Chloroquine sulfate 68mg/5ml oral solution
Requires a prescription from a doctor or prescriber
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MHRA alerts for Chloroquine sulfate
Safety monitoring data
Yellow Card reports
The MHRA Yellow Card scheme collects reports of suspected side effects from healthcare professionals and patients. View the Drug Analysis Profile (iDAP) for real-world adverse reaction data.
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Suspected adverse reactions reported for Chloroquine sulfate
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Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
EudraVigilance
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Suspected adverse reactions reported for Chloroquine sulfate
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2 branded products available
WHO defined daily dose (DDD)
500 mg
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via the NHS dm+d supplementary mapping files (NHSBSA). Contains public sector information licensed under the Open Government Licence v3.0.
Therapeutically similar medicines
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
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Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
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SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing the 50 most relevant studies.
Reviews & meta-analyses: 9 · Randomised trials: 3 · 1969–2026
Showing the 50 most relevant studies, sorted by most relevant.
Minwuyelet A, Yewhalaw D, Siferih M, et al.
2025
BackgroundMalaria during pregnancy poses significant risks to both the mother and the developing fetus. For pregnant women, the infection can result in severe illness and even death. Parasite sequestration in the placenta can cause maternal anemia and increase the risk of mortality both during and after childbirth. Malaria is also a major contributor to stillbirths and preterm births. Infected placental tissue can impede fetal growth, resulting in low birth weight, which is linked to delayed growth and cognitive development in the child. Furthermore, malaria during pregnancy remains a major contributor to perinatal, neonatal, and infant mortality.ObjectivesTo review the epidemiological patterns of malaria in pregnancy and its impact on maternal and neonatal health, and to analyze the availability and effectiveness of drug treatment options.MethodsRelevant articles published only in English were searched using electronic databases such as PubMed, Web of Science, Scopus, and Pro-Quest. Keywords including "'malaria in pregnancy", "placental malaria", "congenital malaria", "treatment options", and "nutrition intervention and intermittent preventive treatment" were used in combination. Of the total of 4,486 articles identified, 139 articles were ultimately included. Whereas, others were excluded due to duplication, irrelevant abstract, title, and quality assessment.ResultsFrom 139 included studies, 47 focused on epidemiology of malaria in pregnancy, 58 on its impact and 16 on treatment options and 18 on nutrition intervention and intermittent treatment. Plasmodium falciparum is the leading cause of complications in pregnant women and is primarily found in Africa, while P.vivax is recognized as an emerging global threat, and causing serious consequences. Other species, such as P.knowlesi, P.ovale, and P.malariae are less common. Malaria prevalence in pregnancy can reach 60% in sub-Saharan Africa and 36% globally, with placental malaria affecting up to 28% of cases. The disease causes serious complications such as maternal anemia, premature birth, and low birth weight, severe anemia and increased maternal and infant mortality. Prevention strategies like intermittent preventive treatment (IPTp), insecticide-treated nets (ITNs) and Indoor residual spray (IRS) are essential. Early diagnosis and treatment can reverse adverse effects on placental and congenital function. Artesunate is recommended for severe malaria in all trimesters. Even resistance to chloroquine reported in some areas, it is the drug of choice for uncomplicated P.vivax infections.ConclusionsMalaria during pregnancy significantly impacts maternal and fetal health, leading to anemia, growth restriction, preterm birth, and neonatal death. Infants born to mothers with malaria are more likely to contract the disease. Further research and improved treatment strategies are needed to address this issue effectively.
Abstract licence: CC BY-NC-ND
Michael Takla, Kamalan Jeevaratnam
2020
Abstract Background The COVID-19 pandemic has required clinicians to urgently identify new treatment options or the repurposing of existing drugs. Several drugs are now being repurposed with the aim of identifying if these drugs provide some level of disease resolution. Of particular interest are chloroquine (CQ) and hydroxychloroquine (HCQ), first developed as an antimalarial therapy. There is increasing concern with regards to the efficacy and safety of these agents. The aims of this review are to systematically identify and collate studies describing the use of CQ and HCQ in human clinical trials and provide a detailed synthesis of evidence of its efficacy and safety. Methods and Findings Searches for (“COVID” AND “chloroquine”[title/abstract] AND “outcomes”[full text]) and two (“COVID” AND “hydroxychloroquine”[title/abstract] AND “outcomes”[full text]) yielded 272 unique articles. Unique articles were manually checked for inclusion and exclusion criteria and also subjected to a quality appraisal assessment. A total of 19 articles were included in the systematic review. Seventy-five percent of observational studies employing an endpoint specific to efficacy recorded no significant difference in the attainment of outcomes, between COVID-19 patients given a range of CQ and/or HCQ doses, and the control groups. All clinical trials and 82% of observational studies examining an indicator unique to drug safety discovered a higher probability of adverse events in those treated patients suspected of, and diagnosed with, COVID-19. Seventy-five percent of the total papers focusing on cardiac side-effects found a greater incidence among patients administered a wide range of CQ and/or HCQ doses, with QTc prolongation the most common finding, in addition to its consequences of VT and cardiac arrest. Of the total studies using mortality rate as an end-point, 60% reported no significant change in the risk of death, while 30% showed an elevation, and 10% a depression, in treated relative to control patients. Conclusion The strongest available evidence suggests that, relative to standard in-hospital management of symptoms, the use of CQ and HCQ to treat hospitalised COVID-19 patients has likely been unsafe. At the very least, the poor quality of data failing to find any significant changes in the risk of VT should preclude definitive judgment on drug safety until the completion of high-quality randomised clinical trials.
