Ipratropium bromide 500micrograms/2ml nebuliser liquid unit dose vials
Requires a prescription from a doctor or prescriber
Safety information for pregnancy and breastfeeding
Pregnancy
Ipratropium was not shown to present carcinogenesis, teratogenesis not mutagenesis potential and it did not present effects on fertility.
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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Safety monitoring data
Yellow Card reports
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Suspected adverse reactions reported for Ipratropium
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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 Ipratropium
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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.
23 branded products available
Part of the Atrovent brand family (generic: Ipratropium)
MHRA licensed products
View all licensed products for Ipratropium on the MHRA register
Atrovent 500micrograms/2ml nebuliser liquid UDVs
Ipratropium 500micrograms/2ml nebuliser liquid Steri-Neb unit dose vials
Ipratropium bromide 500micrograms/2ml nebuliser liquid unit dose vials
Ipratropium bromide 500micrograms/2ml nebuliser liquid unit dose vials
Ipratropium bromide 500micrograms/2ml nebuliser liquid unit dose vials
Ipratropium bromide 500micrograms/2ml nebuliser liquid unit dose vials
Ipratropium bromide 500micrograms/2ml nebuliser liquid unit dose vials
Ipratropium bromide 500micrograms/2ml nebuliser liquid unit dose vials
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)
300 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 BNF/ATC 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
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(1)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
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Supply & safety information
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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
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 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: 13 · 1975–2026
Showing the 50 most relevant studies, sorted by most relevant.
Gustavo J. Rodrigo, Carlos Rodrigo, Omar Burschtin
The American Journal of Medicine, 1999
- Acute Disease
- Administration, Inhalation
- Adrenergic beta-Agonists
R.Gordon Stoodley, Shawn D. Aaron, Robert Dales
Annals of Emergency Medicine, 1999
- Acute Disease
- Administration, Inhalation
- Adrenergic beta-Agonists
Patrick El Khoury, W. A. Abou Hamad, M. Khalaf, et al.
The Laryngoscope, 2023
Hamud AA, Mudawi K, Powell C, et al.
2026
- Asthma
- Ipratropium
- Bronchodilator Agents
Shawn D. Aaron, Shawn D. Aaron
Journal of Asthma, 2001
- Acute Disease
- Administration, Inhalation
- Adrenergic beta-Agonists
Hongzhen Xu, L. Tong, P. Gao, et al.
PLoS ONE, 2020
Gong J, Nie N, Jiang M, et al.
2025
- Ipratropium
- Budesonide
- Heparin
Moustafa HAM, Elbery FH, Al Meslamani AZ, et al.
2025
Objectives: There is a scarcity of pharmacological treatments that efficiently address lung injury in individuals experiencing acute respiratory distress syndrome (ARDS). Early inhaled corticosteroids and ipratropium may reduce pulmonary inflammation and injury of the lungs, minimizing the risk of ARDS. Method: This is a double-blinded randomized control trial conducted on patients at risk of ARDS. Patients were randomly allocated into two groups; the intervention group (63 patients) were administered aerosolized budesonide and ipratropium bromide, and the control group (56) were administered a placebo every eight hours for five days. Alteration in oxygen saturation divided by inspired oxygen (Fio2) (S/F) after five days was the primary outcome. Secondary outcomes included ARDS occurrence, mechanical ventilation (MV) requirement, hospital stay duration, and mortality rates. Results: Of the 604 screened, only 119 patients were included. The intervention group (63 patients) S/F ratio recovered versus the fall of the control group. Both groups had similar organ dysfunction and 28-day mortality. The intervention group had significantly (p Conclusions: The administration of inhaled budesonide and ipratropium bromide improved oxygenation, as assessed by the S/F ratio, and significantly reduced the rate of ARDS development and the requirement of MV versus the control group. Larger multi-center trials including diverse patient populations are needed to validate these results.
Abstract licence: CC BY
Mohammad-Gholizad F, Karimzadeh I, Moghimi-Sarani E, et al.
2024
- Sialorrhea
- Clozapine
- Antipsychotic Agents
Iramain R, Castro-Rodriguez JA, Ortiz J, et al.
2026
- Asthma
- Bronchodilator Agents
- Metered Dose Inhalers
ObjectiveTo evaluate the effectiveness of a new device (SOBIstat-F®) for bronchodilator administration via pMDI compared with the conventional method.IntroductionProtocols for managing severe asthma exacerbations include bronchodilators (short-acting beta-2 agonists and ipratropium bromide) administered by nebulizer or pressurized metered-dose inhaler(pMDI) with a valved holding chamber, corticosteroids IV, and magnesium sulfate IV.MethodsA randomized superiority clinical trial was conducted in children with severe acute asthma at the emergency department. Patients were assigned to one of the following groups: pMDI-SOBx, in which they received bronchodilators in pMDI through the SOBIstat-F® device, or in pMDI with oxygen via cannula or mask (pMDI-OxStand). The primary outcome was the need for hospitalization at the end of 8 h.Results84 patients participated in the study, of which 43 were treated with the pMDI-SOBx device and 41 with pMDI-OxStand. There were no baseline differences between the groups. Children treated with pMDI-SOBx had a lower hospitalization rate compared to those with pMDI-OxStand (9.3% vs. 26.8%, respectively, p = 0.036; absolute risk difference: -17.5% [95% CI: -33.6 to -1.4] and OR: 0.26 [95% CI: 0.08-0.91]). Additionally, a significant clinical improvement (pulmonary score) was observed from 90 min (p p ConclusionsFor the first time, bronchodilator administration using the SOBIstat-F® device was more effective than the conventional method in reducing hospitalizations and improving the clinical condition of children with severe asthma exacerbations.
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
1.6 hours
Mechanism
Ipratropium acts as an antagonist of the muscarinic acetylcholine receptor.
Food interactions
None known
Human targets
3 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
1-2%
Half-life
1.6 hours
[A176945]
Protein binding
0-9%
Volume of distribution
4.6 L/kg
[L5909]
Metabolism
90%
[A176945]…
Elimination
80-100%
[A176945]…
Clearance
2.3 L
[L5909]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Ipratropium as a therapeutic agent was developed by Boehringer Ingelheim and its first monotherapy product was FDA approved in 1986, while the combination product of ipratropium and [albuterol] was approved in 1996.[L5894][L5891]
[A176939]
Asthma exacerbations are characterized by a progressive increase in one or more of asthma symptoms accompanied by a decrease in expiratory flow.
[L5900]
As a single agent, ipratropium was indicated for the symptomatic relief of rhinorrhea associated with the common cold or seasonal allergic rhinitis for patients 5 years or older. It does not alleviate nasal congestion nor sneezing.[FDA label]
Rhinorrhea refers to recurrent or chronic watery nasal discharge. This condition is debilitating and its pathogenesis and etiology is complex and not very well understood presenting very substantial cost burden.
[L5903]
Additionally, ipratropium is indicated as a bronchodilator for maintenance treatment of bronchospasm associated with chronic obstructive pulmonary disease including chronic bronchitis and emphysema.[FDA label]
The chronic obstructive pulmonary disease includes a large number of conditions characterized by breathlessness.
As this includes several conditions, the etiology, symptoms, and treatments are diverse.
[L5906]
Ipratropium has also been studied to be used for the treatment of sialorrhea.
[A176942]
Sialorrhea is a common symptom that accompanies different neurologic conditions and it is characterized by drooling or excessive salivation.
