Carbocisteine 750mg capsules
Requires a prescription from a doctor or prescriber
Dyspnea and cough are common symptoms of chronic obstructive pulmonary disease (COPD)[A231169] and other respiratory conditions characterized by increased mucus production.
Official documents, adverse reaction reporting, and safety monitoring
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Official medicine documents
Safety monitoring data
Yellow Card reports
The MHRA Yellow Card scheme collects reports of suspected side effects from healthcare professionals and patients. View the Drug Analysis Profile (iDAP) for real-world adverse reaction data.
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Suspected adverse reactions reported for Carbocisteine
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Report a side effect
Submit a Yellow Card report to the MHRA
Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
EudraVigilance
The European Medicines Agency (EMA) collects suspected adverse reaction reports from across the EU/EEA through the EudraVigilance system. Search for safety data on this medicine.
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Suspected adverse reactions reported for Carbocisteine
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EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
6 branded products available
MHRA licensed products
View all licensed products for Carbocisteine on the MHRA register
Carbocisteine 750mg capsules
Carbocisteine 750mg capsules
Carbocisteine 750mg capsules
Carbocisteine 750mg capsules
Carbocisteine 750mg capsules
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)
1.5 gram
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 NHS dm+d BNF mapping files. Contains public sector information licensed under the Open Government Licence v3.0.
Therapeutically similar medicines
Similarity based on WHO Anatomical Therapeutic Chemical (ATC) classification and NHS BNF section grouping. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
Clinical guidelines and formulary information
British National Formulary
Carbocisteine
Source: British National Formulary, NICE. Joint Formulary Committee. Contains public sector information licensed under the Open Government Licence v3.0.
NICE clinical guidance(2)
Cough (acute): antimicrobial prescribing (NG120)
Motor neurone disease: assessment and management (NG42)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
Check stock at pharmacies and supply information
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Search for this medicine at major UK pharmacy chains. These links open the retailer's own website — results depend on their current online catalogue.
Supply & product information
Official product databases and supply status monitoring
Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. emc (electronic medicines compendium) is operated by Datapharm Ltd. Shortage information sourced from NHS Specialist Pharmacy Service (SPS), sps.nhs.uk.
Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
Browse tools
SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. BNF codes from NHS Business Services Authority (NHSBSA). 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.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
None known
Half-life
1.33 hours
Mechanism
The hypersecretion of mucus characterizes serious respiratory conditions includi…
Food interactions
1 warning
Human targets
4 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
1 to 1.7 hours
Half-life
1.33 hours
[A230988]
Protein binding
Volume of distribution
[A230988]
Metabolism
Elimination
30%
[A230988]
Clearance
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Several licenses for this drug were withdrawn following serious and fatal paradoxical effects after carbocisteine therapy in children; respiratory dress, dyspnea, and cough aggravation were reported by physicians in France and Italy.[A230993] Carbocisteine is currently not FDA or Health Canada approved, but is approved for use in Asia, Europe, and South America.
[L24484][L24984][L20019]
Known interactions with other medications. Always consult a healthcare professional.
Showing 18 of 18 interactions
[L32378]
An overdose with carbocisteine is likely to result in gastrointestinal discomfort with nausea and vomiting.
[L32373]
It blocks bacterial adherence to cells, preventing pulmonary infections.[A230988] Glycoproteins (fucomucins, sialomucins and sulfomucins) regulate the viscoelastic properties of bronchial mucus. Increased fucomucins can be found in the mucus of patients with COPD. Carbocisteine serves to restore equilibrium between sialomucins and fucomucins, likely by intracellular stimulation of sialyl transferase enzyme, thus reducing mucus viscosity.[A230988]
A study found that L-carbocisteine can inhibit damage to cells by hydrogen peroxide (H2O2) by activating protein kinase B (Akt) phosphorylation, suggesting that carbocisteine may have antioxidant effects and prevent apoptosis of lung cells.[A231003] There is some evidence that carbocisteine suppresses NF-κB and ERK1/2 MAPK signalling pathways, reducing TNF-alpha induced inflammation in the lungs, as well as other inflammatory pathways.[A231134][A231139] An in-vitro study found that L-carbocisteine reduces intracellular adhesion molecule 1 (ICAM-1), inhibiting rhinovirus 14 infection, thereby reducing airway inflammation.[A231144]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A230988]
[A230988]
[A230988]
[A231104]
Reduced metabolism can cause increased exposure to carbocisteine, explaining variable clinical response between patients who may polymorphisms affecting the enzymes responsible for carbocisteine metabolism.
[A230988]
It is generally accepted that sulfodixation is the main metabolic pathway of carbocisteine, however, one group of researchers found a novel urinary metabolite, S-(carboxymethylthio)-L-cysteine (CMTC). No cysteinyl sulfoxide metabolites were found in the urine of patients taking carbocisteine in this study.
[A230998]
[A230988]
Proteins and enzymes this drug interacts with in the body
PMID:14585973 PMID:15379550 PMID:15572695 PMID:15601839 PMID:15983046 PMID:37339955
KEAP1 acts as a key sensor of oxidative and electrophilic stress: in normal conditions, the BCR(KEAP1) complex mediates ubiquitination and degradation of NFE2L2/NRF2, a transcription factor regulating expression of many cytoprotective genes .
PMID:15601839 PMID:16006525
In response to oxidative stress, different electrophile metabolites trigger non-enzymatic covalent modifications of highly reactive cysteine residues in KEAP1, leading to inactivate the ubiquitin ligase activity of the BCR(KEAP1) complex, promoting NFE2L2/NRF2 nuclear accumulation and expression of phase II detoxifying enzymes .
PMID:16006525 PMID:17127771 PMID:18251510 PMID:19489739 PMID:29590092
In response to selective autophagy, KEAP1 is sequestered in inclusion bodies following its interaction with SQSTM1/p62, leading to inactivation of the BCR(KEAP1) complex and activation of NFE2L2/NRF2 .
PMID:20452972
The BCR(KEAP1) complex also mediates ubiquitination of SQSTM1/p62, increasing SQSTM1/p62 sequestering activity and degradation .
PMID:28380357
The BCR(KEAP1) complex also targets BPTF and PGAM5 for ubiquitination and degradation by the proteasome PMID:15379550 PMID:17046835
PMID:11035812 PMID:19489739 PMID:29018201 PMID:31398338
In normal conditions, ubiquitinated and degraded in the cytoplasm by the BCR(KEAP1) complex .
PMID:11035812 PMID:15601839 PMID:29018201
In response to oxidative stress, electrophile metabolites inhibit activity of the BCR(KEAP1) complex, promoting nuclear accumulation of NFE2L2/NRF2, heterodimerization with one of the small Maf proteins and binding to ARE elements of cytoprotective target genes .
PMID:19489739 PMID:29590092
The NFE2L2/NRF2 pathway is also activated in response to selective autophagy: autophagy promotes interaction between KEAP1 and SQSTM1/p62 and subsequent inactivation of the BCR(KEAP1) complex, leading to NFE2L2/NRF2 nuclear accumulation and expression of cytoprotective genes .
PMID:20452972
The NFE2L2/NRF2 pathway is also activated during the unfolded protein response (UPR), contributing to redox homeostasis and cell survival following endoplasmic reticulum stress (By similarity). May also be involved in the transcriptional activation of genes of the beta-globin cluster by mediating enhancer activity of hypersensitive site 2 of the beta-globin locus control region .
PMID:7937919
Also plays an important role in the regulation of the innate immune response and antiviral cytosolic DNA sensing. It is a critical regulator of the innate immune response and survival during sepsis by maintaining redox homeostasis and restraint of the dysregulation of pro-inflammatory signaling pathways like MyD88-dependent and -independent and TNF-alpha signaling (By similarity).
Suppresses macrophage inflammatory response by blocking pro-inflammatory cytokine transcription and the induction of IL6 (By similarity). Binds to the proximity of pro-inflammatory genes in macrophages and inhibits RNA Pol II recruitment. The inhibition is independent of the NRF2-binding motif and reactive oxygen species level (By similarity).
Represses antiviral cytosolic DNA sensing by suppressing the expression of the adapter protein STING1 and decreasing responsiveness to STING1 agonists while increasing susceptibility to infection with DNA viruses .
PMID:30158636
Once activated, limits the release of pro-inflammatory cytokines in response to human coronavirus SARS-CoV-2 infection and to virus-derived ligands through a mechanism that involves inhibition of IRF3 dimerization. Also inhibits both SARS-CoV-2 replication, as well as the replication of several other pathogenic viruses including Herpes Simplex Virus-1 and-2, Vaccinia virus, and Zika virus through a type I interferon (IFN)-independent mechanism PMID:33009401
PMID:16934889 PMID:9822625
Mainly involved in the biosynthesis of ganglioside GM3 but can also use different glycolipids as substrate acceptors such as D-galactosylceramide (GalCer), asialo-GM2 (GA2) and asialo-GM1 (GA1), although less preferentially than beta-D-Gal-(1->4)-beta-D-Glc-(1<->1)-Cer (LacCer) PMID:16934889
Enzymes involved in drug metabolism — important for understanding drug interactions
ATC R05CB03
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)
Carbocisteine
Additional database identifiers
ChemSpider
168055
BindingDB
50213735
PDB
CCS
ZINC
ZINC000001529732
HUGO Gene Nomenclature Committee (HGNC)
HGNC:23177
GeneCards
KEAP1
Guide to Pharmacology
2757
UniProt Accession
KEAP1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:7782
GeneCards
NFE2L2
UniProt Accession
NF2L2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:31822
GeneCards
PLCXD3
UniProt Accession
PLCX3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10872
GeneCards
ST3GAL5
UniProt Accession
SIAT9_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1795
GenAtlas
CDO1
GeneCards
CDO1
GenBank Gene Database
Z31357
GenBank Protein Database
467561
UniProt Accession
CDO1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8582
GenAtlas
PAH
GeneCards
PAH
GenBank Gene Database
K03020
GenBank Protein Database
189937
Guide to Pharmacology
1240
UniProt Accession
PH4H_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10872
GeneCards
ST3GAL5
UniProt Accession
SIAT9_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite the following publications: