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Suspected adverse reactions reported for Glucosamine sulfate
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Suspected adverse reactions reported for Glucosamine sulfate
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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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Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
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: 18 · 1980–2025
Showing the 50 most relevant studies, sorted by most relevant.
Mario Simental‐Mendía, Adriana Sánchez‐García, Félix Vílchez‐Cavazos, et al.
Rheumatology International, 2018
- Chondroitin Sulfates
- Glucosamine
- Single-Blind Method
Young Ho Lee, Jin-Hyun Woo, Seong Jae Choi, et al.
Rheumatology International, 2009
Marc C. Hochberg, Johanne Martel‐Pelletier, Jordi Monfort, et al.
Annals of the Rheumatic Diseases, 2015
- Celecoxib
- Chondroitin Sulfates
- Drug Combinations
Anna Shmagel, Ryan T. Demmer, Daniel Knights, et al.
Nutrients, 2019
- Gastrointestinal Microbiome
- Bacteria
- Chondroitin Sulfates
Anvita Rabade, Gollapalle Lakshminarayanashastry Viswanatha, Krishnadas Nandakumar, et al.
Inflammopharmacology, 2024
- Chondroitin Sulfates
- Glucosamine
Jorge A. Roman‐Blas, Santos Castañeda, Olga Sánchez‐Pernaute, et al.
Arthritis & Rheumatology, 2016
- Chondroitin Sulfates
- Glucosamine
- Arthralgia
Grainne McCarthy, James O’Donovan, B. P. Jones, et al.
The Veterinary Journal, 2006
- Anti-Inflammatory Agents, Non-Steroidal
- Carbazoles
- Chondroitin Sulfates
ZHI Yuan, LIU Haibo, WANG Huiling, et al.
Zhongguo shipin weisheng zazhi, 2025
Anvita Rabade, Gollapalle Lakshminarayanashastry Viswanatha, Krishnadas Nandakumar, et al.
2023
Abstract Aim: This study was aimed to assess the efficacy and safety of oral Symptomatic Slow Acting Drugs for Osteoarthritis (SYSADOAs) such as Glucosamine Sulfate, Chondroitin Sulfate, and their combination regimen in the management of knee osteoarthritis (KOA). Methods: This systematic review was conducted according to PRISMA 2020 guidelines. A detailed literature search was performed from 03/1994 to 31/12/2022 using various electronic databases including PubMed, Embase, Cochrane Library, and Google Scholar using the search terms- Glucosamine sulfate, Chondroitin sulfate, Knee osteoarthritis, Joint pain, Joint disease, and Joint structure for literature concerning glucosamine, chondroitin, and their combination in knee osteoarthritis treatment. Cochrane Collaboration’s Risk assessment tool (version 5.4.1) was used for assessing the risk of bias and the quality of the literature. The data was extracted from the included studies and subjected to statistical analysis to determine the beneficial effect of Glucosamine Sulfate, Chondroitin Sulfate, and their combination. Results: Twenty-five randomized controlled trials (RCTs) were included [9 RCTs are exclusively for Glucosamine sulfate, 13 RCTs are exclusively for Chondroitin sulfate, and only 3 RCTs can be considered for assessing the possible benefits of the combination of Glucosamine sulfate (GS) and Chondroitin sulfate (CS) versus Placebo]. The results of this meta-analysis revealed the following: (1) Pain intensity: Chondroitin sulfate showed a significant reduction in pain intensity, (2) Physical function: Chondroitin sulphate showed a significant improvement in physical function; (3) Joint space narrowing: Glucosamine sulfate showed a significant reduction in tibiofemoral joint space narrowing. Their combination did not reduce pain intensity and showed no improvement in the physical function, whereas it showed a non-significant reduction in joint space narrowing. In the safety aspect, both compounds have a good safety profile and are well tolerated. Conclusion: When the overall effect of these SYSADOAs was evaluated, it was seen that they reduced pain intensity and improved physical function showing their symptom-modifying action and decreased the joint space narrowing significantly showing their disease-modifying action. In the safety aspect, both compounds have a good safety profile and are well tolerated. This meta-analysis revealed that as individual drugs glucosamine sulfate showed a significant reduction in the joint space narrowing while chondroitin sulfate showed a significant reduction in pain intensity and improvement in the physical function. This meta-analysis also showed that the combination did not significantly improve the symptoms or modify the disease. This may be because of the availability of limited trials on the combination of the sulfate forms of the intervention. Thus, further trials on the effect of glucosamine sulfate and chondroitin sulfate are required to establish accurate evidence regarding their use in KOA.
Abstract licence: CC BY 4.0
Knapik JJ, Pope R, Hoedebecke SS, et al.
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 medications. 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
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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)
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 the following publications:
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Structured knowledge from the free knowledge base
ATC classifications (Wikidata)
Linked open data from Wikidata (Q327506), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication.