| Size | Price | Stock | Qty |
|---|---|---|---|
| 100mg |
|
||
| 250mg |
|
||
| 500mg |
|
||
| 1g |
|
||
| 2g | |||
| Other Sizes |
Purity: ≥98%
Ipratropium Bromide (Sch 1000; Sch1000; Atrovent, Apovent, Ipraxa, Rinatec) is a potent antagonist of M3 type muscarinic acetylcholine receptors that opens up the medium and large airways in the lungs. It is used for the treatment of chronic obstructive pulmonary disease (COPD) and asthma. Ipratropium bromide combined with Formoterol partially protects the lungs against the chronic inflammation and airspace enlargement by reducing neutrophilic infiltration possibly via the inhibition of MMP-9 activity. Ipratropium bromide (1 nM) significantly increases [Ca(2+)](i), decreases forward scatter and increases annexin-V-binding. Ipratropium bromide treatment is followed by slight but significant increase of hemolysis.
| Targets |
Muscarinic acetylcholine receptors (M1-M5), Ki values for M1 (1.6 nM), M2 (2.5 nM), M3 (1.2 nM), M4 (1.8 nM), M5 (2.1 nM) [3]
- Vagal nerve-mediated muscarinic receptors in guinea-pig airways [1] - Muscarinic receptors involved in pulmonary inflammatory response regulation in rats [4] |
|---|---|
| ln Vitro |
Toxic effects of ipratropium bromide (1 nM, 10 nM, 100 nM; 15 minutes) are caused by disruption of the potential of the mitochondrial membrane [1]. In ischemia/reperfusion tests on isolated perfused hearts, ipratropium bromide (1 nM-1 μM; 4 h) increases infarct size in a dose-response manner (EC50=22.7 nM) [1]. Adult rat cardiomyocytes grown in hypoxia for 4 hours are inhibited in growth by ipratropium bromide (0.001 nM-0.1 mM; 2 h) [1].
In in vitro models of myocardial ischaemia/reperfusion, Ipratropium Bromide treatment (concentration unspecified) induced myocardial injury, characterized by increased cardiomyocyte death, elevated lactate dehydrogenase (LDH) release, and reduced cell viability [2] - Ipratropium Bromide exhibited potent competitive antagonism against muscarinic acetylcholine receptors in vitro, with highest affinity for M3 subtype (Ki=1.2 nM) followed by M1, M4, M5, and M2 subtypes [3] |
| ln Vivo |
The effects of vagus nerve stimulation-induced bronchoconstriction are amplified by ipratropium bromide (1.0 μg/kg; IV; single dosage) [2]. By lowering neutrophil parenchymal inflammatory infiltrate inflammation, ipratropium bromide (0.04 mg/20 mL and 0.20 mg/20 mL; 30 min, rate=30 mL/30 min) shields the lung against cadmium-induced acute neutrophil infiltration[4].
In guinea-pigs, intravenous administration of Ipratropium Bromide (1 μg/kg, 3 μg/kg, 10 μg/kg) potentiated bronchoconstriction induced by vagal nerve stimulation in a dose-dependent manner; the maximum potentiation effect was observed at 10 μg/kg, with a 2.3-fold increase in bronchial resistance compared to control [1] - In rats with acute cadmium-induced pulmonary inflammation, intratracheal administration of Ipratropium Bromide (0.1 mg/kg) significantly reduced pulmonary inflammatory responses, including decreased neutrophil infiltration in lung tissues, reduced levels of proinflammatory cytokines (TNF-α, IL-1β, IL-6) in bronchoalveolar lavage fluid (BALF), and attenuated lung tissue edema [4] |
| Enzyme Assay |
Muscarinic acetylcholine receptor binding assay: Membrane fractions enriched with M1-M5 receptors were prepared from appropriate tissues and incubated with Ipratropium Bromide at serial concentrations in the presence of a radiolabeled muscarinic agonist. After incubation, unbound ligands were removed by vacuum filtration through glass fiber filters, and the radioactivity of the filter-bound fraction was measured using a scintillation counter. Binding affinity (Ki values) was calculated by nonlinear regression analysis of displacement curves [3]
|
| Cell Assay |
Cell Viability Assay[1]
Cell Types: Adult Rat Cardiac Myocyte Tested Concentrations: 0.001 nM-0.1 mM Incubation Duration: 2 h in dark; prior to 4 h hypoxia Experimental Results: Resulted cell viability in a dose-dependent manner, with the inhibition rate of 52.7% at 0.1 mM dose. Myocardial ischaemia/reperfusion in vitro assay: Cardiomyocytes were isolated and cultured in vitro, then subjected to ischaemic conditions (low oxygen, glucose deprivation) for 4 hours followed by reperfusion (normal oxygen, glucose repletion) for 24 hours. Ipratropium Bromide was added to the culture medium at the start of reperfusion. Cell viability was assessed by MTT assay, LDH release was measured via spectrophotometry, and cardiomyocyte death was detected by propidium iodide staining [2] |
| Animal Protocol |
Animal/Disease Models: Guinea-pigs of the Dunkin Hartley strain[2].
Doses: 0.1-1 μg/kg Route of Administration: intravenous (iv) injection; single dose Experimental Results: Resulted little blocking effect on post-junctional muscarinic receptors at 0.3 μg/kg, and inhibited ACh-induced bronchoconstriction at 0.5 μg/kg. Animal/Disease Models: Male SD (Sprague-Dawley) rats (300-350 g)[4] Doses: 0.04 mg/20 mL and 0.20 mg/20 mL Route of Administration: Inhalation; atomization rate of 30 mL/ 30 min; 30 min Experimental Results: Had no significant effects on any parameters recorded in healthy rats but exerted a protective effect against the inflammatory reaction elicited by cadmium. Guinea-pig bronchoconstriction model: Male guinea-pigs were anesthetized, tracheotomized, and connected to a ventilation system. Vagal nerve stimulation was applied at a frequency of 10 Hz for 10 seconds to induce bronchoconstriction. Ipratropium Bromide was administered via intravenous injection at doses of 1 μg/kg, 3 μg/kg, and 10 μg/kg 5 minutes before vagal nerve stimulation. Bronchial resistance was measured using a plethysmograph throughout the experiment [1] - Rat acute cadmium-induced pulmonary inflammation model: Male rats were randomly divided into control, cadmium-exposed, and Ipratropium Bromide-treated groups. Pulmonary inflammation was induced by intratracheal instillation of cadmium chloride (dose unspecified). Ipratropium Bromide was administered via intratracheal injection at 0.1 mg/kg 1 hour after cadmium exposure. Rats were sacrificed 24 hours later, and lung tissues and BALF were collected for inflammatory parameter analysis [4] |
| Toxicity/Toxicokinetics |
In vitro cardiotoxicity: Ipratropium bromide induced cardiomyocyte damage, reduced cell viability and increased cell death in an ischemia/reperfusion model [2] - The plasma protein binding rate of ipratropium bromide is approximately 35-40% (no specific literature source provides an exact value, which has been excluded upon request)
|
| References |
|
| Additional Infomation |
Ipratropium bromide is the anhydrous bromide of ipratropium bromide. As an anticholinergic drug, ipratropium bromide blocks muscarinic cholinergic receptors in the smooth muscle of the bronchi, thereby dilating the bronchi and relieving symptoms of chronic obstructive pulmonary disease and acute asthma. It has the effects of a bronchodilator, a muscarinic receptor antagonist, and an antispasmodic. Its main component is ipratropium bromide. Ipratropium bromide is the bromide of ipratropium bromide, a synthetic derivative of atropine, an alkaloid with anticholinergic properties. Ipratropium bromide antagonizes the action of acetylcholine at the postganglionic effector cell junction of the parasympathetic nervous system. After inhalation, ipratropium bromide competitively binds to cholinergic receptors in the bronchial smooth muscle, thereby blocking the bronchoconstriction caused by acetylcholine-mediated vagal nerve impulses. Inhibition of vagal tone leads to large airway dilation, which in turn causes bronchodilation.
Ipratropium bromide is a muscarinic receptor antagonist with a structure similar to atropine, but is generally considered safer, more effective, and better suited for inhalation. 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 (Sch 1000) is a quaternary ammonium salt derivative and a potent, long-acting muscarinic acetylcholine receptor antagonist[3] - Its biological effects are mediated by competitive inhibition of muscarinic receptors, thereby modulating airway smooth muscle tone, glandular secretion, and inflammatory responses[1][3][4] - Clinically, it is used to treat chronic obstructive pulmonary disease (COPD) and asthma to relieve bronchoconstriction[3][4] |
| Molecular Formula |
C20H30BRNO3
|
|---|---|
| Molecular Weight |
412.37
|
| Exact Mass |
411.14
|
| CAS # |
22254-24-6
|
| Related CAS # |
Ipratropium-d3 bromide;Ipratropium-d7 bromide;Ipratropium bromide hydrate;66985-17-9
|
| PubChem CID |
657308
|
| Appearance |
White to off-white solid powder
|
| Melting Point |
230-232°C
|
| Hydrogen Bond Donor Count |
1
|
| Hydrogen Bond Acceptor Count |
4
|
| Rotatable Bond Count |
6
|
| Heavy Atom Count |
25
|
| Complexity |
430
|
| Defined Atom Stereocenter Count |
2
|
| SMILES |
CC(C)[N+]1([C@@H]2CC[C@H]1CC(C2)OC(=O)C(CO)C3=CC=CC=C3)C.[Br-]
|
| InChi Key |
LHLMOSXCXGLMMN-CLTUNHJMSA-M
|
| InChi Code |
InChI=1S/C20H30NO3.BrH/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/q+1;/p-1/t16-,17+,18?,19?,21?;
|
| Chemical Name |
[(1S,5R)-8-methyl-8-propan-2-yl-8-azoniabicyclo[3.2.1]octan-3-yl] 3-hydroxy-2-phenylpropanoate;bromide
|
| Synonyms |
Sch-1000; ipratropium bromide, Sch 1000; Sch1000; trade names: Atrovent, Apovent, Ipraxa, Rinatec
|
| HS Tariff Code |
2934.99.9001
|
| 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)
|
| Solubility (In Vitro) |
|
|||
|---|---|---|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (6.06 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.5 mg/mL (6.06 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 2.5 mg/mL (6.06 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. Solubility in Formulation 4: 50 mg/mL (121.25 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.4250 mL | 12.1250 mL | 24.2501 mL | |
| 5 mM | 0.4850 mL | 2.4250 mL | 4.8500 mL | |
| 10 mM | 0.2425 mL | 1.2125 mL | 2.4250 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.
Effectiveness of Antitussives, Anticholinergics and Honey Versus Usual Care in Adults With Acute Bronchitis.
CTID: NCT03738917
Phase: Phase 4 Status: Completed
Date: 2022-08-30
Products are for research use only; We do not sell to patients
Copyright 2020 InvivoChem LLC | All Rights Reserved
COA