Chloroquine sulfate 68mg/5ml oral solution
Requires a prescription from a doctor or prescriber
Official documents, adverse reaction reporting, and safety monitoring
Report a side effect
Submit a Yellow Card report to the MHRA
Official medicine documents
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.
View Drug Analysis Profile
Suspected adverse reactions reported for Chloroquine sulfate
Browse all iDAP reports
Interactive Drug Analysis Profiles for all medicines
Report a side effect
Submit a Yellow Card report to the MHRA
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
The European Medicines Agency (EMA) collects suspected adverse reaction reports from across the EU/EEA through the EudraVigilance system. Search for safety data on this medicine.
View EudraVigilance report
Suspected adverse reactions reported for Chloroquine sulfate
About EudraVigilance
Learn about EU pharmacovigilance and safety monitoring
EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
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 BNF/ATC 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
Check stock at pharmacies and supply information
Pharmacy stock checkers
Search for this medicine at major UK pharmacy chains. These links open the retailer's own website — results depend on their current online catalogue.
Supply & safety information
Official UK regulator monitoring and safety alerts
Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. Shortage and safety information sourced from MHRA drug safety updates (gov.uk, Crown Copyright under OGL v3.0).
Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
Browse tools
SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. BNF code shown is the factual mapping value distributed by NHS Business Services Authority (NHSBSA) in the dm+d supplementary file under OGL v3.0; it is not affiliated with, nor licensed from, the publishers of the British National Formulary. 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 all 23 studies.
Reviews & meta-analyses: 2 · Randomised trials: 1 · 2013–2026
Showing all 23 studies, sorted by most relevant.
I. R. Latarissa, M. Barliana, A. Meiliana, et al.
The Indonesian Biomedical Journal, 2023
BACKGROUND: Before WHO revoked the emergency use authorization for Chloroquine (CQ) and Hydroxychloroquine (HCQ) because of their side effects, it was suggested to use these two drugs for COVID-19 therapy. In addition, another derivate of quinine, namely Quinine Sulfate (QS), showed good in silico and in vitro antiviral activity against SARS-CoV-2. Prior the WHO revocation, this study was conducted to evaluate the efficacy of QS in mild-to-moderate COVID-19 patients.METHODS: This was an adaptive, controlled, multicenter, randomized, double-blind clinical trial involving mild-to-moderate COVID-19 patients in Indonesia. The participants were divided into 2 groups: the control group (standard COVID-19 treatment + placebo) and the treatment group (standard COVID-19 treatment + QS). The primary outcome was the efficacy of QS based on clinical status using a 7-point ordinal scale. The secondary outcomes were the efficacy of QS in terms of the incidence and duration of oxygen supplementation, incidence of mechanical ventilation, and length of stay.RESULTS: No significant difference in the efficacy parameters studied was found between the control group and the treatment group. The difference in the mean oxygen saturation was also measured and the results showed a significant difference where the treatment group had higher mean oxygen saturation than the control group (p=0.001).CONCLUSION: Although not significant, the treatment group showed better therapy outcomes compared to the control group.KEYWORDS: clinical trials, efficacy, quinine, chloroquine, hydroxychloroquine
Abstract licence: CC BY-NC
Sheikh Abdul Khaliq, Muneer Khan, Saquib Azeem, et al.
Liaquat National Journal of Primary Care, 2024
Incidences of dengue-virus infection are increasing globally. Around 3.90 billion population is at high risk of infection. There is no cure/prevention available. Hence aim of the current review was the evaluation of current development and prospects for the production of safe anti-dengue drugs. The data of review was synthesized by PRISMA. Grading of Recommendation Assessment, Development, and Evaluation criteria were employed to establish the quality of the literature. Many drugs/compounds have shown promising prospects. Target site of these drugs on dengue virus were inhibition of replication (N-sulfonyl peptide-hybrids, milk-exosomes, sunitinib, schisandrin-A, cavinafungin, minocycline, 4-hydroxyphenyl retinamide, Goniothalamus umbrosus, Dryopteris crassirhizoma, Morus alba, statins), protease-enzyme (Thiazolidinone-peptide, nelfinavir, carnosine, 1,2-benzisothiazol-3(2H)- one and 1,3,4-oxadiazole), capsid-protein (Juglanin and silymarin), NS4B-gene (Desatinib), entry-in-host-cell (Duramycin, glycodendrimers, curdlan sulfate), RNA-capping (Lanatoside-C), fusion (Chloroquine) and NS3-helicase (Suramina). Many compounds/drugs are found effective by targeting the structural proteins of the dengue virus to use as a therapy in the future.
Abstract licence: CC BY
I. R. Latarissa, M. I. Barliana, A. Meiliana, et al.
Clinical Pharmacology : Advances and Applications, 2021
The coronavirus disease 2019 (COVID-19) pandemic is currently the largest and most serious health crisis in the world. There is no definitive treatment for COVID-19. Vaccine administration has begun in various countries, but no vaccine is 100% effective. Some people are not protected after vaccination, and there are some groups of people who cannot be vaccinated therefore, research on COVID-19 treatment still needs to be done. Of the several drugs under study, chloroquine (CQ) and hydroxychloroquine (HCQ) are quite controversial, although they have good activity against SARS-CoV-2, both drugs have serious side effects. Indonesia with its wealth of natural ingredients has one potential compound, quinine sulfate (QS), which has the same structure and activity as CQ and HCQ and a better safety profile. The aim of this article was to review the potential of QS against the SARS-Cov-2 virus and outline its safety profile. We conclude that QS has the potential to be developed as a COVID-19 treatment with a better safety profile than that of CQ and HCQ.
Abstract licence: CC BY-NC
David J. Browning
Hydroxychloroquine and Chloroquine Retinopathy, 2014
Lara Bull-Otterson, Elizabeth B Gray, D. Budnitz, et al.
Morbidity and Mortality Weekly Report, 2020
- COVID-19 Drug Treatment
- Chloroquine
- Hydroxychloroquine
S. Tunç, O. Duman, B. K. Bozoğlan
Journal of Luminescence, 2013
Yunhao Li, F. jia, Yujuan Gao, et al.
International journal of biological macromolecules, 2023
- Antineoplastic Agents
- Nanocomposites
- Triple Negative Breast Neoplasms
Zhengxuan Liang, G. You
Pharmaceutics, 2023
Organic anion transporter 3 (OAT3), at the basolateral membrane of kidney proximal tubule cells, facilitates the elimination of numerous widely used drugs. Earlier investigation from our laboratory revealed that ubiquitin conjugation to OAT3 leads to OAT3 internalization from the cell surface, followed by degradation in the proteasome. In the current study, we examined the roles of chloroquine (CQ) and hydroxychloroquine (HCQ), two well-known anti-malarial drugs, in their action as proteasome inhibitors and their effects on OAT3 ubiquitination, expression, and function. We showed that in cells treated with CQ and HCQ, the ubiquitinated OAT3 was considerably enhanced, which correlated well with a decrease in 20S proteasome activity. Furthermore, in CQ- and HCQ-treated cells, OAT3 expression and OAT3-mediated transport of estrone sulfate, a prototypical substrate, were significantly increased. Such increases in OAT3 expression and transport activity were accompanied by an increase in the maximum transport velocity and a decrease in the degradation rate of the transporter. In conclusion, this study unveiled a novel role of CQ and HCQ in enhancing OAT3 expression and transport activity by preventing the degradation of ubiquitinated OAT3 in proteasomes.
Abstract licence: CC BY
I. F. Silva, Keiza Priscila Enes, G. Rocha, et al.
Journal of Environmental Science and Health, Part A, 2023
- COVID-19
- Hydroxychloroquine
- COVID-19 Drug Treatment
Letters in Applied NanoBioScience, 2024
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 medications. 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
Show
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 the following publications:
Show earlier publications
Structured knowledge from the free knowledge base
ATC classifications (Wikidata)
Linked open data from Wikidata (Q422438), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication. WHO INN from the World Health Organization.