Umeclidinium bromide 65micrograms/dose dry powder inhaler
Requires a prescription from a doctor or prescriber
Umeclidinium is a long-acting muscarinic antagonist (LAMA) used as a maintenance treatment for symptoms of chronic obstructive pulmonary disease (COPD).
Safety information for pregnancy and breastfeeding
Pregnancy
Always consult your doctor or midwife before taking any medicine during pregnancy or while breastfeeding. Source: DrugBank (CC BY-NC 4.0).
Official documents, adverse reaction reporting, and safety monitoring
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Official medicine documents
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Drug safety updates
MHRA alerts for Umeclidinium bromide
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 Umeclidinium bromide
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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 Umeclidinium bromide
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Learn about EU pharmacovigilance and safety monitoring
EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
7 branded products available
MHRA licensed products
View all licensed products for Umeclidinium bromide on the MHRA register
Incruse Ellipta 55micrograms/dose dry powder inhaler
Incruse Ellipta 55micrograms/dose dry powder inhaler
Incruse Ellipta 55micrograms/dose dry powder inhaler
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)
55 microgram
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 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.
NHS prescribing volume and spending trends
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Supply & safety information
Official UK regulator monitoring and safety alerts
Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. Shortage and safety information sourced from MHRA drug safety updates (gov.uk, Crown Copyright under OGL v3.0).
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. 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: 20 · Randomised trials: 12 · 2012–2026
Showing the 50 most relevant studies, sorted by most relevant.
Marc Decramer, Antonio Anzueto, Edward Kerwin, et al.
The Lancet Respiratory Medicine, 2014
F. Maltais, L. Bjermer, E. Kerwin, et al.
Respiratory Research, 2019
BackgroundProspective evidence is lacking regarding incremental benefits of long-acting dual- versus mono-bronchodilation in improving symptoms and preventing short-term disease worsening/treatment failure in low exacerbation risk patients with chronic obstructive pulmonary disease (COPD) not receiving inhaled corticosteroids.MethodsThe 24-week, double-blind, double-dummy, parallel-group Early MAXimisation of bronchodilation for improving COPD stability (EMAX) trial randomised patients at low exacerbation risk not receiving inhaled corticosteroids, to umeclidinium/vilanterol 62.5/25 μg once-daily, umeclidinium 62.5 μg once-daily or salmeterol 50 μg twice-daily. The primary endpoint was trough forced expiratory volume in 1 s (FEV1) at Week 24. The study was also powered for the secondary endpoint of Transition Dyspnoea Index at Week 24. Other efficacy assessments included spirometry, symptoms, heath status and short-term disease worsening measured by the composite endpoint of clinically important deterioration using three definitions.ResultsChange from baseline in trough FEV1 at Week 24 was 66 mL (95% confidence interval [CI]: 43, 89) and 141 mL (95% CI: 118, 164) greater with umeclidinium/vilanterol versus umeclidinium and salmeterol, respectively (both p < 0.001). Umeclidinium/vilanterol demonstrated consistent improvements in Transition Dyspnoea Index versus both monotherapies at Week 24 (vs umeclidinium: 0.37 [95% CI: 0.06, 0.68], p = 0.018; vs salmeterol: 0.45 [95% CI: 0.15, 0.76], p = 0.004) and all other symptom measures at all time points. Regardless of the clinically important deterioration definition considered, umeclidinium/vilanterol significantly reduced the risk of a first clinically important deterioration compared with umeclidinium (by 16–25% [p < 0.01]) and salmeterol (by 26–41% [p < 0.001]). Safety profiles were similar between treatments.ConclusionsUmeclidinium/vilanterol consistently provides early and sustained improvements in lung function and symptoms and reduces the risk of deterioration/treatment failure versus umeclidinium or salmeterol in symptomatic patients with low exacerbation risk not receiving inhaled corticosteroids. These findings suggest a potential for early use of dual bronchodilators to help optimise therapy in this patient group.
Abstract licence: CC BY 4.0
Zhu H, Lei J, Gao F, et al.
2024
- Pulmonary Disease, Chronic Obstructive
- Benzyl Alcohols
- Chlorobenzenes
BackgroundUMEC/VI administered via a combination inhaler is associated with a clinically significant improvement in lung function and health-related quality of life in patients with mild-to-moderate COPD. However, their efficacy compared to other bronchodilator mono or dual therapies still remains unclear.ObjectiveThe objective of this research was to evaluate the therapeutic efficacy of UMEC/VI dual and UMEC/VI/FF triple therapies versus alternative bronchodilator regimens in COPD patients.MethodsA systematic search was conducted using four electronic databases (PubMed, EMBASE, Scopus, and Cochrane Library) to select publications published in peer-reviewed journals written in English. The odds ratio (OR) and risk ratio (RR) was calculated, along with their 95% confidence intervals. We assessed heterogeneity using Cochrane Q and I [2] statistics and the appropriate p-value. The analysis used RevMan 5.4.ResultsThe current meta-analysis includes 31,814 COPD patients from 17 RCTs. The meta-analysis results demonstrate that the combination of LABA and LAMA provides additive bronchodilation and improved lung function in COPD patients. We found that UMEC/VI dual therapy significantly improved FEV1 (OR 1.98 [95% CI 1.70-2.30]), TDI values (OR 1.97 [95% CI 1.72-2.26]), and reduced SGRQ total scores (OR 1.99 [95% CI 1.71-2.32]), with fewer drug-related adverse events (RR 0.58 [95% CI 0.53-0.64]). Similarly, UMEC/VI/FF triple therapy also showed similar benefits, with significant improvements in FEV1 (OR 1.93 [95% CI 1.73-2.15]), TDI values (OR 2.37 [95% CI 2.15-2.61]), and reduced SGRQ total scores (OR 1.83 [95% CI 1.63-2.05]), and fewer drug-related adverse events (RR 0.53 [95% CI 0.49-0.58]).ConclusionThis systematic review and meta-analysis concludes that UMEC and VI combinations are an efficacious treatment option for symptomatic COPD patients.
Abstract licence: CC BY-NC-ND
Noorduyn SG, Begaj K, Martin A, et al.
2025
IntroductionLong-acting muscarinic antagonist (LAMA) addition to inhaled corticosteroid/long-acting β2-agonist (ICS/LABA) dual therapy is recommended for severe asthma, but its real-world effectiveness is not well established.MethodsA systematic literature review was conducted in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) to investigate clinical outcomes in US adults with asthma receiving ICS + LABA + LAMA as multiple-/single-inhaler triple therapy (MITT/SITT). Real-world/observational studies published in English in Embase/MEDLINE databases (2014-2024) and conference abstracts presented 2022-2024 were eligible for inclusion.ResultsFrom 588 identified records, only 8 articles reporting 6 unique studies were included; 2 assessed SITT and 4 assessed MITT, and 4 treatments were investigated. Exacerbation rates reported in two studies were significantly reduced with tiotropium (TIO) + ICS + LABA MITT versus high-dose ICS + LABA within 6 (64% lower) and 12 months (73%), and fluticasone furoate/umeclidinium/vilanterol (FF/UMEC/VI) 100/62.5/25 mcg SITT versus pre-treatment after 12 months (41%). Oral corticosteroid (OCS) use was reported in two studies. The proportion of patients with ≥ 1 rescue OCS dispensing decreased with TIO 1.25 mcg + ICS + LABA MITT, with greatest reductions for MITT ± leukotriene receptor antagonist (pre-treatment: 68.4%, post treatment: 54.2%). Mean number of OCS dispensings/patient/year significantly decreased (29%, p ConclusionsThis brief communication reports a systematic review that identified few sources of SITT or MITT in US patients with asthma. Although inclusion of observational studies can result in reporting/selection bias, we identified greater clinical benefits with triple therapies versus dual therapies.
Abstract licence: CC BY-NC
Elrosasy A, Zeid MA, Samha R, et al.
2024
- Axilla
- Hyperhidrosis
- Glycopyrrolate
BackgroundHyperhidrosis (HH), characterized by excessive sweating, poses a significant challenge to patients' quality of life. This meta-analysis evaluates the safety and efficacy of topical glycopyrronium bromide (GBP) in treating primary hyperhidrosis, a chronic condition affecting various body regions. Despite its prevalence, primary axillary hyperhidrosis is often undertreated due to a lack of awareness and social stigma.MethodsFollowing PRISMA guidelines, we conducted a systematic review and meta-analysis of randomized controlled trials comparing GBP to a placebo in primary hyperhidrosis patients. Eligibility criteria included outcomes related to perspiration suppression and symptom improvement.ResultsFour RCTs involving 1401 patients were included. GBP significantly increased Hyperhidrosis Disease Severity Scale (HDSS) responders (RR = 2.33, 95% CI [1.99 to 2.74], p ConclusionGBP demonstrated effectiveness in reducing sweat production while improving HDSS and DLQI scores. Adverse events included dry mouth and anticholinergic effects. Dry eye and local skin reactions were not significant, which makes GBP promising in managing primary hyperhidrosis, offering improvements in symptoms and quality of life. While adverse events should be considered, further research with larger sample sizes and long-term follow-up is warranted for comprehensive clinical integration.
Abstract licence: CC BY
Afisi Ismaila, Katrin Haeussler, Alexandrosz Czira, et al.
Advances in Therapy, 2022
- Fluticasone
- Budesonide, Formoterol Fumarate Drug Combination
- Network Meta-Analysis
Marshall J, Sharma A, Darken P, et al.
2023
- Pulmonary Disease, Chronic Obstructive
- Androstadienes
- Benzyl Alcohols
Ioanna Vlachaki, S. Donhauser, A. Madoni, et al.
Health Economics Review, 2025
M. R. Maleki-Yazdi, T. Kaelin, N. Richard, et al.
Respiratory medicine, 2014
- Tiotropium Bromide
- Benzyl Alcohols
- Bronchodilator Agents
Lingling Mao, Yilei Wu, C. Stoumpos, et al.
Journal of the American Chemical Society, 2017
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
11 hours
Mechanism
Umeclidinium is a long-acting muscarinic antagonist, which is often referred to as an anticholinergic.
Food interactions
None known
Human targets
5 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
5 to 15 minutes
Half-life
11 hours
[L44466]
Protein binding
89%
[L44466]
Volume of distribution
86 L
[L44466]
Metabolism
Elimination
58%
Clearance
151 L/h
[L46931]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Maintenance of the airway is controlled by the parasympathetic nervous system, particularly by the abundance of the muscarinic subtype 3 (M3) in the airway smooth muscle.[A7719] Parasympathetic ganglia are associated with the larger airways while postganglionic fibers innervate the smaller diameter bronchioles contributing to airway resistance.[A7719] By blocking the M3 muscarinic receptor, umeclidinium inhibits the binding of acetylcholine and thereby opens up the airways by preventing bronchoconstriction.[A7719] However, even though umeclidinium monotherapy is well-tolerated for up to 14 days, it is more likely to be used in combination therapy, as the international Gold Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines recommended the use of two long-acting bronchodilators with differing mechanisms of action to maximize efficacy and minimize adverse effects.[A7718][A7714]
Umeclidinium was approved by the FDA in April 2014 under the brand name Incruse Ellipta as a standalone product.[L47042] Later, it was further approved as a combination product with [vilanterol] and [vilanterol]/[fluticasone furoate] under the brand name ANORO ELLIPTA and TRELEGY ELLIPTA respectively.[L44461][L44456]. ANORO ELLIPTA was approved in December 2013 while TRELEGY ELLIPTA was approved in September 2017.[L46881][L46886]
[L44466][L46931]
Additionally, umeclidinium also exists as combination products with [vilanterol] or [vilanterol] and [fluticasone furoate].
[L44461][L44456][L46961][L46966]
Both products were indicated for the maintenance treatment of COPD, but only the umeclidinium/[vilanterol]/[fluticasone furoate] product was approved for the maintenance treatment of asthma in patients aged 18 years and older.
[L44461][L44456][L46961][L46966]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 972 interactions
[L44466]
In a perinatal and postnatal developmental study in rats, dams received umeclidinium during late gestation and lactation periods with no evidence of effects on offspring development at doses up to approximately 26 times the MRHDID (on an AUC basis at maternal subcutaneous doses up to 60 mcg/kg/day).
[L44466]
Based on available data, no adjustment of the dosage of umeclidinium in geriatric patients is necessary, but greater sensitivity in some older individuals cannot be ruled out.
Clinical trials of umeclidinium included 810 subjects aged 65 years and older, and, of those, 183 subjects were aged 75 years and older. No overall differences in safety or effectiveness were observed between these subjects and younger subjects, and other reported clinical experience has not identified differences in responses between the elderly and younger subjects.
[L44466]
Umeclidinium produced no treatment-related increases in the incidence of tumors in 2-year inhalation studies in rats and mice at inhaled doses up to 137 and 295/200 mcg/kg/day (male/female), respectively (approximately 20 and 25/20 times the MRHDID in adults on an AUC basis, respectively).
[L44466]
Umeclidinium tested negative in the following genotoxicity assays: the in vitro Ames assay, in vitro mouse lymphoma assay, and in vivo rat bone marrow micronucleus assay.
[L44466]
No evidence of impairment of fertility was observed in male and female rats at subcutaneous doses up to 180 mcg/kg/day and at inhaled doses up to 294 mcg/kg/day, respectively (approximately 100 and 50 times, respectively, the MRHDID in adults on an AUC basis).
[L44466]
No human overdosage data has been reported with umeclidinium High doses of umeclidinium may lead to anticholinergic signs and symptoms.
However, there were no systemic anticholinergic adverse effects following a once-daily inhaled dose of up to 1,000 mcg of umeclidinium (16 times the maximum recommended daily dose) for 14 days in subjects with COPD. Treatment of overdosage consists of discontinuation of INCRUSE ELLIPTA together with institution of appropriate symptomatic and/or supportive therapy.
[L44466]
In clinical trials, the most common adverse effects of umeclidinium were nasopharyngitis, upper respiratory tract infection, cough, and arthralgia. Atrial fibrillation occurred in <1% of patients, but was more common among patients treated with umeclidinium than in those treated with placebo.
Anticholinergics like umeclidinium should be used with caution in patients with narrow-angle glaucoma and in those with prostatic hyperplasia or bladder-neck obstruction. Inhaled medications can cause paradoxical bronchospasm, which can be fatal.
[L44466]
In humans, the M3 receptor has been heavily implicated in the pathophysiology of asthma and COPD. Once the M3 receptor is activated, the phospholipase C would phosphorylate downstream targets, forming inositol 1,4,5-trisphosphate and eventually releasing intracellular Ca2+.[A260091] Increase in intracellular Ca2+ results in muscle contraction, thus worsening COPD and asthma-related bronchoconstriction.[A260091] Additionally, M3 receptor activation also regulates pathways involving CD38, cyclic ADP ribose (cADPR), and ryanodine receptor channels, all of which control the intracellular Ca2+ homeostasis that will lead to muscle contraction.[A260091]
How the body processes this drug — absorption, distribution, metabolism, and elimination
Following repeat dosing of inhaled umeclidinium, steady state was achieved within 14 days with 1.8-fold accumulation.
[L44466]
The absolute bioavailability of inhaled umeclidinium was on average 13% of the dose, with negligible contribution from oral absorption.
[L46931]
[L44466]
[L44466]
[L44466]
[L44466]
[L44466]
[L46931]
Proteins and enzymes this drug interacts with in the body
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that transport this drug across cell membranes
PMID:2897240 PMID:35970996 PMID:8898203 PMID:9038218 PMID:35507548
Catalyzes the flop of phospholipids from the cytoplasmic to the exoplasmic leaflet of the apical membrane. Participates mainly to the flop of phosphatidylcholine, phosphatidylethanolamine, beta-D-glucosylceramides and sphingomyelins .
PMID:8898203
Energy-dependent efflux pump responsible for decreased drug accumulation in multidrug-resistant cells PMID:2897240 PMID:35970996 PMID:9038218
PMID:11388889 PMID:11408531 PMID:12439218 PMID:12719534 PMID:15389554 PMID:16263091 PMID:16272756 PMID:16581093 PMID:19536068 PMID:21128598 PMID:23680637 PMID:24961373 PMID:34040533 PMID:9187257 PMID:9260930 PMID:9655880
Functions as a pH- and Na(+)-independent, bidirectional transporter (By similarity). Cation cellular uptake or release is driven by the electrochemical potential (i.e. membrane potential and concentration gradient) and substrate selectivity (By similarity). Hydrophobicity is a major requirement for recognition in polyvalent substrates and inhibitors (By similarity).
Primarily expressed at the basolateral membrane of hepatocytes and proximal tubules and involved in the uptake and disposition of cationic compounds by hepatic and renal clearance from the blood flow (By similarity). Most likely functions as an uptake carrier in enterocytes contributing to the intestinal elimination of organic cations from the systemic circulation .
PMID:16263091
Transports endogenous monoamines such as N-1-methylnicotinamide (NMN), guanidine, histamine, neurotransmitters dopamine, serotonin and adrenaline .
PMID:12439218 PMID:24961373 PMID:35469921 PMID:9260930
Also transports natural polyamines such as spermidine, agmatine and putrescine at low affinity, but relatively high turnover .
PMID:21128598
Involved in the hepatic uptake of vitamin B1/thiamine, hence regulating hepatic lipid and energy metabolism .
PMID:24961373
Mediates the bidirectional transport of acetylcholine (ACh) at the apical membrane of ciliated cell in airway epithelium, thereby playing a role in luminal release of ACh from bronchial epithelium .
PMID:15817714
Transports dopaminergic neuromodulators cyclo(his-pro) and salsolinol with lower efficency .
PMID:17460754
Also capable of transporting non-amine endogenous compounds such as prostaglandin E2 (PGE2) and prostaglandin F2-alpha (PGF2-alpha) .
PMID:11907186
May contribute to the transport of cationic compounds in testes across the blood-testis-barrier (Probable). Also involved in the uptake of xenobiotics tributylmethylammonium (TBuMA), quinidine, N-methyl-quinine (NMQ), N-methyl-quinidine (NMQD) N-(4,4-azo-n-pentyl)-quinuclidine (APQ), azidoprocainamide methoiodide (AMP), N-(4,4-azo-n-pentyl)-21-deoxyajmalinium (APDA) and 4-(4-(dimethylamino)styryl)-N-methylpyridinium (ASP) PMID:11408531 PMID:15389554 PMID:35469921 PMID:9260930
PMID:9260930 PMID:9687576
Functions as a Na(+)-independent, bidirectional uniporter .
PMID:21128598 PMID:9687576
Cation cellular uptake or release is driven by the electrochemical potential, i.e. membrane potential and concentration gradient .
PMID:15212162 PMID:9260930 PMID:9687576
However, may also engage electroneutral cation exchange when saturating concentrations of cation substrates are reached (By similarity). Predominantly expressed at the basolateral membrane of hepatocytes and proximal tubules and involved in the uptake and disposition of cationic compounds by hepatic and renal clearance from the blood flow .
PMID:15783073
Implicated in monoamine neurotransmitters uptake such as histamine, dopamine, adrenaline/epinephrine, noradrenaline/norepinephrine, serotonin and tyramine, thereby supporting a physiological role in the central nervous system by regulating interstitial concentrations of neurotransmitters .
PMID:16581093 PMID:17460754 PMID:9687576
Also capable of transporting dopaminergic neuromodulators cyclo(his-pro), salsolinol and N-methyl-salsolinol, thereby involved in the maintenance of dopaminergic cell integrity in the central nervous system .
PMID:17460754
Mediates the bidirectional transport of acetylcholine (ACh) at the apical membrane of ciliated cell in airway epithelium, thereby playing a role in luminal release of ACh from bronchial epithelium .
PMID:15817714
Also transports guanidine and endogenous monoamines such as vitamin B1/thiamine, creatinine and N-1-methylnicotinamide (NMN) .