[A176963]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 513 interactions
Ipratropium was not shown to present carcinogenesis, teratogenesis not mutagenesis potential and it did not present effects on fertility. The only effect after high administration of ipratropium was a reduction in the conception rate.[FDA label]
At the cellular level, the diameter of the airways is controlled by the release of acetylcholine into the muscle cells causing them to contract and producing a narrow airway. Thus administration of ipratropium stops the activity of acetylcholine in the smooth muscle preventing the contraction and producing relaxed airways.T457
In clinical trials where ipratropium was used in the initial management of status asthmaticus, it was demonstrated a clear benefit in pulmonary function in children and adults. However, the continuous use of ipratropium after an acute asthmatic attack is not proven to be significantly advantageous[A176939] nor the prophylactic administration of this agent.T542
How the body processes this drug — absorption, distribution, metabolism, and elimination
Serum levels of ipratropium after oral or inhaled administration are very low, corresponding to only 1-2% of the administered dose. These low levels peak after 1-2 hours and it presents a low bioavailability of 2%.T542
[A176945]
[L5909]
[A176945]
From the orally administered dose, about 90% of the dose is excreted unchanged. The absorbed portion is partially metabolized by ester hydrolysis to inactive metabolites, tropic acid and tropane.T85
[A176945]
From the urine eliminated portion, almost all the drug is found unchanged.T542
However, when ipratropium is orally administered, due to its low absorption, most of the dose is recovered in the feces with a very minimal amount found in the urine.T542
[L5909]
Proteins and enzymes this drug interacts with in the body
Proteins that transport this drug across cell membranes
PMID:10454528 PMID:10525100 PMID:10966938 PMID:17509700 PMID:20722056 PMID:33124720
Also transports organic cations such as tetraethylammonium (TEA) without the involvement of sodium.
Relative uptake activity ratio of carnitine to TEA is 11.3 .
PMID:10454528 PMID:10525100 PMID:10966938
In intestinal epithelia, transports the quorum-sensing pentapeptide CSF (competence and sporulation factor) from B.subtilis which induces cytoprotective heat shock proteins contributing to intestinal homeostasis .
PMID:18005709
May also contribute to regulate the transport of organic compounds in testis across the blood-testis-barrier (Probable)
PMID:10215651 PMID:15107849 PMID:15795384 PMID:16729965 PMID:20601551 PMID:22206629 PMID:22569296 PMID:29530864
Functions as a Na(+)-dependent and pH-dependent high affinity microbial symporter of potent food-derived antioxidant ergothioeine .
PMID:15795384 PMID:29530864 PMID:33124720
Transports one sodium ion with one ergothioeine molecule (By similarity). Involved in the absorption of ergothioneine from the luminal/apical side of the small intestine and renal tubular cells, and into non-parenchymal liver cells, thereby contributing to maintain steady-state ergothioneine level in the body .
PMID:20601551
Also mediates the bidirectional transport of acetycholine, although the exact transport mechanism has not been fully identified yet .
PMID:22206629
Most likely exports anti-inflammatory acetylcholine in non-neuronal tissues, thereby contributing to the non-neuronal cholinergic system .
PMID:22206629 PMID:22569296
Displays a general physiological role linked to better survival by controlling inflammation and oxidative stress, which may be related to ergothioneine and acetycholine transports .
PMID:15795384 PMID:22206629
May also function as a low-affinity Na(+)-dependent transporter of L-carnitine through the mitochondrial membrane, thereby maintaining intracellular carnitine homeostasis .
PMID:10215651 PMID:15107849 PMID:16729965
May contribute to regulate the transport of cationic compounds in testis across the blood-testis-barrier PMID:35307651
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 R03BB01
ATC R01AX03
ATC R03AL01
ATC R03AL02
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)
Ipratropium
Additional database identifiers
Drugs Product Database (DPD)
1945
ChemSpider
19962157
Guide to Pharmacology
325
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: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: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: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:8499
GeneCards
ORM2
GenBank Gene Database
BC015964
GenBank Protein Database
16359000
UniProt Accession
A1AG2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10969
GenAtlas
SLC22A5
GeneCards
SLC22A5
GenBank Gene Database
AF057164
GenBank Protein Database
3273741
UniProt Accession
S22A5_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10968
GenAtlas
SLC22A4
GeneCards
SLC22A4
GenBank Gene Database
AB007448
GenBank Protein Database
2605501
UniProt Accession
S22A4_HUMAN
DrugBank citations
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Structured knowledge from the free knowledge base
Linked open data from Wikidata (Q424294), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication.