Pefloxacin 400mg tablets
Requires a prescription from a doctor or prescriber
A synthetic broad-spectrum fluoroquinolone antibacterial agent active against most gram-negative and gram-positive bacteria.
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Safety monitoring data
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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.
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Suspected adverse reactions reported for Pefloxacin
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1 branded products available
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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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
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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: 2 · 1986–2026
Showing the 50 most relevant studies, sorted by most relevant.
Post HK, Blankespoor MG, Ierulli VK, et al.
2023
IntroductionIntra-articular antibiotics have been proposed as a treatment for septic arthritis to allow for high local concentrations without subjecting a patient to the toxicity/side effects of systemic therapy. However, there is concern for chondrotoxicity with intra-articular use of these solutions in high concentrations. The purpose of this systematic review was to evaluate the intra-articular use of antibiotics and antiseptic solutions, and to determine their association with chondrolysis following in vitro or in vivo administration.MethodsA systematic review was conducted following PRISMA guidelines through PubMed, Clinical Key, OVID, and Google Scholar. Studies in English were included if they evaluated for chondrotoxicity following antibiotic exposure.ResultsThe initial search resulted in 228 studies, with 36 studies meeting criteria. These 36 studies included manuscripts that studied 24 different agents. Overall, 7 of the 24 (29%) agents were non-chondrotoxic: minocycline, tetracycline, chloramphenicol, teicoplanin, pefloxacin, linezolid, polymyxin-bacitracin. Eight (33%) agents had inconsistent results: doxycycline, ceftriaxone, gentamicin, vancomycin, ciprofloxacin, ofloxacin, chlorhexidine, and povidone iodine. Chondrotoxicity was evident with 9 (38%) agents, all of which were also dose-dependent chondrotoxic based on reported estimated half maximal inhibitory concentrations (est. IC50): amikacin (est. IC50 = 0.31-2.74 mg/mL), neomycin (0.82), cefazolin (1.67-3.95), ceftazidime (3.16-3.59), ampicillin-sulbactam (8.64 - >25), penicillin (11.61), amoxicillin (14.01), imipenem (>25), and tobramycin (>25). Additionally, chondroprotective effects of doxycycline and minocycline were reported.ConclusionsThis systematic review identified agents that may be used in the treatment of septic arthritis. Nine agents should be avoided due to their dose-dependent chondrotoxic effects. Further studies are needed to clarify the safety of these medications for human intra-articular use.
Abstract licence: CC BY-NC-ND
Li G, Qi X, Wu J, et al.
2024
- Nanocomposites
- Metal Nanoparticles
- Molecular Imprinting
Ahed J Alkhatib, Sani S. Bala, S.S. Bashir, et al.
Indian Research Journal of Pharmacy and Science, 2018
Taherizadeh M, Jahani S, Moradalizadeh M, et al.
2023
- Ofloxacin
- Pefloxacin
- Oxides
Ahmed S, Mahendiran D, Bhat AR, et al.
2023
- Thiosemicarbazones
- Coordination Complexes
- Oxygen
Konyali D, Guzel M, Soyer Y
2023
- Salmonella enterica
- Quinolones
- Salmonella
Salmonella enterica subsp. enterica (Salmonella), one of the most common causes of bacterial foodborne infections, causes salmonellosis, which is usually self-limiting. However, immunocompromised individuals and children often require antimicrobial therapy. The first line of treatment includes fluoroquinolones, to which Salmonella has emerging resistance worldwide. In fact, the WHO classified fluoroquinolone-resistant Salmonella as a high-priority pathogen. Salmonella carrying genes such as blaCTX and blaCMY can show resistance to cephalosporins which are also regularly used for treatment. This study focused on determining the antimicrobial resistance of 373 Salmonella isolates, collected from various foods, humans, and animals, as well as the environmental sludge between 2005 and 2020 in Türkiye. Phenotypic analysis of the resistance was determined by disk diffusion method. Isolates resistant to any of the following: ciprofloxacin, pefloxacin, azithromycin, and ceftriaxone were tested for the presence of quinolone, beta-lactamase, and/or macrolide resistance genes by PCR and gel electrophoresis. Five multi-drug-resistant isolates were then further whole genome sequenced and analyzed. More than 32% (n = 120) of the isolates showed resistance to fluoroquinolones by disc diffusion. A significant number of quinolone-resistant isolates are presented with mutated parC and gyrA. Furthermore, 42% (n = 106) of the isolates were resistant to azithromycin and 10% of them harbored mphA gene. On the bright side, only eight isolates showed resistance to ceftriaxone. Overall, we observed an increase in the number of isolates showing resistance to fluoroquinolones and azithromycin over the years and low resistance to ceftriaxone.
Abstract licence: CC BY-NC-ND
Zhou Y, Wang J
2024
- Hydrogen Peroxide
- Carbon
- Copper
Fan XF, Fu L, Cui GH
2024
Sikorski Ł, Bęś A, Warmiński K
2023
- Araceae
- Quinolones
- Water Pollutants, Chemical
Plant growth and the development of morphological traits in plants are inhibited under exposure to pharmaceuticals that are present in soil and water. The present study revealed that moxifloxacin (MOXI), nalidixic acid (NAL), levofloxacin (LVF) and pefloxacin (PEF) at concentrations of >0.29, >0.48, >0.62 and >1.45 mg × L-1, respectively, inhibited the growth (Ir) of duckweed plants and decreased their yield (Iy). In the current study, none of the tested quinolones (QNs) at any of the examined concentrations were lethal for common duckweed plants. However, at the highest concentration (12.8 mg × L-1), LVF increased Ir and Iy values by 82% on average and increased the values of NAL, PEF and MOXI by 62% on average. All tested QNs led to the loss of assimilation pigments. In consequence, all QNs, except for LVF, induced changes in chlorophyll fluorescence (Fv/Fm), without any effect on phaeophytinization quotient (PQ) values. The uptake of NAL, MOXI, LVF by Lemna minor during the 7-day chronic toxicity test was directly proportional to drug concentrations in the growth medium. Nalidixic acid was absorbed in the largest quantities, whereas in the group of fluoroquinolones (FQNs), MOXI, LVF and PEF were less effectively absorbed by common duckweed. This study demonstrated that biosorption by L. minor occurs regardless of the plants' condition. These findings indicate that L. minor can be used as an effective biological method to remove QNs from wastewater and water and that biosorption should be a mandatory process in conventional water and wastewater treatment.
Abstract licence: CC BY
Li M, Chen D, Guo Y, et al.
2026
- Milk
- Fluoroquinolones
- Ofloxacin
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
1 found
Half-life
8.6 hours
Mechanism
The bactericidal action of pefloxacin results from interference with the activit…
Food interactions
None known
Human targets
2 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
Half-life
8.6 hours
Protein binding
20-30%
Metabolism
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 954 interactions
How the body processes this drug — absorption, distribution, metabolism, and elimination
Proteins and enzymes this drug interacts with in the body
PMID:17567603 PMID:18790802 PMID:22013166 PMID:22323612
May play a role in regulating the period length of BMAL1 transcriptional oscillation (By similarity)
Enzymes involved in drug metabolism — important for understanding drug interactions
ATC J01MA03
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)
Pefloxacin
Additional database identifiers
ChemSpider
46291
BindingDB
57936
ZINC
ZINC000000001894
GenBank Gene Database
L42023
GenBank Protein Database
1574370
UniProt Accession
PARC_HAEIN
GenBank Gene Database
L42023
GenBank Protein Database
1574722
UniProt Accession
GYRA_HAEIN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11989
GenAtlas
TOP2A
GeneCards
TOP2A
GenBank Gene Database
J04088
GenBank Protein Database
292830
Guide to Pharmacology
2637
UniProt Accession
TOP2A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11990
GenAtlas
TOP2B
GeneCards
TOP2B
GenBank Gene Database
X68060
UniProt Accession
TOP2B_HUMAN
UniProt Accession
TOP1_STAAU
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2596
GenAtlas
CYP1A2
GeneCards
CYP1A2
GenBank Gene Database
Z00036
Guide to Pharmacology
1319
UniProt Accession
CP1A2_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