Chondroitin sulfate 0.2%/40ml intravesical solution pre-filled syringes
Class of compounds; sulfated glycosaminoglycan
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Suspected adverse reactions reported for Chondroitin
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1 branded products available
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Supply & safety information
Official UK regulator monitoring and safety alerts
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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
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.
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 30 studies.
Reviews & meta-analyses: 12 · Randomised trials: 1 · 1977–2021
Showing all 30 studies, sorted by most relevant.
Xiaoyue Zhu, Lingli Sang, Dandong Wu, et al.
Journal of Orthopaedic Surgery and Research, 2018
- Chondroitin
- Glucosamine
- Osteoarthritis, Hip
OBJECTIVE: To assess the symptomatic effectiveness and safety of oral symptomatic slow-acting drugs (SYSADOAs) on the treatment of knee and/or hip osteoarthritis, such as chondroitin, glucosamine, and combination treatment with chondroitin plus glucosamine. METHODS: We searched electronic database including PubMed, Embase, Cochrane Library, and the reference lists of relevant articles published from inception to May 22, 2018. An updated meta-analysis was performed to assess the effectiveness of these slow-acting drugs for osteoarthritis. RESULTS: Twenty-six articles describing 30 trials met our inclusion criteria and were included in the meta-analysis. The estimates between chondroitin and placebo showed that chondroitin could alleviate pain symptoms and improve function. Compared with placebo, glucosamine proved significant effect only on stiffness improvement. However, the combination therapy did not have enough evidence to be superior to placebo. Additionally, there was no significant difference in the incidence of AEs and discontinuations of AEs when compared with placebo. CONCLUSIONS: Given the effectiveness of these symptomatic slow-acting drugs, oral chondroitin is more effective than placebo on relieving pain and improving physical function. Glucosamine showed effect on stiffness outcome. Regarding on the limited number of combination therapy, further studies need to investigate the accurate effectiveness. This information accompanied with the tolerability and economic costs of included treatments would be conducive to making decisions for clinicians.
Abstract licence: CC BY
Mario Simental-Mendía, A. Sánchez‐García, F. Vilchez-Cavazos, et al.
Rheumatology International, 2018
- Chondroitin Sulfates
- Glucosamine
- Single-Blind Method
Carl C. L. Schuurmans, M. Mihajlovic, C. Hiemstra, et al.
Biomaterials, 2020
- Chondroitin Sulfates
- Hydrogels
- Cartilage
Hydrogels based on photocrosslinkable Hyaluronic Acid Methacrylate (HAMA) and Chondroitin Sulfate Methacrylate (CSMA) are presently under investigation for tissue engineering applications. HAMA and CSMA gels offer tunable characteristics such as tailorable mechanical properties, swelling characteristics, and enzymatic degradability. This review gives an overview of the scientific literature published regarding the pre-clinical development of covalently crosslinked hydrogels that (partially) are based on HAMA and/or CSMA. Throughout the review, recommendations for the next steps in clinical translation of hydrogels based on HAMA or CSMA are made and potential pitfalls are defined. Specifically, a myriad of different synthetic routes to obtain polymerizable hyaluronic acid and chondroitin sulfate derivatives are described. The effects of important parameters such as degree of (meth)acrylation and molecular weight of the synthesized polymers on the formed hydrogels are discussed and useful analytical techniques for their characterization are summarized. Furthermore, the characteristics of the formed hydrogels including their enzymatic degradability are discussed. Finally, a summary of several recent applications of these hydrogels in applied fields such as cartilage and cardiac regeneration and advanced tissue modelling is presented.
Abstract licence: CC BY
J. A. Roman-Blas, S. Castañeda, O. Sánchez-Pernaute, et al.
Arthritis & Rheumatology, 2017
- Chondroitin Sulfates
- Glucosamine
- Arthralgia
Mamta Bishnoi, Ankit Jain, P. Hurkat, et al.
