first episode of AGEP. Unintentional reexposure may cause a second episode within 2 days.
Hematological adverse reactions have been reported during postmarketing use of chloroquine or other 4-aminoquinoline compounds and include reversible agranulocytosis, aplastic anemia, pancytopenia, neutropenia, and thrombocytopenia. Chloroquine may cause hemolysis and hemolytic anemia in patients with glucose-6-phosphate dehydrogenase deficiency (G6PD deficiency).
During postmarketing use, chloroquine and/or other 4-aminoquinoline compounds have been associated with sensorimotor disorders as well as skeletal muscle myopathy or neuromyopathy leading to progressive weakness (myasthenia) and atrophy of proximal muscle groups, depressed tendon reflexes (hyporeflexia), and abnormal nerve conduction. Periodically test knee and ankle reflexes to detect any evidence of muscular weakness. Discontinue chloroquine if weakness develops.
Nerve type deafness, tinnitus, and reduced hearing (hearing loss) in patients with preexisting auditory damage have been reported during postmarketing use of chloroquine or other 4-aminoquinoline compounds. Discontinue chloroquine with any hearing defects, and monitor the patient closely.
Cardiovascular adverse reactions associated with chloroquine or other 4-aminoquinoline compounds during postmarketing include cardiomyopathy (which may result in cardiac failure and in some cases fatal outcome), electrocardiogram (ECG) changes (particularly, inversion or flattening of the T-wave with widening of the QRS complex), and hypotension. Cardiac arrhythmias, conduction disorders such as bundle-branch block and AV block, QT prolongation, torsade de pointes (TdP), ventricular arrhythmias (e.g., ventricular tachycardia, ventricular fibrillation) have been reported, including fatal cases. The risk is greater with higher doses, although cases have been reported with therapeutic doses. Chronic toxicity should be considered when conduction disorders, such as bundle-branch block or AV block, are diagnosed. Additionally, cases of cardiomyopathy resulting in cardiac failure with some cases of fatal outcome have been reported with chloroquine. Prompt discontinuation of chloroquine may prevent life-threatening complications if cardiotoxicity is suspected.    
Adverse gastrointestinal effects noted with chloroquine or other 4-aminoquinoline compounds during postmarketing include hepatitis, elevated hepatic enzymes, nausea, vomiting, abdominal pain/cramps, diarrhea, and anorexia. Gastric effects can be minimized by taking chloroquine with food.
Nervous system adverse reactions associated with chloroquine or other 4-aminoquinoline compounds during postmarketing include headache (usually mild and transient), seizures, polyneuropathy, acute extrapyramidal symptoms (e.g., dystonia, dyskinesia, tongue protrusion, torticollis), and neuropsychiatric changes including psychosis, delirium, anxiety, agitation, insomnia, hallucinations, confusion, personality changes, depression, and suicidal ideation/behavior. Extrapyramidal symptoms usually resolve after treatment discontinuation and/or symptomatic treatment.
Chloroquine has been shown to cause severe hypoglycemia including loss of consciousness that could be life threatening in patients treated with or without antidiabetic medications. Monitor blood glucose and adjust treatment as necessary in patients presenting with clinical symptoms of hypoglycemia during chloroquine treatment.
Chloroquine is reported in the literature to be a weak genotoxic agent that may elicit both gene mutations and chromosomal/DNA breaks. Mechanisms may involve DNA intercalation or induction of oxidative stress. Both positive and negative results have been reported with in vitro reverse gene mutation assays and with in vivo animal studies. The chromosomal effects were not observed when chloroquine was administered to animals orally.
Antimicrobial resistance to chloroquine therapy is widespread in P. falciparum and is reported in P. vivax. Prior to chloroquine use, it should be ascertained whether chloroquine is appropriate for use based on resistance patterns. Information regarding the geographic areas where resistance to chloroquine occurs is available from the Centers for Disease Control and Prevention.
Use of chloroquine for indications other than acute malaria is contraindicated in patients with ocular disease, specifically those who have retinal or visual field changes of any etiology. Irreversible retinal damage has been observed in some patients who received chloroquine. Significant risk factors for retinal damage include daily doses of chloroquine phosphate more than 2.3 mg/kg of actual body weight, duration of use more than 5 years, subnormal glomerular filtration (renal impairment or renal failure), use of some concomitant drug products such as tamoxifen, and concurrent macular disease. Baseline ophthalmological examination should be performed within the first year of starting chloroquine and should include best corrected distance visual acuity (BCVA), automated threshold visual field (VF) of the central 10 degrees (with retesting if an abnormality is noted), and spectral domain optical coherence tomography (SD-OCT). In Asian patients, retinal toxicity may first be noticed outside the macula, and VF testing should be performed in the central 24 degrees instead of the central 10 degrees. For patients with significant risk factors, monitoring should include annual examinations which include BCVA, VF, and SD-OCT. For individuals without significant risk factors, annual exams can usually be deferred until 5 years of treatment. Discontinue chloroquine if ocular toxicity is suspected, and monitor the patient closely as retinal changes and visual disturbances may progress after cessation of therapy. The use of chloroquine should be approached with caution in patients with Fabry disease, particularly those with ocular symptoms. The drug can cause a keratopathy that is clinically and ultrastructurally indistinguishable from keratopathy caused by Fabry disease; this drug-induced keratopathy is reversible with drug cessation. In addition, chloroquine poses a theoretical risk of decreased intracellular alpha-galactosidase A activity in Fabry disease patients. Chloroquine has been reported to induce clinical symptoms that mimic those of Fabry disease, including formation of inclusion bodies that are biochemically and ultrastructurally similar in most of the cells affected by Fabry disease (e.g., striated muscle, smooth muscle, etc.). The distinguishing factor is that the ultrastructural features of chloroquine toxicity in striated muscle, curvilinear bodies, are not present in renal cells.
Chloroquine is contraindicated in patients with known chloroquine hypersensitivity, or with a known allergy to 4-aminoquinolines. Patients with hydroxychloroquine hypersensitivity may have cross sensitivity to chloroquine.
QT prolongation, torsade de pointes (TdP), and ventricular arrhythmias have been reported with chloroquine use. The risk is greater with higher doses, although cases have been reported with therapeutic doses.     Use chloroquine with caution in patients with conditions that may increase the risk of QT prolongation including congenital long QT syndrome, bradycardia, AV block, heart failure, stress-related cardiomyopathy, myocardial infarction, stroke, hypomagnesemia, hypokalemia, hypocalcemia, or in patients receiving medications known to prolong the QT interval or cause electrolyte imbalances. Females, geriatric patients, patients with sleep deprivation, pheochromocytoma, sickle cell disease, hypothyroidism, hyperparathyroidism, hypothermia, systemic inflammation (e.g., human immunodeficiency virus (HIV) infection, fever, and some autoimmune diseases including rheumatoid arthritis, systemic lupus erythematosus (SLE), and celiac disease) and patients undergoing apheresis procedures (e.g., plasmapheresis [plasma exchange], cytapheresis) may also be at increased risk for QT prolongation.     In patients taking chloroquine with another drug that also prolongs the QT interval (see Therapeutic Drug Monitoring for recommendations specific to azithromycin with chloroquine used together for COVID-19), obtain a pre-treatment QTc using a standard 12-lead ECG, telemetry, or mobile ECG device. Obtain baseline electrolytes, including calcium, magnesium, and potassium. Determine if the patient is currently on any QT-prolonging medications that can be discontinued. Document high-risk cardiovascular and comorbid conditions. If the baseline QTc is 500 msec or more and/or the patient has an inherent tendency to develop an exaggerated QTc response (i.e., change of 60 msec or more), correct contributing electrolyte abnormalities, review and discontinue other unnecessary QTc prolonging medications, and proceed with close QTc surveillance. Obtain an initial on-therapy QTc approximately 2 to 4 hours after the first dose and then again at 48 and 96 hours after treatment initiation. If the baseline QTc is 460 to 499 msec (prepubertal), 470 to 499 msec (postpubertal males), or 480 to 499 msec (postpubertal females), correct contributing electrolyte abnormalities, review and discontinue other unnecessary QTc prolonging medications, and obtain an initial on-therapy QTc 48 and 96 hours after treatment initiation. If the baseline QTc is less than 460 msec (prepubertal), less than 470 msec (postpubertal males), or less than 480 msec (postpuberal females), correct electrolyte abnormalities and obtain an initial on-therapy QTc 48 and 96 hours after treatment initiation. Consider chronic chloroquine toxicity when conduction disorders, such as bundle-branch block or AV block, are diagnosed. Cases of cardiomyopathy resulting in cardiac failure, sometimes fatal, have been reported with chloroquine. Prompt discontinuation of chloroquine may prevent life-threatening complications if cardiotoxicity is suspected.
Chloroquine should not be used in patients with psoriasis unless the benefit to the patient outweighs the potential risks because it may precipitate a severe attack of psoriasis.
Chloroquine should be used with caution in patients with hepatic disease or alcoholism because the drug is metabolized in the liver and accumulation can occur producing toxic effects. Patients receiving other hepatotoxic drugs also should be treated with caution.
Chloroquine should be used with caution in patients with neurological disease including preexisting hearing impairment or seizure disorder. Polyneuritis, ototoxicity, seizures, neuromyopathy, and acute extrapyramidal symptoms (dystonia, dyskinesia, tongue protrusion, torticollis) have occurred with chloroquine therapy. Symptoms of muscle weakness and response of knee and ankle reflexes should be investigated regularly. If muscle weakness, extrapyramidal symptoms, or any defects in hearing occur during chloroquine therapy, the drug should be discontinued immediately and the patient observed closely.
Chloroquine can exacerbate porphyria or may cause hemolysis in patients with glucose-6-phosphate dehydrogenase deficiency (G6PD deficiency). Use chloroquine with caution in patients with these conditions. Blood monitoring for hemolytic anemia in G6PD deficiency patients may be necessary, particularly with concomitant use of other medications associated with hemolysis.
Use chloroquine with caution in patients with hypoglycemia or diabetes mellitus. Chloroquine can cause severe, life-threatening hypoglycemia in patients with or without antidiabetic medications. Warn patients about the risk of hypoglycemia and the associated clinical signs and symptoms. Monitor blood glucose and adjust treatment as necessary in patients presenting with clinical symptoms of hypoglycemia during chloroquine treatment.
Children are especially sensitive to the 4-aminoquinoline compounds. Fatalities have been reported after accidental exposure of chloroquine; some cases involved relatively small doses (e.g., 0.75 g or 1 g in a 3-year-old child). Strongly warn patients to keep chloroquine out of the reach of pediatric patients, including neonates, infants, children, and adolescents.
Weigh the benefit of chloroquine prophylaxis or treatment of malaria against the potential risk to the fetus, and consider the drug's potential to remain in the body for several months after discontinuation of therapy.   In humans at recommended doses for prophylaxis and treatment of malaria, observational studies as well as a meta-analysis, including a small number of prospective studies with chloroquine during pregnancy, have shown no increase in the rate of birth defects or spontaneous abortions. Guidelines recommend chloroquine as a treatment option for acute malaria and for prophylaxis in pregnant women during all trimesters. Chloroquine crosses the placenta, but the potential damage to the mother from malaria is greater than the drug's risk to the fetus. Weekly prophylactic doses appear to have minimal adverse effects when administered during pregnancy.  Animal studies showed embryo-fetal developmental toxicity at doses 3 to 16 times the maximum recommended therapeutic dose and the potential of genotoxicity in some test systems. Autoradiographic studies have shown accumulation in the eyes and ears when chloroquine is administered at the start or end of gestation in animal studies.
