Tenoxicam 20mg powder and solvent for solution for injection vials
Tenoxicam, an antiinflammatory agent with analgesic and antipyretic properties, is used to treat osteoarthritis and control acute pain.
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Tenoxicam 20mg powder and solvent for solution for injection vials
Tenoxicam 20mg powder and solvent for solution for injection vials
Alliance Healthcare (Distribution) Ltd
Tenoxicam 20mg powder and solvent for solution for injection vials
WHO defined daily dose (DDD)
20 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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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 25 studies.
Reviews & meta-analyses: 2 · Randomised trials: 2 · 2021–2025
Showing all 25 studies, sorted by most relevant.
Bliźniak F, Chęciński M, Chęcińska K, et al.
2024
Objectives: This systematic review was designed to summarize randomized controlled trials of intra-articular administration of non-steroidal anti-inflammatory drugs (NSAIDs) for temporomandibular disorders. Methods: Randomized controlled trials regarding intra-articular injections of non-steroidal anti-inflammatory drugs for temporomandibular disorders were included in the review. The final search was conducted on 16 June 2024 in the Bielefeld Academic Search Engine, PubMed, and Scopus databases. Results: Of the 173 identified studies, 6 were eligible for review. In trials comparing arthrocentesis alone to arthrocentesis with NSAIDs, slight differences in joint pain were noted. For tenoxicam, differences were under 1 point on a 0–10 scale after 4 weeks, with inconsistent results. Piroxicam showed no significant difference, and pain levels were minimal in both groups. For maximum mouth opening (MMO), tenoxicam showed no significant difference. Piroxicam increased MMO by nearly 5 mm, based on one small trial with bias concerns. Conclusions: Currently, there is no strong scientific evidence supporting the injection of NSAIDs into the temporomandibular joint to relieve pain or increase jaw movement. Preliminary reports on piroxicam with arthrocentesis and tenoxicam or diclofenac without rinsing justify further research.
Abstract licence: CC BY
Z. Bayramoğlu, G. Yavuz, Aydın Keskinruzgar, et al.
BMC Oral Health, 2023
- Osteoarthritis
- Temporomandibular Joint Disorders
- Arthrocentesis
BACKGROUND: Temporomandibular joint osteoarthritis (TMJ-OA) is a degenerative disease and manifests itself with pain and limitation of movement in the jaws. Arthrocentesis alone or in combination with intraarticular injections is one of the most commonly used treatment methods in these patients. The aim of the study is to examine the effectiveness of arthrocentesis plus tenoxicam injection and to compare it with arthrocentesis alone in patients with TMJ-OA. METHODS: Thirty patients with TMJ-OA who were treated randomly with either arthrocentesis plus tenoxicam injection (TX group) or arthrocentesis alone (control group) were examined. Maximum mouth opening (MMO), visual analog scale (VAS) pain values, and joint sounds were the outcome variables, which were evaluated at pre-treatment and at 1, 4, 12, and 24 weeks after treatment. Statistical significance was set at p < 0.05. RESULTS: The gender distribution and mean age were not significantly different between the two groups. Pain values (p < 0.001), MMO (p < 0.001), and joint sounds (p < 0.001) improved significantly in both groups. However, there was no significant difference between the groups in terms of outcome variables [pain (p = 0.085), MMO (p = 0.174), joint sounds (p = 0.131)]. CONCLUSIONS: Arthrocentesis plus tenoxicam injection showed no better outcomes in terms of MMO, pain, and joint sounds compared with arthrocentesis alone in patients with TMJ-OA. TRIAL REGISTRATION: Injection of Tenoxicam Versus Arthrocentesis Alone in the Treatment of Temporomandibular Joint Osteoarthritis, NCT05497570. Registered 11 May 2022. Retrospectively registered, https://register. CLINICALTRIALS: gov/prs/app/action/SelectProtocol?sid=S000CD7A&selectaction=Edit&uid=U0006FC4&ts=6&cx=f3anuq.
Abstract licence: CC BY
N. Kashevarova, E. Taskina, E. Strebkova, et al.
Modern Rheumatology Journal, 2023
Local forms of non-steroidal anti-inflammatory drugs (NSAIDs) are characterized by a high safety profile due to low systemic absorption. They do not increase the risk of developing class-specific gastrointestinal, cardiovascular and kidney adverse events (AEs), which makes it possible to prescribe them even in severe comorbid pathology, which is typical for patients with osteoarthritis (OA). Objective : to evaluate the efficacy and safety of Artoxan gel (tenoxicam) 1% in comparison with Diclofenac gel 1% in patients with knee OA in a prospective comparative randomized trial. Material and methods . The study included 60 patients with Kellgren–Lawrence stages II–III knee OA, aged 41 to 78 years. The patients were randomly divided into two groups: the 1st group received Artoxan gel 1%, 5 cm 2 times a day for 14 days; 2nd – Diclofenac gel 1% according to the same scheme. During therapy, we assessed pain using a visual analog scale, the WOMAC index, quality of life using the EQ-5D questionnaire, satisfaction with therapy, and time to effect. Results and discussion . It has been demonstrated that local forms of NSAIDs have a positive effect on all clinical manifestations of OA: effectively reduce pain, stiffness, improve the functional state of the joints and quality of life. They also have a good safety profile and a fast symptomatic response. Comparison of the two groups showed that in patients receiving the local form of tenoxicam, there was a tendency to a more rapid and pronounced analgesic effect. Conclusion . The results of the study confirm the good efficacy and safety of local forms of NSAIDs.
Abstract licence: CC BY
Colceriu-Șimon IM, Feștilă D, Emoke H, et al.
2025
Orthodontic treatment is commonly associated with pain, leading to reduced patient compliance and treatment adherence. Non-steroidal anti-inflammatory drugs (NSAIDs) are effective in reducing this pain by inhibiting prostaglandin synthesis. However, this mechanism may also interfere with orthodontic tooth movement (OTM) by affecting bone remodeling. This narrative review investigates the existing literature published between 2004 and 2024 to assess the impact of various NSAIDs on OTM and identify those that balance pain relief with minimal impact on tooth movement. Evidence shows that NSAIDs such as aspirin, ketorolac, diclofenac, and nimesulide significantly reduce OTM. The results for ibuprofen, meloxicam, and celecoxib were inconsistent with both no influence or a reduction in OTM, depending on dosage, mode, and duration of administration. Conversely, tenoxicam, nabumetone, etoricoxib, and parecoxib appear to have no effect on OTM. Among these, etoricoxib appears particularly promising due to its favorable gastrointestinal profile, high COX-2 selectivity, and negligible influence on OTM in clinical doses. However, the limited number of human trials highlights the need for further research to develop evidence-based guidelines for pain management that preserve treatment efficiency in orthodontics.
Abstract licence: CC BY
Soha Talal Al-Goul, Huda Salem AlSalem, Mona Saad Binkadem, et al.
Journal of Photochemistry and Photobiology A: Chemistry, 2023
Mohamed A, Dayo M, Alahmadi S, et al.
2024
In this study, an easy, efficient, economical, and eco-friendly green bio-synthesis method was utilized to synthesize silver nanoparticles (AgNPs) using the extracts of four plants: Ginkgo biloba, Cichorium Intybus, Adiantum Capillus-Veneris, and Rosmarinus Officinalis. The synthesis of AgNPs was confirmed by using a uv-vis spectrometer, which showed distinct surface plasmon resonance (SPR) bands. The surface of AgNPs was characterized using scanning electron microscopy and Fourier-transform infrared spectroscopy. The anti-inflammatory activity of Tenoxicam/Meloxicam-loaded AgNPs has been studied using the inhibition of albumin denaturation method. Tenoxicam-loaded AgNPs showed higher % Inhibition, but Meloxicam-loaded AgNPs showed lower % Inhibition. Furthermore, the AgNPs showed excellent antimicrobial activity on both Gram-negative and Gram-positive bacteria.
Abstract licence: CC BY
F. Shakeel, P. Alam, N. Haq, et al.
ACS Omega, 2023
There is a dearth of information in the literature regarding environmentally benign high-performance thin-layer chromatography (HPTLC) methods to determine tenoxicam (TNX). Therefore, designing and validating an HPTLC method to detect TNX in commercial tablets and capsules was the goal of this investigation. The green mobile phase utilized was the combination of ethanol/water/ammonia solution (50:45:5 v/v/v). The TNX was quantified at a wavelength of 375 nm. The proposed method's greenness profile was established using the Analytical GREEnness (AGREE) approach. The proposed methodology for determining TNX was linear in the range of 25-1400 ng/band. The proposed methodology for measuring TNX was accurate (% recoveries = 98.24-101.48), precise (% RSD = 0.87-1.02), robust (% RSD = 0.87-0.94), sensitive (LOD = 0.98 ng/band and LOQ = 2.94 ng/band), and environmentally friendly. The AGREE scale for the present methodology was derived to be 0.75, indicating an outstanding greenness profile. TNX was found to be highly stable under acidic, base, and thermal stress conditions. However, it completely decomposed under oxidative stress conditions. Commercial tablets and capsules were found to have 98.46 and 101.24% TNX, respectively. This finding supports the validity of the current methodology for measuring TNX in commercial formulations. The outcomes of this work showed that the proposed eco-friendly HPTLC methodology can be used for the routine analysis of TNX in commercial formulations.
Abstract licence: CC BY-NC-ND
S. Osman, T. M. Yassin, Ahmed M Mohammed, et al.
AAPS PharmSciTech, 2023
- Piroxicam
- Drug Delivery Systems
- Anti-Inflammatory Agents, Non-Steroidal
R. El-Dahmy, M. EL-NABARAWI, Hassan Gamal Mostafa, et al.
International journal of pharmaceutics, 2025
- Anti-Inflammatory Agents, Non-Steroidal
- Drug Carriers
- Osteoarthritis
Uswatul Hasanah, Yesica Azfitri, Lili Fitriani, et al.
International Journal of Applied Pharmaceutics, 2024
Objective: Tenoxicam is classified as a nonsteroidal anti-inflammatory drug employed for managing musculoskeletal conditions. However, its effectiveness is obstructed by its restricted ability to dissolve in water. This investigation aims to create a multicomponent crystal involving tenoxicam and tromethamine to augment tenoxicam's solubility and dissolution rate. Methods: Using the solvent drop grinding technique, the multicomponent crystal was synthesized by combining tenoxicam and tromethamine in equimolar proportions. The physicochemical properties of multicomponent crystal were assessed through powder X-ray diffraction (PXRD), differential scanning calorimetry (DSC), and FT-IR spectroscopy. Solubility test and dissolution rate profile were conducted to evaluate the effectiveness of multicomponent crystal formation in compared to intact tenoxicam. The solubility test occurred in CO2-free distilled water over 48 h and was quantified using UV spectrophotometry at 368 nm. Dissolution rate profiles were conducted using a USP type II dissolution apparatus in HCl 0.1 N, and CO2-free distilled water as the dissolution media. Results: The multicomponent crystal displayed distinctive characteristics in the diffractogram, including altered melting points, and shifts in the FT-IR spectrum peaks. Within the multicomponent crystal system, the solubility of tenoxicam exhibited a notable increase, specifically by a factor of 11.130. Moreover, the dissolution efficiency of tenoxicam in HCl 0.1 N solution and CO2-free distilled water showed substantial enhancements, with respective increases of 2.600-fold and 8.605-fold observed at the 60-minute mark. Conclusion: In conclusion, the tenoxicam and tromethamine multicomponent crystal formation using a solvent drop grinding technique resulted in a novel crystalline structure, enhancing the solubility and dissolution of tenoxicam both in CO2-free distilled water and HCl 0.1 N.
Abstract licence: CC BY
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
150 found
Half-life
72 hours
Mechanism
The antiinflammatory effects of tenoxicam may result from the inhibition of the…
Food interactions
1 warning
Human targets
2 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
100%
Half-life
72 hours
Protein binding
99%
Metabolism
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 1590 interactions
How the body processes this drug — absorption, distribution, metabolism, and elimination
Proteins and enzymes this drug interacts with in the body
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)
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)
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that transport this drug across cell membranes
PMID:14586168 PMID:15644426 PMID:15846473 PMID:16455804 PMID:31553721
Transports organic anions such as estrone 3-sulfate (E1S) and urate in exchange for dicarboxylates such as glutarate or ketoglutarate (2-oxoglutarate) .
PMID:14586168 PMID:15846473 PMID:15864504 PMID:22108572 PMID:23832370
Plays an important role in the excretion of endogenous and exogenous organic anions, especially from the kidney and the brain .
PMID:11306713 PMID:14586168 PMID:15846473
E1S transport is pH- and chloride-dependent and may also involve E1S/cGMP exchange .
PMID:26377792
Responsible for the transport of prostaglandin E2 (PGE2) and prostaglandin F2(alpha) (PGF2(alpha)) in the basolateral side of the renal tubule .
PMID:11907186
Involved in the transport of neuroactive tryptophan metabolites kynurenate and xanthurenate .
PMID:22108572 PMID:23832370
Functions as a biopterin transporters involved in the uptake and the secretion of coenzymes tetrahydrobiopterin (BH4), dihydrobiopterin (BH2) and sepiapterin to urine, thereby determining baseline levels of blood biopterins .
PMID:28534121
May be involved in the basolateral transport of steviol, a metabolite of the popular sugar substitute stevioside .
PMID:15644426
May participate in the detoxification/ renal excretion of drugs and xenobiotics, such as the histamine H(2)-receptor antagonists fexofenadine and cimetidine, the antibiotic benzylpenicillin (PCG), the anionic herbicide 2,4-dichloro-phenoxyacetate (2,4-D), the diagnostic agent p-aminohippurate (PAH), the antiviral acyclovir (ACV), and the mycotoxin ochratoxin (OTA), by transporting these exogenous organic anions across the cell membrane in exchange for dicarboxylates such as 2-oxoglutarate .
PMID:11669456 PMID:15846473 PMID:16455804
Contributes to the renal uptake of potent uremic toxins (indoxyl sulfate (IS), indole acetate (IA), hippurate/N-benzoylglycine (HA) and 3-carboxy-4-methyl-5-propyl-2-furanpropionate (CMPF)), pravastatin, PCG, E1S and dehydroepiandrosterone sulfate (DHEAS), and is partly involved in the renal uptake of temocaprilat (an angiotensin-converting enzyme (ACE) inhibitor) .
PMID:14675047
May contribute to the release of cortisol in the adrenals .
PMID:15864504
Involved in one of the detoxification systems on the choroid plexus (CP), removes substrates such as E1S or taurocholate (TC), PCG, 2,4-D and PAH, from the cerebrospinal fluid (CSF) to the blood for eventual excretion in urine and bile (By similarity). Also contributes to the uptake of several other organic compounds such as the prostanoids prostaglandin E(2) and prostaglandin F(2-alpha), L-carnitine, and the therapeutic drugs allopurinol, 6-mercaptopurine (6-MP) and 5-fluorouracil (5-FU) (By similarity). Mediates the transport of PAH, PCG, and the statins pravastatin and pitavastatin, from the cerebrum into the blood circulation across the blood-brain barrier (BBB).
In summary, plays a role in the efflux of drugs and xenobiotics, helping reduce their undesired toxicological effects on the body (By similarity)
ATC M01AC02
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)
Tenoxicam
Additional database identifiers
Drugs Product Database (DPD)
1220
ChemSpider
10442339
BindingDB
92332
ZINC
ZINC000100006429
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:2623
GenAtlas
CYP2C9
GeneCards
CYP2C9
GenBank Gene Database
AY341248
Guide to Pharmacology
1326
UniProt Accession
CP2C9_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10972
GeneCards
SLC22A8
GenBank Gene Database
AF097491
GenBank Protein Database
4378059
Guide to Pharmacology
1027
UniProt Accession
S22A8_HUMAN
DrugBank citations
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Structured knowledge from the free knowledge base
ATC classifications (Wikidata)
Linked open data from Wikidata (Q45050), 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.