Glycoconjugate Journal, 2016
- Chondroitin Sulfates
- Osteoarthritis
- Cell Adhesion
T. Mikami, H. Kitagawa
Biochimica et biophysica acta, 2013
- Chondroitin Sulfates
- Enzymes
J. Singh, S. Noorbaloochi, R. MacDonald, et al.
The Cochrane database of systematic reviews, 2015
- Anti-Inflammatory Agents, Non-Steroidal
- Chondroitin Sulfates
- Glucosamine
Scott Dyck, Soheila Karimi-Abdolrezaee
Experimental neurology, 2015
- Brain Injuries
- Central Nervous System
- Nerve Regeneration
N. Volpi
Molecules, 2019
- Chondroitin Sulfates
- Osteoarthritis
- Dietary Supplements
The industrial production of chondroitin sulfate (CS) uses animal tissue sources as raw material derived from different terrestrial or marine species of animals. CS possesses a heterogeneous structure and physical-chemical profile in different species and tissues, responsible for the various and more specialized functions of these macromolecules. Moreover, mixes of different animal tissues and sources are possible, producing a CS final product having varied characteristics and not well identified profile, influencing oral absorption and activity. Finally, different extraction and purification processes may introduce further modifications of the CS structural characteristics and properties and may lead to extracts having a variable grade of purity, limited biological effects, presence of contaminants causing problems of safety and reproducibility along with not surely identified origin. These aspects pose a serious problem for the final consumers of the pharmaceutical or nutraceutical products mainly related to the traceability of CS and to the declaration of the real origin of the active ingredient and its content. In this review, specific, sensitive and validated analytical quality controls such as electrophoresis, eHPLC (enzymatic HPLC) and HPSEC (high-performance size-exclusion chromatography) able to assure CS quality and origin are illustrated and discussed.
Abstract licence: CC BY
M.B. Keough, James A. Rogers, Ping Zhang, et al.
Nature Communications, 2016
- Remyelination
- Animals, Newborn
- Astrocytes
Remyelination is the generation of new myelin sheaths after injury facilitated by processes of differentiating oligodendrocyte precursor cells (OPCs). Although this repair phenomenon occurs in lesions of multiple sclerosis patients, many lesions fail to completely remyelinate. A number of factors have been identified that contribute to remyelination failure, including the upregulated chondroitin sulfate proteoglycans (CSPGs) that comprise part of the astrogliotic scar. We show that in vitro, OPCs have dramatically reduced process outgrowth in the presence of CSPGs, and a medication library that includes a number of recently reported OPC differentiation drugs failed to rescue this inhibitory phenotype on CSPGs. We introduce a novel CSPG synthesis inhibitor to reduce CSPG content and find rescued process outgrowth from OPCs in vitro and accelerated remyelination following focal demyelination in mice. Preventing CSPG deposition into the lesion microenvironment may be a useful strategy to promote repair in multiple sclerosis and other neurological disorders.
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
None known
Half-life
15 hours
Mechanism
Chondroitin sulfate functions as a major component of the intricate extracellular matrix.
Food interactions
None known
Human targets
4 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
10%
[A32063]…
Half-life
15 hours
[A32066]…
Protein binding
0.23%
[A32070]
Volume of distribution
0.40 ml
Metabolism
[A32066]
Reports have indicated the presence in plasma of mono-, oligo- and polysaccharides…
Elimination
37%
[A32063]…
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
[L1527]
This supplement is reported to improve joint function and slow disease progression.
[L1528]
Osteoarthritis is characterized by progressive structural and metabolic changes in joint tissues, mainly cartilage degradation, subchondral bone sclerosis and inflammation of synovial membrane.
[A32066]
Studies have proposed the potential use of chondroitin sulfate as a nutraceutical in dietary supplements.
[A32065]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 734 interactions
[L1527]
On tolerability assays, it has been shown to present great safety and good tolerability without significant severe side effects.
[A32066]
The anti-inflammatory effect of chondroitin sulfate is thought to be caused by the inhibition of the synthesis of inflammatory intermediates such as the inhibition of nitric oxide synthase, COX-2, microsomal prostaglandin synthase 1 and prostaglandin E2. It is reported also an inhibitory activity in the toll-like receptor 4 which will later inhibit inflammatory cytokines, NFkB and MyD88. This activity suggests a modulation of the MAP kinase pathway. On the other hand, some reports have pointed out an induction on the PKC/PI3K/Akt pathway in neuroblastoma.[A32066]
The anabolic effect of chondroitin sulfate is suggested to be caused by the inhibition of metalloproteinases such as MMP-1, -3 and -13 as well as ADAMTS-4 and -5.[A32066]
It is also registered an anabolic effect of chondroitin sulfate in which it induces the synthesis of hyaluronate in synovial cells, it increases type II collagen and proteoglycan synthesis.[A32066]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A32063]
The absorbed portion reaches a ratio of 10% as unchanged chondroitin sulfate and 90% as depolymerized low-molecular-weight derivatives. This absorption depends on the sulfation status. The bioavailability of chondroitin sulfate ranges from 10-20% following oral administration.
