Dexketoprofen 25mg tablets
Requires a prescription from a doctor or prescriber
Dexketoprofen is a non-steroidal anti-inflammatory drug.
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Suspected adverse reactions reported for Dexketoprofen
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Suspected adverse reactions reported for Dexketoprofen
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2 branded products available
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View all licensed products for Dexketoprofen on the MHRA register
Keral 25mg tablets
This is the NHS Drug Tariff indicative price used for reimbursement purposes. It may not reflect the price paid by patients or pharmacies.
View full Drug TariffSource: NHS Drug Tariff via NHSBSA. Derived from dm+d VMPP (Virtual Medicinal Product Pack) pricing data. Contains public sector information licensed under the Open Government Licence v3.0.
WHO defined daily dose (DDD)
75 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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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. 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: 13 · Randomised trials: 29 · 1996–2026
Showing the 50 most relevant studies, sorted by most relevant.
R Andrew Moore, Jodie Barden
BMC Clinical Pharmacology, 2008
- Acute Disease
- Anti-Inflammatory Agents, Non-Steroidal
- Chronic Disease
Bhattarai BP, Selvido DI, Rokaya D
2024
This study aims to compare the analgesic efficacy of dexketoprofen trometamol (DT) with other analgesic drugs for pain relief after third molar surgery. The PubMed, Scopus, and Web of Science databases were searched to identify randomized controlled trials comparing DT with other analgesics for third molar surgery. The outcome measures were the sum of pain intensity differences (SPID), total pain relief (TOTPAR) at the 6th and 8th postoperative hours, time to rescue medication, and tolerability. In total, four studies met our inclusion criteria. A total of 660 third molar surgeries were performed: 365 in the DT group and 295 in the active control group. Compared to other analgesics, DT produced significantly better pain relief at the 6th postoperative hour: SPID (MD, 0.33; P = 0.01) and TOTPAR (MD, 0.41; P = 0.02). However, there were no statistically significant differences in the efficiency of pain relief at the 8th postoperative hour, time to rescue medication, or tolerability. Overall, a 25 mg dose produced the best results for pain relief. In conclusion, DT (25 mg) is a viable alternative to contemporary analgesics for pain relief after third molar surgery, particularly during the early postoperative period.
Abstract licence: CC BY-NC
Vicente Esparza‐Villalpando, Amaury Pozos‐Guillén, David Masuoka‐Ito, et al.
Drug Development Research, 2017
- Analgesics
- Anti-Inflammatory Agents, Non-Steroidal
- Ketoprofen
Baohua Yang, Zhili Xu, Linglong Chen, et al.
Medicine, 2019
- Anti-Inflammatory Agents, Non-Steroidal
- Ketoprofen
- Migraine Disorders
Abstract Background: The efficacy of dexketoprofen for migraine attack remains controversial. We conduct a systematic review and meta-analysis to explore the influence of dexketoprofen supplementation versus placebo on pain control in migraine attack patients. Methods: We search PubMed, EMbase, Web of science, EBSCO, and Cochrane library databases through March 2019 for randomized controlled trials (RCTs) assessing the effect of dexketoprofen supplementation versus placebo on pain control for migraine attack patients. This meta-analysis is performed using the random-effect model. Results: Five RCTs involving 794 patients are included in the meta-analysis. Overall, compared with control group for migraine attack, dexketoprofen supplementation is associated with substantially increased pain free at 2 hours (RR = 1.90; 95% CI = 1.43–2.53; P < .0001), pain free at 48 hours (RR = 1.63; 95% CI = 1.07–2.49; P = .02), good or excellent treatment (RR = 1.48; 95% CI = 1.24–1.78; P < .0001) and pain relief at 2 hours (RR = 1.80; 95% CI = 1.17–2.77; P = .007), as well as reduced need for rescue drug (RR = 0.64; 95% CI = 0.43–0.94; P = .02), with no significant increase in adverse events (RR = 1.51; 95% CI = 0.87–2.62; P = .14). Conclusion: Dexketoprofen supplementation benefits to improve pain control at 48 hours and reduce the need for rescue drug in migraine attack patients.
Abstract licence: CC BY-NC 4.0
Joanna Kuczyńska, Angelika Pawlak, Barbara Nieradko-Iwanicka
Polish Hyperbaric Research, 2021
Abstract Introduction. Dexketoprofen(DEX) belongs to nonsteroidal anti-inflammatory drugs (NSAIDs) and has analgesic, anti-inflammatory, and antipyretic properties. DEX is an enantiomer of ketoprofen (S+) and has a stronger effect than ketoprofen. It is highly effective even after the administration of small doses. The therapy with DEX does not cause serious side effects and is additionally tolerated by the body. Aim. The review aimed to find original scientific publications on DEX in recent years and its therapeutic efficacy, safety, and tolerability. Method. A systematic review of scientific articles published no earlier than 2015 was carried out. Materials from the PubMed, Google Scholar, and Medline Complete databases were used. The literature review was carried out in November 2021. Among the publications found, 28 scientific articles were selected for analysis. Results and discussion. Over the recent years, there have been many publications about DEX. Articles describing new data on DEX in the treatment of pain were analyzed, compared with other drugs and mesotherapy, the latest reports of its combination with tramadol and thiocolchicoside were reviewed, and a new slow release form of DEX and new therapeutic applications of this drug were investigated. After analyzing all the studies, it was found that DEX produced similar or more effective analgesia compared to other drugs and reduced the need for emergency medications. In addition, it was noted that using DEX in combination therapy was far better than taking it alone, and was also found to be effective in raising the epileptic threshold. Mesotherapy achieved higher results in the treatment of pain symptoms compared to DEX. The side effects that appeared as a result of the use of DEX therapy were not life-threatening. Conclusion. The results of the review confirm that DEX is a very good analgesic, which is more potent than paracetamol and diclofenac sodium while having similar effects to dexmedetomidine and lidocaine. DEX in combination with tramadol or thiocolchicoside is more effective than when the two drugs are used alone. Scientists are working on the long-acting DEX and are looking for new applications of the drug in epilepsy and oncology.
Abstract licence: CC BY-NC-ND 3.0
H J McQuay, Rachel Moore, A. Berta, et al.
British Journal of Anaesthesia, 2016
- Analgesics, Opioid
- Anti-Inflammatory Agents, Non-Steroidal
- Ketoprofen
Cosme Gay‐Escoda, Magdi Hanna, A. Alcántara Montero, et al.
BMJ Open, 2019
- Acetaminophen
- Ketoprofen
- Molar, Third
R Andrew Moore, H J McQuay, Janusz Tomaszewski, et al.
BMC Anesthesiology, 2016
- Analgesics, Opioid
- Hysterectomy
- Ketoprofen
Pamela Delgado-García, Juan Bautista Alcocer-Herrera, Adelfia Urenda-Quezada, et al.
Clinical Drug Investigation, 2024
- Tromethamine
- Ketoprofen
- Pyridoxine
Y. Kaba, A. Demirbaş, N. Kütük, et al.
Medicina Oral, Patología Oral y Cirugía Bucal, 2023
- Tramadol
- Ketoprofen
- Orthognathic Surgery
Background The purpose of this study was to evaluate the effect of a single-dose intravenous dexketoprofen administration for preventive analgesia on postoperative pain and reducing swelling in double jaw surgery. Material and Methods The authors designed a prospective, randomized, and double-blind cohort study. Patients who have Class III malocclusion were randomly divided in two groups. 50 mg intravenous dexketoprofen trometamol were administrated 30 minutes before incision in treatment group, while intravenous sterile saline was administrated 30 minutes before incision in placebo group. The primary predictor variable was treatment group. Primary outcomes were pain, swelling and 24-hour opioid intake. Patient- controlled analgesia with tramadol was given for management of postoperative pain. Other variables were demographic and operation related parameters. Visual analogue scale was used to evaluate postoperative pain. 3dMD Face System (3dMD, USA) was used to measure postoperative swelling. Data were analysed using two independent samples t test and Mann Whitney U test. Results The study sample was composed of 30 patients with a mean age of 20,63 years and 21 were female. Preemptive dexketoprofen administration decreased postoperative tramadol consumption by 25.9% compared to placebo group, and there was a statistically significant decrease in VAS scores (p0,05). Conclusions Preventive administration of intravenous dexketoprofen provides adequate analgesic effect in the postoperative 24-hour period and reduces opioid consumption in orthognathic surgery. Key words:Preventive analgesia, pain, swelling, orthognathic surgery, dexketoprofen, opioid, 3dMD.
Abstract licence: CC BY 4.0
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
160 found
Half-life
1.65 h
Mechanism
It is a non-steroidal anti-inflammatory drug (NSAID) that reduces prostaglandin…
Food interactions
None known
Human targets
2 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
30 minutes
Half-life
1.65 h
Protein binding
[L1299]
Volume of distribution
0.25 L/kg
Metabolism
25 mg
[L1304]…
Elimination
70 to 80%
[L1301]…
Clearance
[L1299]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
[L1302]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 1463 interactions
Severe toxicity can lead to thrombocytopenia and anemia with bleeding episodes. Dexketoprofen is associated with a small increased risk of myocardial infarction .
[L1302]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[L1299]
[L1304]
In one study, after oral administration of 25 mg of dexketoprofen to young healthy adults, Tmax was approximately 30 min for a Cmax of 3.7 ± 0.72 mg/l .
[L1305]
Dexketoprofen trometamol is metabolized by the hepatic cytochrome P450 enzymes (CYP2C8 and CYP2C9) .
[L1305]
Dexketoprofen trometamol has a number of metabolites, with hydroxyl derivatives making up the greatest volume .
[L1305]
In humans, hydroxylation plays a minor role.
Dexketoprofen is primarily conjugated to an acyl-glucuronide [L1305]
[L1301]
[L1299]
Proteins and enzymes this drug interacts with in the body
The insertion of a second molecule of O2 (bis-oxygenase activity) yields a hydroperoxy group in PGG2 that is then reduced to PGH2 by two electrons .
PMID:7947975
Involved in the constitutive production of prostanoids in particular in the stomach and platelets. In gastric epithelial cells, it is a key step in the generation of prostaglandins, such as prostaglandin E2 (PGE2), which plays an important role in cytoprotection. In platelets, it is involved in the generation of thromboxane A2 (TXA2), which promotes platelet activation and aggregation, vasoconstriction and proliferation of vascular smooth muscle cells (Probable).
Can also use linoleate (LA, (9Z,12Z)-octadecadienoate, C18:2(n-6)) as substrate and produce hydroxyoctadecadienoates (HODEs) in a regio- and stereospecific manner, being (9R)-HODE ((9R)-hydroxy-(10E,12Z)-octadecadienoate) and (13S)-HODE ((13S)-hydroxy-(9Z,11E)-octadecadienoate) its major products (By similarity)
PMID:11939906 PMID:16373578 PMID:19540099 PMID:22942274 PMID:26859324 PMID:27226593 PMID:7592599 PMID:7947975 PMID:9261177
The cyclooxygenase activity oxygenates AA to the hydroperoxy endoperoxide prostaglandin G2 (PGG2), and the peroxidase activity reduces PGG2 to the hydroxy endoperoxide prostaglandin H2 (PGH2), the precursor of all 2-series prostaglandins and thromboxanes .
PMID:16373578 PMID:22942274 PMID:26859324 PMID:27226593 PMID:7592599 PMID:7947975 PMID:9261177
This complex transformation is initiated by abstraction of hydrogen at carbon 13 (with S-stereochemistry), followed by insertion of molecular O2 to form the endoperoxide bridge between carbon 9 and 11 that defines prostaglandins. The insertion of a second molecule of O2 (bis-oxygenase activity) yields a hydroperoxy group in PGG2 that is then reduced to PGH2 by two electrons .
PMID:16373578 PMID:22942274 PMID:26859324 PMID:27226593 PMID:7592599 PMID:7947975 PMID:9261177
Similarly catalyzes successive cyclooxygenation and peroxidation of dihomo-gamma-linoleate (DGLA, C20:3(n-6)) and eicosapentaenoate (EPA, C20:5(n-3)) to corresponding PGH1 and PGH3, the precursors of 1- and 3-series prostaglandins .
PMID:11939906 PMID:19540099
In an alternative pathway of prostanoid biosynthesis, converts 2-arachidonoyl lysophopholipids to prostanoid lysophopholipids, which are then hydrolyzed by intracellular phospholipases to release free prostanoids .
PMID:27642067
Metabolizes 2-arachidonoyl glycerol yielding the glyceryl ester of PGH2, a process that can contribute to pain response .
PMID:22942274
Generates lipid mediators from n-3 and n-6 polyunsaturated fatty acids (PUFAs) via a lipoxygenase-type mechanism. Oxygenates PUFAs to hydroperoxy compounds and then reduces them to corresponding alcohols .
PMID:11034610 PMID:11192938 PMID:9048568 PMID:9261177
Plays a role in the generation of resolution phase interaction products (resolvins) during both sterile and infectious inflammation .
PMID:12391014
Metabolizes docosahexaenoate (DHA, C22:6(n-3)) to 17R-HDHA, a precursor of the D-series resolvins (RvDs) .
PMID:12391014
As a component of the biosynthetic pathway of E-series resolvins (RvEs), converts eicosapentaenoate (EPA, C20:5(n-3)) primarily to 18S-HEPE that is further metabolized by ALOX5 and LTA4H to generate 18S-RvE1 and 18S-RvE2 .
PMID:21206090
In vascular endothelial cells, converts docosapentaenoate (DPA, C22:5(n-3)) to 13R-HDPA, a precursor for 13-series resolvins (RvTs) shown to activate macrophage phagocytosis during bacterial infection .
PMID:26236990
In activated leukocytes, contributes to oxygenation of hydroxyeicosatetraenoates (HETE) to diHETES (5,15-diHETE and 5,11-diHETE) .
PMID:22068350 PMID:26282205
Can also use linoleate (LA, (9Z,12Z)-octadecadienoate, C18:2(n-6)) as substrate and produce hydroxyoctadecadienoates (HODEs) in a regio- and stereospecific manner, being (9R)-HODE ((9R)-hydroxy-(10E,12Z)-octadecadienoate) and (13S)-HODE ((13S)-hydroxy-(9Z,11E)-octadecadienoate) its major products (By similarity).
During neuroinflammation, plays a role in neuronal secretion of specialized preresolving mediators (SPMs) 15R-lipoxin A4 that regulates phagocytic microglia (By similarity)
Enzymes involved in drug metabolism — important for understanding drug interactions
ATC M02AA27
ATC N02AJ14
ATC M01AE17
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)
Dexketoprofen
Additional database identifiers
ChemSpider
580922
BindingDB
50088570
PDB
9KL
ZINC
ZINC000000005560
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9604
GenAtlas
PTGS1
GeneCards
PTGS1
GenBank Gene Database
M31822
GenBank Protein Database
387018
Guide to Pharmacology
1375
UniProt Accession
PGH1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9605
GenAtlas
PTGS2
GeneCards
PTGS2
GenBank Gene Database
L15326
GenBank Protein Database
291988
Guide to Pharmacology
1376
UniProt Accession
PGH2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9604
GenAtlas
PTGS1
GeneCards
PTGS1
GenBank Gene Database
M31822
GenBank Protein Database
387018
Guide to Pharmacology
1375
UniProt Accession
PGH1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9605
GenAtlas
PTGS2
GeneCards
PTGS2
GenBank Gene Database
L15326
GenBank Protein Database
291988
Guide to Pharmacology
1376
UniProt Accession
PGH2_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
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Structured knowledge from the free knowledge base
Linked open data from Wikidata (Q425440), 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.