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Last update 28 Nov 2025
Ipratropium Bromide
Last update 28 Nov 2025
Overview
Basic Info
Drug Type Small molecule drug |
Synonyms Ipratropium bromide (USP), Ipratropium Bromide Hydrate, Ipratropium bromide hydrate (JP17) + [8] |
Target |
Action antagonists |
Mechanism mAChRs antagonists(Muscarinic acetylcholine receptor antagonists) |
Therapeutic Areas |
Active Indication |
Inactive Indication |
Originator Organization |
Inactive Organization |
License Organization- |
Drug Highest PhaseApproved |
First Approval Date Japan (25 Oct 1980), |
Regulation- |
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Structure/Sequence
Molecular FormulaC20H32BrNO4 |
InChIKeyKEWHKYJURDBRMN-ZEODDXGYSA-M |
CAS Registry66985-17-9 |
Related
115
Clinical Trials associated with Ipratropium BromideCTR20252731
单中心、随机、开放、两序列、两周期交叉设计评估中国健康研究参与者非炭阻、空腹状态下经口吸入异丙托溴铵吸入气雾剂的生物等效性试验
[Translation] A single-center, randomized, open-label, two-sequence, two-period crossover design to evaluate the bioequivalence of oral ipratropium bromide inhalation aerosol in participants of the China Health Study in the non-carbuncle-free, fasting state
CTR20250540
异丙托溴铵吸入气雾剂人体生物等效性研究
[Translation] Study on the bioequivalence of ipratropium bromide inhalation aerosol in healthy volunteers
CTIS2024-514065-19-00
PHASE III, DOUBLE-BLIND, RANDOMIZED, CONTROLLED, NON-INFERIORITY, PHASE III CLINICAL TRIAL TO EVALUATE THE EFFICACY OF SALBUTAMOL MONOTHERAPY COMPARED TO SALBUTAMOL PLUS IPRATROPIUM BROMIDE IN THE MANAGEMENT OF MODERATE ACUTE ASTHMATIC EXARCEBATIONS IN CHILDREN IN THE EMERGENCY DEPARTMENT
100 Clinical Results associated with Ipratropium Bromide
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100 Translational Medicine associated with Ipratropium Bromide
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100 Patents (Medical) associated with Ipratropium Bromide
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2,214
Literatures (Medical) associated with Ipratropium Bromide18 Oct 2025Cureus Journal of Medical Science
Asthma Management-Induced Diabetic Ketoacidosis: A Case Report
Article
Author: Alzahrani, Abdulrahman Y ; Banoon, Elaf ; Adam, Alyaa M
Diabetic ketoacidosis (DKA) is an acute, life‑threatening complication of diabetes mellitus, often triggered by infection, missed insulin doses, or physiological stress. Less commonly, medications such as glucocorticoids and repeated short‑acting beta‑agonists (SABAs) may precipitate DKA by exacerbating insulin resistance and promoting gluconeogenesis. We describe a 50‑year‑old diabetic woman who presented during the Hajj season with acute respiratory distress, wheezing, and tachycardia and was initially treated as an acute asthma exacerbation with four consecutive nebulized salbutamol/ipratropium and a methylprednisolone 125 mg IV. Although her breathing improved, persistent tachycardia and progressive hyperglycemia led to further work‑up. She had missed her insulin injections for two days prior to admission. Venous blood gas analysis shortly thereafter revealed a pH of 7.21, elevated lactate, and severe hyperglycemia (random glucose >500 mg/dL), confirming DKA. Initiation of standard DKA management (insulin IV, fluid resuscitation, and electrolyte replacement) resulted in stabilization. This case highlights the risk of rapid metabolic decompensation in vulnerable patients even after a single dose of corticosteroids combined with high-dose SABA therapy and insulin omission. Atypical presentation in early DKA may include respiratory alkalosis and wheezing, which can delay diagnosis. Clinicians must maintain a high index of suspicion for DKA in diabetic patients presenting with unexplained tachycardia, respiratory symptoms, or gastrointestinal signs, especially when corticosteroids or SABAs are administered. Early recognition and prompt initiation of appropriate therapy are essential to prevent morbidity and improve outcomes.
12 Sep 2025Scientific Reports
Amitriptyline inhibits bronchoconstriction independent of direct receptor binding and reduces number of caveolae.
Article
Author: Martin, Christian ; Katona, Istvan ; Klein, Virag ; Hempel, Paulina ; Michely, Anna ; Verjans, Eva ; Tenbrock, Klaus
Bronchial asthma is a chronic inflammatory disease with rising prevalence worldwide. Apart from the immunological role of the tricyclic antidepressant amitriptyline in bronchial asthma, there is emerging evidence that inhaled amitriptyline directly reduces acute bronchoconstriction. However, the mechanism by which amitriptyline influences bronchial tone remains poorly understood. To influence bronchoconstriction, rat precision-cut lung slices treated with varying concentrations of amitriptyline (0-5 µM) and incubated with inhibitors targeting different signaling pathways. Amitriptyline reduces acetylcholine- and serotonin-induced bronchoconstriction. Neither the muscarinic antagonist ipratropium nor the phospholipase C inhibitor U73122, nor the protein kinase C inhibitor chelerythrine diminished the effect of amitriptyline. Inhibition of calcium sensitizing and induction failed to alter amitriptyline's effect on bronchoconstriction. Caveolae-as part of the plasma membrane-display a microenvironment, where regulation of signal transduction takes place. Similar to methyl ß cyclodextrin (MBCD), a common substance to destroy caveolae, amitriptyline dramatically reduced the number of caveolae in lung tissue. However, unlike MBCD, this effect could not be explained by cholesterol depletion alone, as cholesterol repletion did not reverse amitriptyline's effect. Furthermore, neither simvastatin (a lipid lowering agent) nor cytochalasin D (an inhibitor of actin polymerization), influenced the inhibitory effect of amitriptyline on bronchoconstriction. In conclusion, amitriptyline inhibits bronchoconstriction independently of direct receptor binding or interaction. It also reduces the total number of caveolae without effects on cholesterol lowering pathways or actin depolymerization. A more general mechanism seems likely, as inhibition of single signal transduction pathways failed. Further studies are required to elucidate the underlying mechanisms.
08 Aug 2025Cureus Journal of Medical Science
Stepwise Management of Status Asthmaticus Refractory to Initial Therapy: A Case Report
Article
Author: Singh, Sumi ; Chowdhury, Shafayath ; Shen, Kevin ; Weissman, Brandon
Asthma is one of the most prevalent chronic respiratory illnesses, significantly impacting patients through shortness of breath and even death. Acute exacerbations are usually controlled with a short-acting beta agonist, such as an albuterol inhaler, as well as long-acting agents to prevent the occurrence of exacerbations and status asthmaticus. Status asthmaticus is an emergent episode of asthma that is refractory to standard treatment. This disease presents as tachycardia, tachypnea, and dyspnea. The forced expiratory volume measures the severity of asthma in one second and the serial peak expiratory flow rate. Proper treatment is vital for patient survival. This case report reviews the proper treatment of a patient in her mid-30s presenting to the emergency department due to an asthmatic attack refractory to albuterol. The patient went through a five-stage treatment plan. First, the patient was treated with inhaled beta-2 agonist (albuterol) and corticosteroids (prednisone, dexamethasone, and methylprednisolone). The patient did not improve with these treatments and was given the anticholinergic agent ipratropium bromide in an attempt to increase bronchodilation. Nebulized racemic epinephrine was then added to the patient to optimize maximum bronchodilation and vasoconstriction in an attempt to reduce airway edema and inflammation. To reduce ventilator peak airway pressures through sedation and paralytics, rocuronium and cisatracurium (Nimbex) were administered. Ketamine was added as a sedative and bronchodilator. Propofol and midazolam (Versed) were used to sedate the patient for mechanical ventilation. After the acute episode, maintenance therapy included inhaled corticosteroids (budesonide), a long-acting beta-2 agonist (arformoterol), a long-acting muscarinic antagonist (revefenacin), and montelukast (a leukotriene receptor antagonist). This case illustrates the importance of status asthmaticus treatment as a vital, stepwise process that focuses on bronchodilation, maintaining the airway, mechanical ventilation, sedation, and reducing inflammation and paralysis.
20
News (Medical) associated with Ipratropium Bromide
05 Jul 2025
Drug Approval
100 Deals associated with Ipratropium Bromide
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External Link
| KEGG | Wiki | ATC | Drug Bank |
|---|---|---|---|
| D02212 | Ipratropium Bromide |
R&D Status
Approved
10 top approved records. to view more data
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| Indication | Country/Location | Organization | Date |
|---|---|---|---|
| Rhinitis, Allergic, Seasonal | United States | 27 Oct 2000 | |
| Common Cold | United States | 20 Oct 1995 | |
| Rhinitis | United States | 20 Oct 1995 | |
| Bronchial Spasm | United States | 29 Sep 1993 | |
| Pulmonary Disease, Chronic Obstructive | United States | 29 Sep 1993 | |
| Asthma | Japan | 25 Oct 1980 | |
| Bronchitis, Chronic | Japan | 25 Oct 1980 | |
| Pulmonary Emphysema | Japan | 25 Oct 1980 |
Developing
10 top R&D records. to view more data
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| Indication | Highest Phase | Country/Location | Organization | Date |
|---|---|---|---|---|
| Dyspnea | Clinical | Canada | 01 Oct 2008 |
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Clinical Result
Clinical Result
Indication
Phase
Evaluation
View All Results
Not Applicable | 141 | (Levalbuterol) | mwmvbblcvz = hptebfufcj lpcycaelhu (xvmjotezsa, tjiwiricgx - pxjdbplzup) View more | - | 16 May 2022 | ||
(Levalbuterol Plus Ipratropium) | mwmvbblcvz = umzqwxurnz lpcycaelhu (xvmjotezsa, pdraafyzrd - afvzkofgnc) View more | ||||||
Phase 4 | 40 | minhbjqfet(gqlrtbbymm) = pjwwovvyrc nqbkghoyay (aklzihdyyb, 25.2) View more | - | 10 Jun 2021 | |||
(Dry Powder Inhaler) | minhbjqfet(gqlrtbbymm) = xqcazsdzdd nqbkghoyay (aklzihdyyb, 19.8) View more | ||||||
Phase 4 | 20 | Placebo (Placebo) | zszjbbdbhg(khvuyfyodv) = yqznzkiotz wstqcixroj (atnqqwvyzv, dweeaadfsb - cszjynafdw) View more | - | 05 Jun 2020 | ||
(Ipratropium Bromide) | zszjbbdbhg(khvuyfyodv) = ymyxfqukac wstqcixroj (atnqqwvyzv, ymhptdcsim - ectlvkpbiy) View more | ||||||
Phase 4 | 20 | (Ipratropium) | tdsjsugoxv(dzctrqljnk) = cgfxwbqlwu towedtofov (dofozuhavi, xtryveopsz - oatdmntwac) View more | - | 12 Oct 2016 | ||
(Theophylline) | tdsjsugoxv(dzctrqljnk) = bqbyobkvdo towedtofov (dofozuhavi, kywzcdspan - fynpiogqcn) View more | ||||||
Phase 4 | 192 | placebo | lqlcvvnbux(fgrckhqlus) = qkuopyjzfq xwjxyzlqcl (dkyvnamphb, 29.35) View more | - | 12 Sep 2016 | ||
Phase 3 | 15 | (Albuterol-sulphate) | hfzsdhxemf(brdvirkwsl) = kmmihigtfz tujvfozrrl (dmvvplnbnc, 13.6) View more | - | 02 Jun 2016 | ||
(Ipratropium-bromide (Atrovent ®)) | hfzsdhxemf(brdvirkwsl) = tcefkwsmur tujvfozrrl (dmvvplnbnc, 10.9) View more | ||||||
Not Applicable | - | Salbutamol, Prednisolone, and Ipratropium Bromide | tfebxlagzw(mkkwzrkssx) = yaxzojwgxk uiyfuskqir (xdzbtyuewi ) View more | - | 01 Feb 2015 | ||
Salbutamol and Prednisolone | tfebxlagzw(mkkwzrkssx) = yhvssptqtr uiyfuskqir (xdzbtyuewi ) View more | ||||||
Phase 4 | 581 | (Symbicort Turbuhaler + Ipratropium + Theophylline SR) | bintdthude(xlnxfbegsd) = hjggmuzcyl iltduosbtp (zevffrfdjw, alktdbqxgp - rivdbmkkct) View more | - | 26 Aug 2014 | ||
(Ipratropium + Theophylline SR) | bintdthude(xlnxfbegsd) = nvxujfciqp iltduosbtp (zevffrfdjw, ljbfolkomv - ubpqccjvdv) View more | ||||||
Phase 4 | 56 | (Albuterol/Salbutamol Followed by Ipratropium) | dknufsgoji(ovmpsciozn) = iqrbaeragd zlqbiusuxi (hbfoslhoub, 0.0394) View more | - | 25 Dec 2013 | ||
(Ipratropium Followed by Albuterol/Salbutamol) | dknufsgoji(ovmpsciozn) = yahclslhgx zlqbiusuxi (hbfoslhoub, 0.0372) View more |
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