Abstract licence: CC BY-NC-ND
I. R. Latarissa, M. Barliana, A. Meiliana, et al.
The Indonesian Biomedical Journal, 2023
Latarissa IR, Khairinisa MA, Iftinan GN, et al.
2025
E. Mcchesney
The American journal of medicine, 1983
M. Michaelides, Niamh B. Stover, P. Francis, et al.
Archives of ophthalmology, 2011
Michel Cot, A. Roisin, D. Barro, et al.
The American journal of tropical medicine and hygiene, 1992
M. Ishihara, N. Fedarko, H. Conrad
The Journal of biological chemistry, 1986
O. Sharma
Archives of neurology, 1998
Masaki Yanagishita, V. C. Hascall
The Journal of biological chemistry, 1984
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
66 found
Half-life
20-60 days
Mechanism
Chloroquine inhibits the action of heme polymerase in malarial trophozoites, pre…
Food interactions
1 warning
Human targets
7 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
52-102%
[A191676]
…
Half-life
20-60 days
[A191676]
Protein binding
46-74%
[A191673]
(-)-chloroquine binds more strongly to alpha-1-acid glycoprotein and (+)-chloroquine binds more strongly to serum albumin.
[A191667]
…
Volume of distribution
200-800L/kg
[A191676]
Metabolism
[A38847][A191661][A39300][A191676]
…
Elimination
50%
[A191676]
50% of a dose is recovered in the urine as unchanged chloroquine, with 10% of the dose recovered in the urine as desethylchloroquine.
[A191676]
…
Clearance
0.35-1L/h
[A191676]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
The FDA emergency use authorization for [hydroxychloroquine] and chloroquine in the treatment of COVID-19 was revoked on 15 June 2020.[L14312]
Chloroquine was granted FDA Approval on 31 October 1949.[L12054]
[L12051]
It is also used to treat extraintestinal amebiasis.
[L12051]
Chloroquine is also used off label for the treatment of rheumatic diseases,[A191655] as well as treatment and prophylaxis of Zika virus.
[A191649][A191652]
Chloroquine is currently undergoing clinical trials for the treatment of COVID-19.
[A191631]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 1649 interactions
[L12051]
Overdose should be managed with symptomatic and supportive treatment which may include prompt emesis, gastric lavage, and activated charcoal.
[L12051]
Chloroquine passively diffuses through cell membranes and into endosomes, lysosomes, and Golgi vesicles; where it becomes protonated, trapping the chloroquine in the organelle and raising the surrounding pH.[A191676][A191628] The raised pH in endosomes, prevent virus particles from utilizing their activity for fusion and entry into the cell.[A191625]
Chloroquine does not affect the level of ACE2 expression on cell surfaces, but inhibits terminal glycosylation of ACE2, the receptor that SARS-CoV and SARS-CoV-2 target for cell entry.[A191628][A191625] ACE2 that is not in the glycosylated state may less efficiently interact with the SARS-CoV-2 spike protein, further inhibiting viral entry.[A191625]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A191676]
Intravenous chloroquine reaches a Cmax of 650-1300µg/L and oral chloroquine reaches a Cmax of 65-128µg/L with a Tmax of 0.5h.
[A191676]
[A191676]
[A191673]
(-)-chloroquine binds more strongly to alpha-1-acid glycoprotein and (+)-chloroquine binds more strongly to serum albumin.
[A191667]
[A191676]
[A38847][A191661][A39300][A191676]
It is N-dealkylated to a lesser extent by CYP3A5, CYP2D6, and to an ever lesser extent by CYP1A1.
[A38847][A191661][A39300][A191676]
N-desethylchloroquine can be further N-dealkylated to N-bidesethylchloroquine, which is further N-dealkylated to 7-chloro-4-aminoquinoline.
[A191676]
[A191676]
50% of a dose is recovered in the urine as unchanged chloroquine, with 10% of the dose recovered in the urine as desethylchloroquine.
[A191676]
[A191676]
Proteins and enzymes this drug interacts with in the body
Acts as a receptor for chemokines including CCL2, CCL5, CCL7, CCL11, CCL13, CCL14, CCL17, CXCL5, CXCL6, IL8/CXCL8, CXCL11, GRO, RANTES, MCP-1 and TARC. May regulate chemokine bioavailability and, consequently, leukocyte recruitment through two distinct mechanisms: when expressed in endothelial cells, it sustains the abluminal to luminal transcytosis of tissue-derived chemokines and their subsequent presentation to circulating leukocytes; when expressed in erythrocytes, serves as blood reservoir of cognate chemokines but also as a chemokine sink, buffering potential surges in plasma chemokine levels
Impairs regulatory T-cells (Treg) function in individuals with rheumatoid arthritis via FOXP3 dephosphorylation. Up-regulates the expression of protein phosphatase 1 (PP1), which dephosphorylates the key 'Ser-418' residue of FOXP3, thereby inactivating FOXP3 and rendering Treg cells functionally defective .
PMID:23396208
Key mediator of cell death in the anticancer action of BCG-stimulated neutrophils in combination with DIABLO/SMAC mimetic in the RT4v6 bladder cancer cell line .
PMID:16829952 PMID:22517918 PMID:23396208
Induces insulin resistance in adipocytes via inhibition of insulin-induced IRS1 tyrosine phosphorylation and insulin-induced glucose uptake. Induces GKAP42 protein degradation in adipocytes which is partially responsible for TNF-induced insulin resistance (By similarity).
Plays a role in angiogenesis by inducing VEGF production synergistically with IL1B and IL6 .
PMID:12794819
Promotes osteoclastogenesis and therefore mediates bone resorption (By similarity)
PMID:14716310
Acts via MYD88 and TRAF6, leading to NF-kappa-B activation, cytokine secretion and the inflammatory response .
PMID:11564765 PMID:17932028
Controls lymphocyte response to Helicobacter infection (By similarity).
Upon CpG stimulation, induces B-cell proliferation, activation, survival and antibody production PMID:23857366
PMID:33147444
Proposed to be an universal biosensor for nucleic acids. Promotes host inflammatory response to sterile and infectious signals and is involved in the coordination and integration of innate and adaptive immune responses.
In the cytoplasm functions as a sensor and/or chaperone for immunogenic nucleic acids implicating the activation of TLR9-mediated immune responses, and mediates autophagy. Acts as a danger-associated molecular pattern (DAMP) molecule that amplifies immune responses during tissue injury .
PMID:27362237
Released to the extracellular environment can bind DNA, nucleosomes, IL-1 beta, CXCL12, AGER isoform 2/sRAGE, lipopolysaccharide (LPS) and lipoteichoic acid (LTA), and activates cells through engagement of multiple surface receptors .
PMID:34743181
In the extracellular compartment fully reduced HMGB1 (released by necrosis) acts as a chemokine, disulfide HMGB1 (actively secreted) as a cytokine, and sulfonyl HMGB1 (released from apoptotic cells) promotes immunological tolerance .
PMID:23446148 PMID:23519706 PMID:23994764 PMID:25048472
Has proangiogdenic activity (By similarity). May be involved in platelet activation (By similarity).
Binds to phosphatidylserine and phosphatidylethanolamide (By similarity). Bound to RAGE mediates signaling for neuronal outgrowth (By similarity). May play a role in accumulation of expanded polyglutamine (polyQ) proteins such as huntingtin (HTT) or TBP PMID:23303669 PMID:25549101
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that transport this drug across cell membranes
PMID:2897240 PMID:35970996 PMID:8898203 PMID:9038218 PMID:35507548
Catalyzes the flop of phospholipids from the cytoplasmic to the exoplasmic leaflet of the apical membrane. Participates mainly to the flop of phosphatidylcholine, phosphatidylethanolamine, beta-D-glucosylceramides and sphingomyelins .
PMID:8898203
Energy-dependent efflux pump responsible for decreased drug accumulation in multidrug-resistant cells PMID:2897240 PMID:35970996 PMID:9038218
Proteins that carry this drug through the body
PMID:19021548
Major calcium and magnesium transporter in plasma, binds approximately 45% of circulating calcium and magnesium in plasma (By similarity).
Potentially has more than two calcium-binding sites and might additionally bind calcium in a non-specific manner (By similarity). The shared binding site between zinc and calcium at residue Asp-273 suggests a crosstalk between zinc and calcium transport in the blood (By similarity). The rank order of affinity is zinc > calcium > magnesium (By similarity).
