| Size | Price | Stock | Qty |
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| 250mg |
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| 500mg |
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| Targets |
Ipratropium bromide acts as a competitive antagonist of muscarinic acetylcholine receptors (mAChRs) in bronchial smooth muscle. By binding to these receptors, it blocks the bronchoconstrictor actions of acetylcholine released from vagal nerve terminals. Anticholinergic agents like ipratropium prevent the increases in intracellular cyclic GMP concentration that result from acetylcholine interaction with muscarinic receptors on bronchial smooth muscle. The bronchodilation following inhalation is primarily a local, site-specific effect rather than a systemic one. Ipratropium bromide does not penetrate the blood-brain barrier due to its quaternary ammonium structure.
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| ln Vitro |
In 15 minutes, ipratropium bromide hydrate (1 nM, 10 nM, 100 nM) causes damage to mitochondrial membrane potential [1]. In 4 hours, ipratropium bromide hydrate (1 nM-1 μM) increases infarct size in ischemia/reperfusion experiments in isolated perfused hearts [1], and in 2 hours, ipratropium bromide hydrate (0.001 nM-0.1 mM) inhibits the growth of adult rat cardiomyocytes following 4 hours of hypoxia [1].
In vitro studies demonstrate that ipratropium bromide competitively binds to cholinergic receptors, thereby blocking the bronchoconstrictor effects of acetylcholine. The compound exhibits concentration-dependent inhibition of acetylcholine-induced contraction in isolated airway smooth muscle preparations. Functional antagonism studies show that ipratropium effectively shifts the acetylcholine concentration-response curve to the right in a competitive manner. The compound's anticholinergic activity is specific to muscarinic receptors, with no significant effects on nicotinic receptors at therapeutic concentrations. |
| ln Vivo |
Ipratropium bromide hydrate (1.0 μg/kg; IV; single dosage) potentiates vagal nerve stimulation that produces bronchoconstriction [2]. Ipratropium bromide hydrate (0.04 mg/20 mL and 0.20 mg/20 mL; inhalation over 30 minutes, rate=30 mL/30 minutes) protects the lungs from cadmium by lowering parenchymal inflammatory infiltration of neutrophils Effects of induced acute neutrophilic inflammation. 4].
In vivo, ipratropium bromide produces significant bronchodilation following inhalation. In controlled 12-week studies in patients with bronchospasm associated with COPD, significant improvements in pulmonary function (FEV1 increases of 15% or more) occurred within 15 to 30 minutes, reached a peak in 1 to 2 hours, and persisted for periods of 4 to 5 hours in the majority of patients. About 25% to 38% of patients demonstrated improvements for at least 7 to 8 hours. Continued effectiveness was demonstrated throughout the 12-week period. Significant increases in forced vital capacity (FVC) have also been demonstrated. |
| Enzyme Assay |
Muscarinic receptor binding assays are performed using membrane preparations from tissues or cells expressing muscarinic receptor subtypes. Radioligand binding studies typically utilize [3H]-N-methylscopolamine or [3H]-QNB as the tracer. Membranes are incubated with varying concentrations of ipratropium bromide and a fixed concentration of radioligand in appropriate binding buffer for 60 minutes at room temperature. Non-specific binding is determined in the presence of 1 μM atropine. Bound radioligand is separated by rapid filtration and counted. Functional assays measure the inhibition of acetylcholine-induced contraction in isolated smooth muscle preparations, where ipratropium causes concentration-dependent rightward shifts of the acetylcholine concentration-response curve.
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| Cell Assay |
Cell viability assay [1]
Cell Types: adult rat cardiomyocytes Tested Concentrations: 0.001 nM-0.1 mM Incubation Duration: 2 hrs (hours) in the dark; 4 hrs (hours) before hypoxia Experimental Results: Cell viability was dose-dependent, and the inhibition rate was at the 0.1 mM dose 52.7%. Cellular assays for anticholinergic activity typically use cell lines expressing muscarinic receptor subtypes (M1-M5). Cells are loaded with calcium-sensitive dyes, and receptor activation is measured by monitoring intracellular calcium increases upon acetylcholine stimulation. Cells are pre-incubated with ipratropium bromide for 10-15 minutes before acetylcholine addition. The compound's antagonist activity is quantified by the degree of inhibition of the acetylcholine-induced calcium response. Alternatively, assays measuring IP3 accumulation or cAMP modulation can be employed depending on the specific muscarinic receptor subtype being studied. |
| Animal Protocol |
Animal/Disease Models: Dunkin Hartley strain guinea pig [2]
Doses: 0.1-1 μg/kg Route of Administration: intravenous (iv) (iv)injection; intravenous (iv) (iv)injection. Single dose Experimental Results: 0.3 μg/kg had little blocking effect on postligation muscarinic receptors, and 0.5 μg/kg inhibited ACh-induced bronchoconstriction. Animal/Disease Models: Male SD (SD (Sprague-Dawley)) rat (300-350 g) [4] Doses: 0.04 mg/20 mL and 0.20 mg/20 mL Route of Administration: Inhalation; Inhalation; Nebulization rate 30 mL/30 minutes; 30 minute Experimental Results: Has no significant effect on any parameters recorded in healthy rats, but has a protective effect on cadmium-induced inflammatory responses. In vivo efficacy is typically evaluated in animal models of bronchoconstriction, such as guinea pigs or rats challenged with acetylcholine, histamine, or other bronchoconstrictor agents. Ipratropium is administered via inhalation or intravenous routes, and airway resistance or pulmonary function parameters are measured. In humans, clinical studies involve inhalation administration to patients with COPD or asthma, with spirometry measurements (FEV1, FVC) conducted at multiple time points post-dose. Twelve-week controlled studies are standard for evaluating long-term efficacy and safety. Inhaled doses typically range from 20-80 μg per administration. |
| ADME/Pharmacokinetics |
Following nebulization of a 2 mg dose, approximately 7% of the dose is absorbed into the systemic circulation either from the lung surface or from the gastrointestinal tract. Much of the administered dose is swallowed but not absorbed, as shown by fecal excretion studies. The elimination half-life is approximately 1.6 hours after intravenous administration. Ipratropium bromide is minimally (0 to 9% in vitro) bound to plasma albumin and α1-acid glycoproteins. It is partially metabolized. Autoradiographic studies in rats have shown that ipratropium bromide does not penetrate the blood-brain barrier. Peak plasma concentrations following inhalation are low (approximately 59 pg/mL).
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| Toxicity/Toxicokinetics |
Ipratropium bromide is generally well-tolerated. Common adverse effects are related to its anticholinergic activity and include dry mouth, cough, and throat irritation. Because of its quaternary ammonium structure and poor systemic absorption, systemic anticholinergic side effects are minimal at recommended doses. Preclinical and clinical evidence suggest no deleterious effect on airway mucous secretion, mucociliary clearance, or gas exchange. The compound has not been extensively studied in patients with hepatic or renal insufficiency and should be used with caution in those populations.
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| References |
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| Additional Infomation |
Ipratropium bromide hydrate is the monohydrate form of ipratropium bromide. Ipratropium bromide is an anticholinergic drug that blocks muscarinic cholinergic receptors in the smooth muscle of the bronchi in the lungs, thereby dilating the bronchi and relieving symptoms of chronic obstructive pulmonary disease and acute asthma. It is both a muscarinic receptor antagonist and a bronchodilator. It contains ipratropium bromide. Ipratropium bromide is a muscarinic receptor antagonist with a structure related to atropine, but it is generally considered safer and more effective when inhaled. It is used to treat various bronchial diseases, rhinitis, and can be used as an antiarrhythmic drug. See also: Ipratropium bromide (note moved to).
Ipratropium bromide is FDA-approved for the treatment of bronchospasm associated with COPD and is available under brand names including Atrovent. It is also used off-label for asthma, particularly in acute exacerbations in combination with beta-agonists. Clinical trials have demonstrated its efficacy in both COPD and asthma patients. It is often used in fixed-dose combinations with albuterol sulfate for symptomatic management of bronchospasm in patients requiring a second bronchodilator. The compound is on the WHO Model List of Essential Medicines. |
| Molecular Formula |
C20H32BRNO4
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| Molecular Weight |
430.3764
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| Exact Mass |
413.156
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| CAS # |
66985-17-9
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| Related CAS # |
Ipratropium bromide;22254-24-6;Ipratropium-d3 bromide;Ipratropium-d7 bromide
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| PubChem CID |
16738693
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| Appearance |
White to off-white solid powder
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| LogP |
0.026
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| Hydrogen Bond Donor Count |
2
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| Hydrogen Bond Acceptor Count |
5
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| Rotatable Bond Count |
6
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| Heavy Atom Count |
26
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| Complexity |
430
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| Defined Atom Stereocenter Count |
2
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| SMILES |
[Br-].O(C(C([H])(C1C([H])=C([H])C([H])=C([H])C=1[H])C([H])([H])O[H])=O)C1([H])C([H])([H])C2([H])C([H])([H])C([H])([H])C([H])(C1([H])[H])[N+]2(C([H])([H])[H])C([H])(C([H])([H])[H])C([H])([H])[H].O([H])[H]
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| InChi Key |
KEWHKYJURDBRMN-XFQAGIBXSA-M
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| InChi Code |
InChI=1S/C20H30NO3.BrH.H2O/c1-14(2)21(3)16-9-10-17(21)12-18(11-16)24-20(23)19(13-22)15-7-5-4-6-8-15;;/h4-8,14,16-19,22H,9-13H2,1-3H3;1H;1H2/q+1;;/p-1/t16-,17+,18?,19?,21?;;
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| Chemical Name |
[(1R,5S)-8-methyl-8-propan-2-yl-8-azoniabicyclo[3.2.1]octan-3-yl] 3-hydroxy-2-phenylpropanoate;bromide;hydrate
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: Please store this product in a sealed and protected environment, avoid exposure to moisture. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
H2O : ~62.5 mg/mL (~145.22 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: 50 mg/mL (116.18 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with sonication.
(Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.3235 mL | 11.6176 mL | 23.2353 mL | |
| 5 mM | 0.4647 mL | 2.3235 mL | 4.6471 mL | |
| 10 mM | 0.2324 mL | 1.1618 mL | 2.3235 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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