PMID:12089365 PMID:15212162 PMID:17072098 PMID:24961373 PMID:9260930
Mediates the uptake and efflux of quaternary ammonium compound choline .
PMID:9260930
Mediates the bidirectional transport of polyamine agmatine and the uptake of polyamines putrescine and spermidine .
PMID:12538837 PMID:21128598
Able to transport non-amine endogenous compounds such as prostaglandin E2 (PGE2) and prostaglandin F2-alpha (PGF2-alpha) .
PMID:11907186
Also involved in the uptake of xenobiotic 4-(4-(dimethylamino)styryl)-N-methylpyridinium (ASP) .
PMID:12395288 PMID:16394027
May contribute to regulate the transport of organic compounds in testis across the blood-testis-barrier (Probable)
Proteins that carry this drug through the body
PMID:19021548
Major calcium and magnesium transporter in plasma, binds approximately 45% of circulating calcium and magnesium in plasma (By similarity).
Potentially has more than two calcium-binding sites and might additionally bind calcium in a non-specific manner (By similarity). The shared binding site between zinc and calcium at residue Asp-273 suggests a crosstalk between zinc and calcium transport in the blood (By similarity). The rank order of affinity is zinc > calcium > magnesium (By similarity).
Binds to the bacterial siderophore enterobactin and inhibits enterobactin-mediated iron uptake of E.coli from ferric transferrin, and may thereby limit the utilization of iron and growth of enteric bacteria such as E.coli .
PMID:6234017
Does not prevent iron uptake by the bacterial siderophore aerobactin PMID:6234017
Appears to function in modulating the activity of the immune system during the acute-phase reaction
ATC R03AL08
ATC R03AL03
ATC R03BB07
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)
Additional database identifiers
Drugs Product Database (DPD)
22230
ChemSpider
9693858
BindingDB
50267614
ZINC
ZINC000034608502
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1952
GenAtlas
CHRM3
GeneCards
CHRM3
GenBank Gene Database
X15266
GenBank Protein Database
32324
Guide to Pharmacology
15
UniProt Accession
ACM3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1951
GenAtlas
CHRM2
GeneCards
CHRM2
GenBank Gene Database
M16404
GenBank Protein Database
177990
Guide to Pharmacology
14
UniProt Accession
ACM2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1950
GenAtlas
CHRM1
GeneCards
CHRM1
GenBank Gene Database
X52068
GenBank Protein Database
34451
Guide to Pharmacology
13
UniProt Accession
ACM1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1953
GenAtlas
CHRM4
GeneCards
CHRM4
GenBank Gene Database
M16405
GenBank Protein Database
61970253
Guide to Pharmacology
16
UniProt Accession
ACM4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1954
GenAtlas
CHRM5
GeneCards
CHRM5
GenBank Gene Database
M80333
GenBank Protein Database
177988
Guide to Pharmacology
17
UniProt Accession
ACM5_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2625
GenAtlas
CYP2D6
GeneCards
CYP2D6
GenBank Gene Database
M20403
GenBank Protein Database
181350
Guide to Pharmacology
1329
UniProt Accession
CP2D6_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:399
GenAtlas
ALB
GeneCards
ALB
GenBank Gene Database
V00494
GenBank Protein Database
28590
UniProt Accession
ALBU_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8498
GenAtlas
ORM1
GeneCards
ORM1
GenBank Gene Database
X02544
GenBank Protein Database
757907
UniProt Accession
A1AG1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:40
GenAtlas
ABCB1
GeneCards
ABCB1
GenBank Gene Database
M14758
GenBank Protein Database
307180
Guide to Pharmacology
768
UniProt Accession
MDR1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10963
GeneCards
SLC22A1
GenBank Gene Database
X98332
GenBank Protein Database
2511670
Guide to Pharmacology
1019
UniProt Accession
S22A1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10966
GeneCards
SLC22A2
GenBank Gene Database
X98333
GenBank Protein Database
2281942
Guide to Pharmacology
1020
UniProt Accession
S22A2_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