Dequalinium chloride 250microgram lozenges
Dequalinium is an antibacterial agent with multi-targeted actions.
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Suspected adverse reactions reported for Dequalinium
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1 branded products available
WHO defined daily dose (DDD)
1.5 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.
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Codes for healthcare professionals and prescribing systems
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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. 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 the 50 most relevant studies.
Reviews & meta-analyses: 4 · Randomised trials: 4 · 1969–2026
Showing the 50 most relevant studies, sorted by most relevant.
Fanny Eckel, Alex Farr, Julia Deinsberger, et al.
Journal of Lower Genital Tract Disease, 2023
- Vaginosis, Bacterial
- Candidiasis, Vulvovaginal
- Vulvovaginitis
Objective/Purpose Women at reproductive age frequently experience vulvovaginal infections and vaginitis. The most common etiologies are vulvovaginal candidiasis (VVC), bacterial vaginosis (BV), desquamative inflammatory vaginitis/aerobic vaginitis, and trichomoniasis. Various treatment options are available for these infections, such as specific antimicrobial or antiseptic agents. Dequalinium chloride (DQC) is a local antiseptic agent with a broad antimicrobial and antifungal spectrum. Multiple studies suggest that DQC is an efficient treatment for vaginal infections; however, it is not widely recommended as a first-line treatment. This systematic review and meta-analysis aims to evaluate the efficacy of DQC compared with that of standard treatment. Methods Our systematic review was conducted according to the PRISMA guidelines. PubMed/MEDLINE, EMBASE, CENTRAL, and clinicaltrials.org were searched to retrieve relevant reports up to October 2022. Results Four randomized controlled studies and 1 observational study were included in this review. Overall, DQC showed noninferiority to the reference treatments for BV and VVC, and to the evaluated treatment options for desquamative inflammatory vaginitis/aerobic vaginitis. For BV and VVC, this could also be confirmed in a meta-analysis including 3 randomized controlled studies. No serious adverse events were reported in any of these studies. Conclusions Dequalinium chloride offers a safe, well-tolerated, and efficient treatment option for vulvovaginal infections of different etiologies. However, further studies are needed to confirm our findings and allow inclusion of DQC as a first-line treatment into guidelines.
Abstract licence: CC BY-NC-ND 4.0
Mila Permata Sari, Dovy Djanas, Andani Eka Putra
Andalas Obstetrics and Gynecology Journal, 2025
Introduction: Vulvovaginitis affects pregnancy outcomes and managing it involves the use of metronidazole or nystatin, which can cause local or systemic side effects. Dequalinium chloride (DQC) is suggested as a new treatment option for vulvovaginitis during pregnancy with minimal side effects. Objective: To compare the effectiveness of dequalinium chloride (DQC) versus metronidazole + nystatin (MN) in treating vulvovaginitis in pregnant women during their second and third trimesters. Method: A single-blind randomized controlled trial was conducted at the Andalas Public Health Center, Padang, from January to May 2024. Pregnant women in their second and third trimesters, meeting the inclusion and exclusion criteria, were enrolled. The participants were randomly assigned to either the DQC or MN group. Vaginal swabs were taken before and after a 6-day treatment, and PCR analysis was performed. Results: Eighteen patients were treated with DQC and MN. Most participants had bacterial vaginosis (DQC 78%, MN 83%), with half having candidiasis (DQC and MN 50%) and fewer cases of trichomoniasis (28% in both groups). Significant improvements were seen in the DQC group for symptoms (p=0.000), Gardnerella vaginalis (p=0.035), and Candida albicans (p=0.021). In the MN group, significant improvements were noted for symptoms (p=0.000) and Gardnerella vaginalis (p=0.002). No significant differences were observed between the groups for symptom resolution or microbial reduction. Conclusion: DQC is as effective as metronidazole + nystatin in treating bacterial vaginosis and candidiasis in pregnancy. Keywords: Vulvovaginitis, pregnancy, dequalinium chloride, metronidazole, nystatin
Abstract licence: CC BY 4.0
M. J. Weiss, James R. Wong, C. S. Ha, et al.
Proceedings of the National Academy of Sciences of the United States of America, 1987
Xiao-Xing Wang, Yang-Bing Li, Hong-Juan Yao, et al.
Biomaterials, 2011
E. Weissenbacher, G. Donders, V. Unzeitig, et al.
Gynecologic and Obstetric Investigation, 2011
Volkmar Weissig, Jürgen Lasch, Gregory Erdos, et al.
Pharmaceutical Research, 1998
Rebecca Haydock, Trish Hepburn, Jonathan Ross, et al.
Trials, 2022
- Vaginosis, Bacterial
- Dequalinium
- Anti-Infective Agents
Abstract Background Bacterial vaginosis (BV) is the most common cause of vaginal discharge in women of reproductive age, and it is estimated that up to a third of women will experience it at some point in their lives. BV produces an offensive vaginal odour and it is associated with serious sequelae. The most frequently prescribed treatment for BV in the UK is 7-day oral metronidazole but recurrences are common following it. Dequalinium chloride (Fluomizin©) is an anti-infective, antiseptic agent administered as a vaginal tablet. Small studies have shown this to be an effective alternative to antibiotics as a BV treatment. This trial aims to investigate whether dequalinium is as effective as current antibiotic treatments for the treatment of BV 1 month after treatment start. Methods DEVA is a multi-centre, randomised, open-label, parallel group, non-inferiority trial of dequalinium chloride versus usual care antibiotics for the treatment of BV. Recruitment will take place in 15 GUM clinics in the UK with Leeds Sexual Health also managing remote recruitment via the trial website. Women will be randomised 1:1 to receive dequalinium or usual care antibiotics. The primary outcome is to determine if the proportion of women reporting resolution of BV symptoms 4 weeks after treatment (without the need for additional treatment) is not worse in women treated with dequalinium chloride compared to usual care antibiotics. Questionnaire follow-up will take place 4 and 12 weeks after starting treatment, and remotely recruited patients will also provide a week 4 BV vaginal smear. The sample size is 904. Discussion This trial will provide high-quality evidence on the use of dequalinium chloride as a BV treatment, which could result in patients reducing the number of antibiotics they take. Trial registration ISRCTN ISRCTN91800263. Prospectively registered on 20 January 2020.
Abstract licence: CC BY 4.0
Phillip Hay
Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature, 2017
W. Mendling, E. Weissenbacher, S. Gerber, et al.
Archives of Gynecology and Obstetrics, 2015
BackgroundVaginal infections are responsible for a large proportion of gynaecological outpatient visits. Those are bacterial vaginosis (BV), vulvovaginal candidosis (VVC), aerobic vaginitis (AV) associated with aerobic bacteria, and mixed infections. Usual treatments show similar acceptable short-term efficacy, but frequent recurrences and increasing microbial resistance are unsolved issues. Furthermore, vaginal infections are associated with a variety of serious adverse outcomes in pregnancy and generally have a major impact on quality of life. Identifying the correct therapy can be challenging for the clinician, particularly in mixed infections.FindingsDequalinium chloride (DQC) is an anti-microbial antiseptic agent with a broad bactericidal and fungicidal activity. Systemic absorption after vaginal application of DQC is very low and systemic effects negligible. Vaginal DQC (Fluomizin®vaginal tablets) has been shown to have equal clinical efficacy as clindamycin in the treatment of BV. Its broad antimicrobial activity makes it appropriate for the treatment of mixed vaginal infections and in case of uncertain diagnosis. Moreover, resistance of pathogens is unlikely due to its multiple mode of action, and vaginal DQC provides also a reduced risk for post-treatment vaginal infections.ConclusionsVaginal DQC (10 mg) as 6-day therapy offers a safe and effective option for empiric therapy of different vaginal infections in daily practice. This review summarizes the available and relevant pharmacological and clinical data for the therapy of vaginal infections with vaginal DQC and provides the rationale for its use in daily gynaecologic practice.
Abstract licence: CC BY 4.0
Yuehai Pan, Shuai Zhao, Fan Chen
Clinical and Experimental Pharmacology and Physiology, 2021
- Glioma
- Dequalinium
- Antineoplastic Agents
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
None known
Half-life
Not available
Mechanism
Dequalinium has multiple modes of action.
Food interactions
None known
Human targets
10 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
2000 to 4000 mg/L
Half-life
Protein binding
Volume of distribution
Metabolism
Elimination
Clearance
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
First used as an antiseptic and disinfectant in the 1950s, dequalinium is still found in various OTC products to treat conditions of oral infections and inflammation.[A249255] It is also used in vaginal tablets to treat bacterial vaginosis.[L42190]
[A249255]
As vaginal tablets, dequalinium is indicated for the treatment of bacterial vaginosis in adult women under 55 years of age.
[L42190]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 54 interactions
[L42260]
There is limited clinical experience of drug overdose with dequalinium. While dequalinium is generally well tolerated and considered as safe at recommended therapeutic doses, dequalinium is a neurotoxic agent and mitochondrial poison. At a high dose in mice, the drug caused damages to the liver and kidneys, and caused renal and hepatic failure.
[A249255]
Dequalinium can also precipitate nucleic acids, as it can intercalate one of its quinoline chromophores between DNA base pairs.[A19280][A249255] Depending on the drug concentration, dequalinium can lyse the bacterial cell by promoting osmotic imbalance.[A19280][A19293]
As with other quaternary ammonium compounds similar to dequalinium, gram-positive bacteria are more sensitive to dequalinium than gram-negative bacteria.[A19293][L42190] The bactericidal and fungicidal effects of dequalinium can occur within 30 to 60 minutes.[A19294] According to in vitro studies, the minimal inhibitory concentration (MIC) for dequalinium against relevant vaginal pathogens ranges from 0.2 to ≥ 1024 µg/mL.[L42190]
There is evidence that dequalinium exhibits anticancer activity in human leukemia cells: dequalinium induces a cytotoxic effect by altering redox balance, downregulating Raf/MEK/ERK1/2 and PI3K/Akt signalling pathways, and promoting apoptosis of leukemic cells.[A19290][A19291][A19292] Dequalinium was also shown to block small conductance Ca2+-activated K+ channels, called SK channels, which are often expressed in some cancer cells to play a role in cell proliferation and migration.[A249255] One study showed that dequalinium reduced macrophage motility in mice, inhibiting macrophage infiltration of irradiated tumours and attenuating local metastasis.[A19289]
Interestingly, dequalinium was shown to modulate and induce self-oligomerization of alpha-synuclein, a synaptic protein known to cause aggregates in several neurodegenerative disorders. This finding highlights the neuroprotective actions of dequalinium; however, further investigations are warranted as dequalinium is a neurotoxic agent.[A249255]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[L42190]
Proteins and enzymes this drug interacts with in the body
PMID:11257230 PMID:11257231 PMID:11447297 PMID:12121969 PMID:12620238 PMID:17560374 PMID:17967870 PMID:19473982 PMID:20154138 PMID:22103349 PMID:9230442
Acts as a direct caspase inhibitor .
PMID:11257230 PMID:11257231 PMID:12620238
Directly bind to the active site pocket of CASP3 and CASP7 and obstructs substrate entry .
PMID:11257230 PMID:11257231 PMID:16352606 PMID:16916640
Inactivates CASP9 by keeping it in a monomeric, inactive state .
PMID:12620238
Acts as an E3 ubiquitin-protein ligase regulating NF-kappa-B signaling and the target proteins for its E3 ubiquitin-protein ligase activity include: RIPK1, RIPK2, MAP3K2/MEKK2, DIABLO/SMAC, AIFM1, CCS, PTEN and BIRC5/survivin .
PMID:17560374 PMID:17967870 PMID:19473982 PMID:20154138 PMID:22103349 PMID:22607974 PMID:29452636 PMID:30026309
Acts as an important regulator of innate immunity by mediating 'Lys-63'-linked polyubiquitination of RIPK2 downstream of NOD1 and NOD2, thereby transforming RIPK2 into a scaffolding protein for downstream effectors, ultimately leading to activation of the NF-kappa-B and MAP kinases signaling .
PMID:19667203 PMID:22607974 PMID:29452636 PMID:30026309
'Lys-63'-linked polyubiquitination of RIPK2 also promotes recruitment of the LUBAC complex to RIPK2 .
PMID:22607974 PMID:29452636
Regulates the BMP signaling pathway and the SMAD and MAP3K7/TAK1 dependent pathways leading to NF-kappa-B and JNK activation .
PMID:17560374
Ubiquitination of CCS leads to enhancement of its chaperone activity toward its physiologic target, SOD1, rather than proteasomal degradation .
PMID:20154138
Ubiquitination of MAP3K2/MEKK2 and AIFM1 does not lead to proteasomal degradation .
PMID:17967870 PMID:22103349
Plays a role in copper homeostasis by ubiquitinating COMMD1 and promoting its proteasomal degradation .
PMID:14685266
Can also function as E3 ubiquitin-protein ligase of the NEDD8 conjugation pathway, targeting effector caspases for neddylation and inactivation .
PMID:21145488
Ubiquitinates and therefore mediates the proteasomal degradation of BCL2 in response to apoptosis .
PMID:29020630
Protects cells from spontaneous formation of the ripoptosome, a large multi-protein complex that has the capability to kill cancer cells in a caspase-dependent and caspase-independent manner .
PMID:22095281
Suppresses ripoptosome formation by ubiquitinating RIPK1 and CASP8 .
PMID:22095281
Acts as a positive regulator of Wnt signaling and ubiquitinates TLE1, TLE2, TLE3, TLE4 and AES .
PMID:22304967
Ubiquitination of TLE3 results in inhibition of its interaction with TCF7L2/TCF4 thereby allowing efficient recruitment and binding of the transcriptional coactivator beta-catenin to TCF7L2/TCF4 that is required to initiate a Wnt-specific transcriptional program PMID:22304967
Upon photon absorption cGMP levels decline leading to channel closure and membrane hyperpolarization that ultimately slows neurotransmitter release and signals the presence of light, the end point of the phototransduction cascade. Conducts cGMP- and cAMP-gated ion currents, with permeability for monovalent and divalent cations. The selectivity for Ca(2+) over Na(+) increases with cGMP concentrations, whereas the selectivity among monovalent ions is independent of the cGMP levels
PMID:12808432 PMID:20562108 PMID:31155282 PMID:36502918
The current is characterized by a voltage-independent activation, an intracellular calcium concentration increase-dependent activation and a single-channel conductance of 10 picosiemens .
PMID:12808432 PMID:20562108 PMID:31155282 PMID:36502918
Also presents an inwardly rectifying current, thus reducing its already small outward conductance of potassium ions, which is particularly the case when the membrane potential displays positive values, above + 20 mV .
PMID:12808432
Activation is followed by membrane hyperpolarization. Thought to regulate neuronal excitability by contributing to the slow component of synaptic afterhyperpolarization (By similarity)
PMID:10991935 PMID:33242881 PMID:9287325
The current is characterized by a voltage-independent activation, an intracellular calcium concentration increase-dependent activation and a single-channel conductance of about 3 picosiemens .
PMID:10991935
Also presents an inwardly rectifying current, thus reducing its already small outward conductance of potassium ions, which is particularly the case when the membrane potential displays positive values, above + 20 mV .
PMID:10991935
The inward rectification could be due to a blockade of the outward current by intracellular divalent cations such as calcium and magnesium and could also be due to an intrinsic property of the channel pore, independent of intracellular divalent ions. There are three positively charged amino acids in the S6 transmembrane domain, close to the pore, that collectively control the conductance and rectification through an electrostatic mechanism. Additionally, electrostatic contributions from these residues also play an important role in determining the intrinsic open probability of the channel in the absence of calcium, affecting the apparent calcium affinity for activation.
Forms an heteromeric complex with calmodulin, which is constitutively associated in a calcium-independent manner. Channel opening is triggered when calcium binds the calmodulin resulting in a rotary movement leading to the formation of the dimeric complex to open the gate (By similarity). Plays a role in the repolarization phase of cardiac action potential PMID:13679367
PMID:17142458 PMID:8781233 PMID:9287325
The current is characterized by a voltage-independent activation, an intracellular calcium concentration increase-dependent activation and a single-channel conductance of about 3 picosiemens .
