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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. 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: 18 · Randomised trials: 22 · 1980–2026
Showing the 50 most relevant studies, sorted by most relevant.
M. Hochberg, J. Martel-Pelletier, J. Monfort, et al.
Annals of the Rheumatic Diseases, 2015
Brian H. Rowe, Jennifer A. Bretzlaff, Chris Bourdon, et al.
Annals of Emergency Medicine, 2000
A. Shmagel, R. Demmer, D. Knights, et al.
Nutrients, 2019
Jorge A. Roman-Blas, S. Castañeda, O. Sánchez-Pernaute, et al.
Arthritis & Rheumatology, 2017
ZHI Yuan, LIU Haibo, WANG Huiling, et al.
Zhongguo shipin weisheng zazhi, 2025
Li Y, Wang R, Xu J, et al.
2026
BackgroundKnee osteoarthritis (OA) is a common cause of pain and disability without a cure. Glucosamine is widely used as a symptomatic treatment owing to its safety, yet its clinical efficacy remains uncertain amid mixed trial results and conflicting guidelines. This umbrella review synthesized evidence from published systematic reviews and meta-analyses on the effectiveness and safety of glucosamine in knee OA.MethodsWe searched MEDLINE (via PubMed), Embase, Web of Science, and the Cochrane Library up to November 2025. Eligible studies were systematic reviews or meta-analyses of randomized trials in adults with knee OA comparing glucosamine (any formulation) with placebo or other non-surgical comparators and reporting pain, physical function, or joint structure. Two reviewers independently screened, extracted data, and assessed quality (AMSTAR-2). Key outcomes were pain (visual analog scale [VAS] and WOMAC [Western Ontario and McMaster Universities Osteoarthritis Index]), functional measures, joint space narrowing (JSN), and adverse events. Overlap among shared primary trials was quantified using the corrected covered area, and the resulting dependence was addressed using robust variance estimation to pool standardized mean differences (SMDs), with p ResultsNineteen reviews were included (most low or critically low quality). Glucosamine produced a small but statistically significant reduction in VAS pain (SMD - 0.36, p = 0.02), whereas WOMAC pain showed no significant difference. Functional outcomes (WOMAC total and function) showed no significant improvement. Glucosamine was associated with significant slowing of JSN progression (SMD - 0.32, p = 0.01), though this signal derived mainly from long-duration sulfate trials. The magnitude of the significant effects was at or below accepted MCID thresholds. Adverse event rates did not differ from placebo.ConclusionGlucosamine demonstrated at most minimal-to-modest efficacy for knee OA, yielding a small pain reduction and possible slowing of radiographic progression but no clear functional benefit, with effects at or below the threshold of clinical importance. Given the low quality of evidence, extensive overlap among reviews, and the predominantly out-of-pocket nature of glucosamine use, these findings should be interpreted with caution and weighed against cost in shared decision-making.Systematic review registrationhttps://www.crd.york.ac.uk/prospero/, identifier (CRD420251207513).
Abstract licence: CC BY
Calzada-Gonzales N, Aguirre-Ipenza R, Serna-Alarcón V, et al.
2026
BackgroundGlucosamine has been proposed as a therapeutic option for temporomandibular disorders (TMD), particularly temporomandibular joint osteoarthritis (TMJ OA), but its effectiveness and safety remain uncertain.ObjectiveTo evaluate the benefits and harms of oral glucosamine supplementation in patients with TMJ OA and other/unspecified TMD.MethodsA systematic review was conducted in PubMed/MEDLINE, CENTRAL, Scopus, and Embase through October 8, 2025. Randomized controlled trials (RCTs) evaluating oral glucosamine supplementation in patients with any type of TMD, including TMJ OA, were selected. Meta-analyses were performed using random-effects models, and the GRADE methodology was applied to assess the certainty of the evidence.ResultsSeven RCTs were included. In patients with TMJ OA, compared with placebo, glucosamine may not result in a clinically important reduction in pain at ≤3 months (MD -1.58 mm; 95% CI -5.98 to 2.83; low certainty) and probably does not provide a clinically important reduction at 6 months despite statistical significance (MD -7.02 mm; 95% CI -11.95 to -2.09; moderate certainty). Glucosamine improved quality of life at 12 months (MD -4.14; 95% CI -6.41 to -1.87; high certainty). Compared with active controls, the effect on pain was uncertain, although quality of life may improve at 3 months. In patients with other/unspecified TMD, glucosamine may not meaningfully reduce pain but may increase maximum pain-free mandibular opening at 3 months. Evidence regarding adverse and serious adverse events was very uncertain across comparisons.ConclusionOral glucosamine does not provide a clinically important reduction in pain in TMJ OA or other/unspecified TMD but may improve quality of life in TMJ OA. Evidence for functional outcomes and adverse events remains uncertain, highlighting the need for high-quality randomized trials.Systematic review registrationhttps://www.crd.york.ac.uk/PROSPERO/view/CRD42024531131, identifier CRD42024531131.
Abstract licence: CC BY
Yan Y, Xu M, Wang R, et al.
2026
Background and aimThis systematic review and meta-analysis aimed to evaluate whether habitual glucosamine use is associated with colorectal cancer risk and survival outcomes in the general population.MethodsFollowing PRISMA 2020 guidance, we systematically searched PubMed, Embase, Web of Science, and the Cochrane Database of Systematic Reviews from inception to January 10, 2026. Prospective cohort studies comparing glucosamine users with non-users and reporting adjusted effect estimates were eligible. Two reviewers independently extracted data and assessed study quality using the Newcastle-Ottawa Scale. Adjusted hazard ratios or relative risks were pooled using fixed- or random-effects models based on heterogeneity quantified with I².ResultsFrom 347 records, 18 prospective cohort studies met eligibility criteria; five outcomes (colorectal cancer incidence, colorectal cancer-specific mortality, all-cause mortality, cardiovascular mortality, and overall cancer mortality) were quantitatively synthesized. Glucosamine use was associated with a lower incidence of colorectal cancer across 5 studies (pooled HR 0.87, 95% CI 0.82 to 0.92; I² = 36%). For colorectal cancer-specific mortality, the evidence was limited to only 2 studies with substantial heterogeneity (I² = 81%) and effect estimates in opposite directions, and the pooled estimate showed no clear association (pooled RR 0.99, 95% CI 0.57 to 1.71); this outcome should therefore be regarded as inconclusive. Glucosamine use was also associated with lower all-cause mortality in 4 studies (pooled HR 0.84, 95% CI 0.76 to 0.94; I² = 65%), lower cardiovascular mortality in 4 studies (pooled HR 0.82, 95% CI 0.75 to 0.89; I² = 44%), and a modest reduction in overall cancer mortality in 4 studies (pooled HR 0.94, 95% CI 0.91 to 0.98; I² = 7%). Results were stable in leave-one-out sensitivity analyses. All estimates represent associations derived from observational cohort studies and cannot establish causation.ConclusionsCurrent cohort evidence indicates that glucosamine use is associated with a modestly lower risk of developing colorectal cancer and with lower mortality from all causes, cardiovascular disease, and cancer overall. The evidence for colorectal cancer-specific mortality was based on only 2 studies with substantial heterogeneity and remains inconclusive. Because all included studies were observational, these findings represent associations rather than evidence of a causal protective effect. Given the modest effect sizes, healthy-user bias and residual confounding are plausible and possibly major explanations for the observed associations, and even a small degree of unmeasured confounding could account for part or all of them. Well-designed studies with improved exposure characterization, and ideally causal designs such as Mendelian randomization, are needed to determine whether these associations are causal and clinically meaningful.
Abstract licence: CC BY
Chen K, Sun Y, Cui L, et al.
2026
PurposeKnee osteoarthritis (KOA) creates a substantial global socioeconomic burden. Celecoxib remains a standard pharmacological treatment, but its long-term safety profile raises concerns. Several adjuvant therapies-probiotics, metformin, krill oil, and glucosamine/chondroitin (CS+GH)-have produced encouraging results in individual trials; however, direct head-to-head comparisons are absent. This network meta-analysis (NMA) compares the efficacy and safety of these five interventions to inform individualized treatment decisions in clinical practice.MethodsRCTs published from database inception through February 2026 were retrieved from PubMed, Web of Science, Embase, and the Cochrane Library. A random-effects NMA was conducted using Stata 18.0 and R (MetaInsight). Continuous outcomes were synthesized as mean differences (MD) and dichotomous safety endpoints as risk ratios (RR). Interventions were ranked by surface under the cumulative ranking curve (SUCRA), and evidence quality was assessed using the GRADE framework.ResultsTwenty-three RCTs met the inclusion criteria. No significant network inconsistency (P > 0.05) or publication bias was detected. For analgesic efficacy, celecoxib ranked highest on VAS pain improvement (MD = -0.48, 95% CI -0.78 to -0.17, SUCRA = 0.93) and WOMAC total scores (SUCRA = 0.912), followed by CS+GH (0.756). Probiotics (0.66) and metformin (0.63) showed potential efficacy, but the final network certainty for most of these auxiliary comparisons was low or very low, mainly due to severe imprecision and the absence of direct head-to-head trials. These SUCRA-based rankings should therefore be interpreted cautiously in clinical settings. On WOMAC subscales, celecoxib was associated with the largest improvements in pain and physical function; krill oil ranked highest on the pain subscale (SUCRA = 0.99), while probiotics and metformin had the most favorable safety profiles (SUCRA = 0.885 and 0.724, respectively).Systematic review registrationhttps://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD420261345598, identifier: CRD420261345598.
Abstract licence: CC BY
J. Knapik, R. Pope, S. S. Hoedebecke, et al.
Journal of special operations medicine : a peer reviewed journal for SOF medical professionals, 2018
- Joints
- Osteoarthritis
- Pain
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
15 hours
Mechanism
The mechanism of action of glucosamine in joint health is unclear,[A231894] howe…
Food interactions
None known
Human targets
4 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
88.7%
Half-life
15 hours
[A232279]
…
Volume of distribution
15.4 L/kg
Metabolism
[A232274]
Metabolism information for glucosamine is limited in the literature.
Elimination
11.3%
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
[L32699]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 50 interactions
[L32684]
Symptoms of an overdose with glucosamine may include nausea, vomiting, abdominal pain, and diarrhea (common side effects of this drug). Severe and life-threatening hypersensitivity reactions to glucosamine may occur in patients with a shellfish allergy or asthma.
[L32774]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A232274]
In a pharmacokinetic study of 12 healthy adults receiving oral crystalline glucosamine, plasma levels increased up to 30 times the baseline levels and Cmax was 10 microM with a 1,500 mg once-daily dose. Tmax was about 3 hours. AUC was 20,216 ± 5021 after a 15,000 mg dose.
[A232279]
[A232279]
After a bolus intravenous injection of 1005 mg crystalline glucosamine sulfate, the parent drug has an apparent half life of 1.11 hours.
[A232274]
[A232279]
Human pharmacokinetic data for glucosamine is limited in the literature, however, a large animal model study of horses revealed a mean apparent volume of distribution of 15.4 L/kg. Concentrations of glucosamine ranged from 9-15 microM after an intravenous dose, and 0.3-0.7 microM after nasogastric dosing. These concentrations remained in the range of 0.1-0.7 microM in the majority of horses 12 hours after dosing,[A2356] suggesting effectiveness of a once-daily dose.
In rats and dogs, radioactivity from a C-14 labeled dose of glucosamine is detected in the liver, kidneys, articular cartilage, and other areas.
[A232274]
[A232274]
Metabolism information for glucosamine is limited in the literature.
[A232279]
Urinary elimination was found to be 1.19% within the first 8 hours post-administration.
[A232274]
Proteins and enzymes this drug interacts with in the body
PMID:10653850 PMID:12794819 PMID:28331908 PMID:3920526
Initially discovered as the major endogenous pyrogen, induces prostaglandin synthesis, neutrophil influx and activation, T-cell activation and cytokine production, B-cell activation and antibody production, and fibroblast proliferation and collagen production .
PMID:3920526
Promotes Th17 differentiation of T-cells. Synergizes with IL12/interleukin-12 to induce IFNG synthesis from T-helper 1 (Th1) cells .
PMID:10653850
Plays a role in angiogenesis by inducing VEGF production synergistically with TNF and IL6 .
PMID:12794819
Involved in transduction of inflammation downstream of pyroptosis: its mature form is specifically released in the extracellular milieu by passing through the gasdermin-D (GSDMD) pore .
PMID:33377178 PMID:33883744
Acts as a sensor of S.pyogenes infection in skin: cleaved and activated by pyogenes SpeB protease, leading to an inflammatory response that prevents bacterial growth during invasive skin infection PMID:28331908
PMID:21645528
Positively regulates postnatal regression of retinal hyaloid vessels via suppression of VEGFR2/KDR activity, downstream of OPN5 (By similarity)
PMID:16914093 PMID:8666937
Primarily signals through the JAK-STAT pathway after interaction with its receptor IFNGR1 to affect gene regulation .
PMID:8349687
Upon IFNG binding, IFNGR1 intracellular domain opens out to allow association of downstream signaling components JAK2, JAK1 and STAT1, leading to STAT1 activation, nuclear translocation and transcription of IFNG-regulated genes. Many of the induced genes are transcription factors such as IRF1 that are able to further drive regulation of a next wave of transcription .
PMID:16914093
Plays a role in class I antigen presentation pathway by inducing a replacement of catalytic proteasome subunits with immunoproteasome subunits .
PMID:8666937
In turn, increases the quantity, quality, and repertoire of peptides for class I MHC loading .
PMID:8163024
Increases the efficiency of peptide generation also by inducing the expression of activator PA28 that associates with the proteasome and alters its proteolytic cleavage preference .
PMID:11112687
Up-regulates as well MHC II complexes on the cell surface by promoting expression of several key molecules such as cathepsins B/CTSB, H/CTSH, and L/CTSL .
PMID:7729559
Participates in the regulation of hematopoietic stem cells during development and under homeostatic conditions by affecting their development, quiescence, and differentiation (By similarity)
The dimers bind at kappa-B sites in the DNA of their target genes and the individual dimers have distinct preferences for different kappa-B sites that they can bind with distinguishable affinity and specificity. Different dimer combinations act as transcriptional activators or repressors, respectively. The NF-kappa-B heterodimeric RELA-NFKB1 and RELA-REL complexes, for instance, function as transcriptional activators.
NF-kappa-B is controlled by various mechanisms of post-translational modification and subcellular compartmentalization as well as by interactions with other cofactors or corepressors. NF-kappa-B complexes are held in the cytoplasm in an inactive state complexed with members of the NF-kappa-B inhibitor (I-kappa-B) family. In a conventional activation pathway, I-kappa-B is phosphorylated by I-kappa-B kinases (IKKs) in response to different activators, subsequently degraded thus liberating the active NF-kappa-B complex which translocates to the nucleus.
The inhibitory effect of I-kappa-B on NF-kappa-B through retention in the cytoplasm is exerted primarily through the interaction with RELA. RELA shows a weak DNA-binding site which could contribute directly to DNA binding in the NF-kappa-B complex. Besides its activity as a direct transcriptional activator, it is also able to modulate promoters accessibility to transcription factors and thereby indirectly regulate gene expression.
Associates with chromatin at the NF-kappa-B promoter region via association with DDX1. Essential for cytokine gene expression in T-cells .
PMID:15790681
The NF-kappa-B homodimeric RELA-RELA complex appears to be involved in invasin-mediated activation of IL-8 expression. Key transcription factor regulating the IFN response during SARS-CoV-2 infection PMID:33440148
Proteins that transport this drug across cell membranes
PMID:16186102 PMID:23396969 PMID:28083649 PMID:8027028 PMID:8457197
Likely mediates the bidirectional transfer of glucose across the plasma membrane of hepatocytes and is responsible for uptake of glucose by the beta cells; may comprise part of the glucose-sensing mechanism of the beta cell .
PMID:8027028
May also participate with the Na(+)/glucose cotransporter in the transcellular transport of glucose in the small intestine and kidney .
PMID:3399500
Also able to mediate the transport of dehydroascorbate PMID:23396969
PMID:10227690 PMID:10954735 PMID:18245775 PMID:19449892 PMID:25982116 PMID:27078104 PMID:32860739
Has a very broad substrate specificity; can transport a wide range of aldoses including both pentoses and hexoses .
PMID:18245775 PMID:19449892
Most important energy carrier of the brain: present at the blood-brain barrier and assures the energy-independent, facilitative transport of glucose into the brain .
PMID:10227690
In association with BSG and NXNL1, promotes retinal cone survival by increasing glucose uptake into photoreceptors (By similarity). Required for mesendoderm differentiation (By similarity)
PMID:26176916 PMID:32860739 PMID:9477959
Can also mediate the uptake of various other monosaccharides across the cell membrane .
PMID:26176916 PMID:9477959
Mediates the uptake of glucose, 2-deoxyglucose, galactose, mannose, xylose and fucose, and probably also dehydroascorbate .
PMID:26176916 PMID:9477959
Does not mediate fructose transport .
PMID:26176916 PMID:9477959
Required for mesendoderm differentiation (By similarity)
ATC M01AX05
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)
Glucosamine
Matched from: Glucosamine sulfate
Additional database identifiers
ChemSpider
388352
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5992
GenAtlas
IL1B
GeneCards
IL1B
GenBank Gene Database
K02770
GenBank Protein Database
307043
UniProt Accession
IL1B_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3023
GenAtlas
DRD2
GeneCards
DRD2
GenBank Gene Database
M30625
GenBank Protein Database
181432
Guide to Pharmacology
215
UniProt Accession
DRD2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5438
GenAtlas
IFNG
GeneCards
IFNG
GenBank Gene Database
X13274
GenBank Protein Database
32692
UniProt Accession
IFNG_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9955
GeneCards
RELA
Guide to Pharmacology
3280
UniProt Accession
TF65_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11006
GenAtlas
SLC2A2
GeneCards
SLC2A2
GenBank Gene Database
J03810
GenBank Protein Database
307125
UniProt Accession
GTR2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11005
GenAtlas
SLC2A1
GeneCards
SLC2A1
GenBank Gene Database
K03195
GenBank Protein Database
183303
Guide to Pharmacology
875
UniProt Accession
GTR1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11009
GenAtlas
SLC2A4
GeneCards
SLC2A4
GenBank Gene Database
M20747
GenBank Protein Database
307076
UniProt Accession
GLUT4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11007
GeneCards
SLC2A3
UniProt Accession
GTR3_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