Binds to the bacterial siderophore enterobactin and inhibits enterobactin-mediated iron uptake of E.coli from ferric transferrin, and may thereby limit the utilization of iron and growth of enteric bacteria such as E.coli .
PMID:6234017
Does not prevent iron uptake by the bacterial siderophore aerobactin PMID:6234017
Appears to function in modulating the activity of the immune system during the acute-phase reaction
ATC P01BB52
ATC P01BA01
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
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Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Chloroquine
Matched from: Chloroquine sulfate
Additional database identifiers
Drugs Product Database (DPD)
6547
Drugs Product Database (DPD)
6549
ChemSpider
2618
BindingDB
22985
PDB
CLQ
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4035
GeneCards
ACKR1
UniProt Accession
ACKR1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4627
GenAtlas
GSTA2
GeneCards
GSTA2
GenBank Gene Database
M16594
GenBank Protein Database
306811
UniProt Accession
GSTA2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11892
GenAtlas
TNF
GeneCards
TNF
GenBank Gene Database
M16441
GenBank Protein Database
339741
UniProt Accession
TNFA_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:15633
GenAtlas
TLR9
GeneCards
TLR9
GenBank Gene Database
AF259262
GenBank Protein Database
8099652
Guide to Pharmacology
1759
UniProt Accession
TLR9_HUMAN
GenBank Gene Database
AF426836
UniProt Accession
GST_PLAF7
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4983
GenAtlas
HMGB1
GeneCards
HMGB1
GenBank Gene Database
X12597
Guide to Pharmacology
3279
UniProt Accession
HMGB1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4632
GenAtlas
GSTM1
GeneCards
GSTM1
GenBank Gene Database
X08020
GenBank Protein Database
31924
UniProt Accession
GSTM1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:13557
GenAtlas
ACE2
GeneCards
ACE2
GenBank Gene Database
AF291820
GenBank Protein Database
9802433
Guide to Pharmacology
1614
UniProt Accession
ACE2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2622
GenAtlas
CYP2C8
GeneCards
CYP2C8
GenBank Gene Database
M17397
Guide to Pharmacology
1325
UniProt Accession
CP2C8_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2638
GenAtlas
CYP3A5
GeneCards
CYP3A5
GenBank Gene Database
J04813
GenBank Protein Database
181346
Guide to Pharmacology
1338
UniProt Accession
CP3A5_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2625
GenAtlas
CYP2D6
GeneCards
CYP2D6
GenBank Gene Database
M20403
GenBank Protein Database
181350
Guide to Pharmacology
1329
UniProt Accession
CP2D6_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2595
GeneCards
CYP1A1
GenBank Gene Database
K03191
GenBank Protein Database
181276
Guide to Pharmacology
1318
UniProt Accession
CP1A1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:399
GenAtlas
ALB
GeneCards
ALB
GenBank Gene Database
V00494
GenBank Protein Database
28590
UniProt Accession
ALBU_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8498
GenAtlas
ORM1
GeneCards
ORM1
GenBank Gene Database
X02544
GenBank Protein Database
757907
UniProt Accession
A1AG1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8499
GeneCards
ORM2
GenBank Gene Database
BC015964
GenBank Protein Database
16359000
UniProt Accession
A1AG2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:40
GenAtlas
ABCB1
GeneCards
ABCB1
GenBank Gene Database
M14758
GenBank Protein Database
307180
Guide to Pharmacology
768
UniProt Accession
MDR1_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite:
- DrugBank 6.02024Recommended citationKnox C., Wilson M., Klinger C.M., et alDrugBank 6.0: the DrugBank Knowledgebase for 2024Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
- DrugBank 5.02018Wishart D.S., Feunang Y.D., Guo A.C., et alDrugBank 5.0: a major update to the DrugBank database for 2018Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
- DrugBank 4.02014Law V., Knox C., Djoumbou Y., et alDrugBank 4.0: shedding new light on drug metabolismNucleic Acids Res. 2014 Jan 142(1):D1091-7
- DrugBank 3.02011Knox C., Law V., Jewison T., et alDrugBank 3.0: a comprehensive resource for 'omics' research on drugsNucleic Acids Res. 2011 Jan39(Database issue):D1035-41
- DrugBank 2.02008Wishart D.S., Knox C., Guo A.C., et alDrugBank: a knowledgebase for drugs, drug actions and drug targets.Nucleic Acids Research2008 Jan36(Database issue):D901-6
- DrugBank 1.02006Wishart D.S., Knox C., Guo A.C., et alDrugBank: a comprehensive resource for in silico drug discovery and exploration.Nucleic Acids Research2006 Jan 134(Database issue):D668-72