Use caution when administering chloroquine to breast-feeding women. Chloroquine is excreted into breast milk. The excretion of chloroquine and the major metabolite, desethylchloroquine, in breast milk was investigated in 11 lactating mothers following a single oral dose of chloroquine (600 mg base).The maximum daily dose of the drug that the infant received from breast-feeding was about 0.7% of the maternal start dose of the drug in malaria chemotherapy. Separate chemoprophylaxis for an infant is required. However, previous American Academy of Pediatrics (AAP) recommendations consider chloroquine usually compatible with breast-feeding, and chloroquine has an established dosage in infants.
Chloroquine should be used with caution in males because animal studies suggest that infertility is possible; after 30 days of oral treatment, testosterone levels and weight of testes, epididymis, seminal vesicles, and prostate decreased.
Chloroquine, a 4-aminoquinoline, is an anti-protozoal agent. The precise mechanism is unknown. Chloroquine may exert its effect against Plasmodium species by concentrating in the acid vesicles of the parasite and by inhibiting polymerization of heme. It can also inhibit certain enzymes by its interaction with DNA. Chloroquine is not active against gametocytes and the exoerythrocytic forms, including the hypnozoite stage (P. vivax and P. ovale) of the Plasmodium parasites. Organisms with reduced susceptibilities to hydroxychloroquine also show reduced susceptibilities to chloroquine.
Although the mechanisms underlying the antiinflammatory and immunomodulatory effects of chloroquine are unknown, several possible mechanisms of action have been proposed. It is unclear if these mechanisms work similarly for rheumatic and autoimmune diseases. Potential mechanisms include reduced cytokine production, inhibition of immune effector cells, inhibition of platelet function, protection of the cell surface from external disturbances, competitive binding to nucleic acid ligands or toll-like receptors (TLRs), interference with lysosomal function, reduction of leakage of lysosomal enzymes, and interference with endosomal NADPH oxidase (NOX).  
There are several potential mechanisms by which chloroquine may be active against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). These include inhibition of viral enzymes or processes such as viral DNA and RNA polymerase, viral protein glycosylation, virus assembly, new virus particle transport, and virus release. Other mechanisms may also involve ACE2 cellular receptor inhibition, acidification at the surface of the cell membrane inhibiting fusion of the virus, and immunomodulation of cytokine release.        
Chloroquine is administered orally. It is widely distributed into body tissues, with higher concentrations in the liver, kidneys, spleen, and lungs. Leukocytes also concentrate the drug. Smaller amounts of the drug are found in the brain and spinal cord. Cells containing melanin in the eyes and skin bind strongly to chloroquine. The drug also concentrates in erythrocytes and is bound to platelets and granulocytes. It is about 55% bound to plasma protein.  
Excretion of chloroquine is largely through urine, but this is a slow process and may be increased by acidification of the urine. Chloroquine undergoes appreciable degradation in the body, and the major metabolite is desethylchloroquine. Slightly more than half of a dose is excreted in urine as unchanged drug and about 25% as the major metabolite; bisdesethylchloroquine and other metabolic products are found in small amounts. A small portion of the unabsorbed drug is excreted in the feces. Elimination appears to take place in a biphasic manner. The elimination half-life is 108 to 291 hours.  
Affected cytochrome P450 isoenzymes and drug transporters: CYP2C8, CYP2D6, CYP3A4, P-gp
In vitro data suggest that chloroquine is metabolized primarily by CYP2C8 and CYP3A4, and to a much lesser extent, by CYP2D6.  It has also been shown to be an inhibitor of the drug transporter P-glycoprotein (P-gp).
After oral administration, chloroquine is rapidly and almost completely absorbed from the gastrointestinal tract. The Tmax is 2.7 to 6.9 hours with a Cmax of 283 to 1,430 ng/mL and an AUC of 8.2 to 140 mcg x hour/mL. A single study showed that the AUC in patients with malaria was higher than in normal volunteers (281 vs. 122 mcg x mL/L x hour).
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