PMID:8781233
Also presents an inwardly rectifying current, thus reducing its already small outward conductance of potassium ions, which is particularly the case when the membrane potential displays positive values, above + 20 mV (Probable). Activation is followed by membrane hyperpolarization (By similarity). Thought to regulate neuronal excitability by contributing to the slow component of synaptic afterhyperpolarization (By similarity)
ATC D08AH01
ATC R02AA02
ATC G01AC05
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)
Dequalinium
Additional database identifiers
Drugs Product Database (DPD)
5913
ChemSpider
2886
BindingDB
50048403
PDB
DEQ
Guide to Pharmacology
2313
ZINC
ZINC000001655706
HUGO Gene Nomenclature Committee (HGNC)
HGNC:592
GenAtlas
BIRC4
GeneCards
XIAP
GenBank Gene Database
U45880
GenBank Protein Database
1184320
Guide to Pharmacology
2790
UniProt Accession
XIAP_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2148
GeneCards
CNGA1
Guide to Pharmacology
394
UniProt Accession
CNGA1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6292
GeneCards
KCNN3
GenBank Gene Database
AF031815
GenBank Protein Database
3309531
Guide to Pharmacology
383
UniProt Accession
KCNN3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6291
GeneCards
KCNN2
GenBank Gene Database
AF239613
GenBank Protein Database
10334701
Guide to Pharmacology
382
UniProt Accession
KCNN2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6290
GeneCards
KCNN1
GenBank Gene Database
U69883
GenBank Protein Database
1575661
Guide to Pharmacology
381
UniProt Accession
KCNN1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2149
GeneCards
CNGA2
Guide to Pharmacology
395
UniProt Accession
CNGA2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6284
GenAtlas
KCNMA1
GeneCards
KCNMA1
GenBank Gene Database
U13913
GenBank Protein Database
537439
Guide to Pharmacology
380
UniProt Accession
KCMA1_HUMAN
GenBank Gene Database
X56628
GenBank Protein Database
46660
UniProt Accession
QACR_STAAU
UniProt Accession
RAMR_STRCO
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9393
GenAtlas
PRKCA
GeneCards
PRKCA
GenBank Gene Database
X52479
GenBank Protein Database
35483
Guide to Pharmacology
1482
UniProt Accession
KPCA_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9395
GenAtlas
PRKCB1
GeneCards
PRKCB
GenBank Gene Database
M13975
GenBank Protein Database
189969
Guide to Pharmacology
1483
UniProt Accession
KPCB_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9399
GenAtlas
PRKCD
GeneCards
PRKCD
GenBank Gene Database
L07860
Guide to Pharmacology
1485
UniProt Accession
KPCD_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9401
GenAtlas
PRKCE
GeneCards
PRKCE
GenBank Gene Database
X65293
Guide to Pharmacology
1486
UniProt Accession
KPCE_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9402
GeneCards
PRKCG
Guide to Pharmacology
1484
UniProt Accession
KPCG_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9404
GeneCards
PRKCI
GenBank Gene Database
L18964
GenBank Protein Database
432274
Guide to Pharmacology
1490
UniProt Accession
KPCI_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9410
GenAtlas
PRKCQ
GeneCards
PRKCQ
GenBank Gene Database
L01087
GenBank Protein Database
558099
Guide to Pharmacology
1488
UniProt Accession
KPCT_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9412
GeneCards
PRKCZ
Guide to Pharmacology
1491
UniProt Accession
KPCZ_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11138
GenAtlas
SNCA
GeneCards
SNCA
GenBank Gene Database
L08850
GenBank Protein Database
437365
Guide to Pharmacology
3285
UniProt Accession
SYUA_HUMAN
UniProt Accession
MSHC_MYCTA
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1442
GeneCards
CALM1
UniProt Accession
CALM1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1445
GeneCards
CALM2
UniProt Accession
CALM2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1449
GeneCards
CALM3
UniProt Accession
CALM3_HUMAN
GenBank Gene Database
M94248
GenBank Protein Database
290406
UniProt Accession
ACRB_ECOLI
DrugBank citations
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