Reports have shown a consistent accumulation of the compound in joint tissue. The steady-state is attained after 3-4 days and it takes around 3-6 months to obtain the maximal effect.
[A32066]
After intramuscular administration of chondroitin sulfate, the peak plasma level of 3.8 mcg/ml was reached after 90 min. When given orally, the peak plasma concentration of 4.6 mcg/ml was reached after 240 min.
[A32068]
[A32066]
After intramuscular administration of chondroitin sulfate in humans, the elimination half-life of the chondroitin sulfate was of 275 min. When administered orally, the elimination half-life was presented at 310 min.
[A32068]
[A32070]
[A32068]
[A32066]
Reports have indicated the presence in plasma of mono-, oligo- and polysaccharides with a molecular weight of less of 5 kDa which are derived from the partial digestion of exogenous chondroitin sulfate.
[A32068]
The reported degradation of chondroitin sulfate seems to be very complex and led by the formation of smaller digestion derivatives of the original form.
[L1536]
[A32063]
After intramuscular administration, about 37% of the administered dose is excreted by urine during the first 24 hours as high- and low-molecular-weight derivatives.
[A32068]
Proteins and enzymes this drug interacts with in the body
PMID:11152678
During development, promotes the survival and differentiation of selected neuronal populations of the peripheral and central nervous systems. Participates in axonal growth, pathfinding and in the modulation of dendritic growth and morphology. Major regulator of synaptic transmission and plasticity at adult synapses in many regions of the CNS.
The versatility of BDNF is emphasized by its contribution to a range of adaptive neuronal responses including long-term potentiation (LTP), long-term depression (LTD), certain forms of short-term synaptic plasticity, as well as homeostatic regulation of intrinsic neuronal excitability
PMID:8493557
Acts by binding to its coreceptor, GFRA1, leading to autophosphorylation and activation of the RET receptor .
PMID:10829012 PMID:25242331 PMID:31535977
Involved in the development of the neural crest PMID:15242795
PMID:35455969
Involved in protecting cells from hypoxia-mediated cell death (By similarity)
PMID:10529171 PMID:10587439 PMID:9837883
Signals through binding and activation of CCR2 and induces a strong chemotactic response and mobilization of intracellular calcium ions .
PMID:10587439 PMID:9837883
Exhibits a chemotactic activity for monocytes and basophils but not neutrophils or eosinophils .
PMID:8195247 PMID:8627182 PMID:9792674
May be involved in the recruitment of monocytes into the arterial wall during the disease process of atherosclerosis PMID:8107690
Enzymes involved in drug metabolism — important for understanding drug interactions
ATC M01AX25
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)
Chondroitin sulfate
Matched from: Chondroitin
Additional database identifiers
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1033
GenAtlas
BDNF
GeneCards
BDNF
GenBank Gene Database
M37762
UniProt Accession
BDNF_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4232
GenAtlas
GDNF
GeneCards
GDNF
GenBank Gene Database
L19063
UniProt Accession
GDNF_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12680
GenAtlas
VEGF
GeneCards
VEGFA
GenBank Gene Database
M32977
GenBank Protein Database
181971
UniProt Accession
VEGFA_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10618
GenAtlas
CCL2
GeneCards
CCL2
GenBank Gene Database
M24545
GenBank Protein Database
307163
UniProt Accession
CCL2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4696
GenAtlas
GUSB
GeneCards
GUSB
GenBank Gene Database
M15182
GenBank Protein Database
183233
UniProt Accession
BGLR_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4879
GenAtlas
HEXB
GeneCards
HEXB
GenBank Gene Database
M13519
GenBank Protein Database
179462
UniProt Accession
HEXB_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:4122
GenAtlas
GALNS
GeneCards
GALNS
GenBank Gene Database
D17629
GenBank Protein Database
870751
UniProt Accession
GALNS_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5389
GeneCards
IDS
UniProt Accession
IDS_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5391
GeneCards
IDUA
UniProt Accession
IDUA_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:714
GeneCards
ARSB
UniProt Accession
ARSB_HUMAN
DrugBank citations
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Structured knowledge from the free knowledge base
ATC classifications (Wikidata)
Linked open data from Wikidata (Q408014), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication.