Bopindolol
Bopindolol ((±)-Bopindolol) is an orally active antagonist of β-adrenoceptors (ARs) with partial agonist activity. Bopindolol is non-selective for β1- and β2-ARs and has low affinity for β3-AR subtype. Bopindolol has intrinsic sympathomimetic as well as membrane stabilizing actions, inhibits renin secretion, and interacts with 5-HT receptors. Bopindolol is a proagent of Pindolol (HY-B0982). Bopindolol can be used for essential and renovascular hypertension research.
For research use only. We do not sell to patients.
- CAS No.: 62658-63-3
- Formula: C23H28N2O3
- Molecular Weight:380.48
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
IC50 & Target
[1]|
β2 adrenoceptor |
Beta-1 adrenergic receptor |
Beta-3 adrenergic receptor |
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Male Wistar rats (260-300 g)[2]
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Dosage:0.3, 1 and 3 mg/kg
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Administration:IP; single dosage
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Result:Produced dose dependent decreases in diastolic blood pressure, and the decrease of about 8 mmHg at 3 mg/kg.
Decreased the heart rate in a dose-dependent manner.
Chemical Information
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CAS No. 62658-63-3
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Molecular Weight 380.48
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Formula C23H28N2O3
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SMILES
CC(N1)=CC2=C1C=CC=C2OCC(OC(C3=CC=CC=C3)=O)CNC(C)(C)C
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Synonyms
(±)-Bopindolol
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Research Protocol for Cardiovascular Diseases
Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.
Purity & Documentation
References
[1]. Harron DW, et al. Bopindolol. A review of its pharmacodynamic and pharmacokinetic properties and therapeutic efficacy. Drugs. 1991 Jan;41(1):130-49. [Content Brief]
[2]. H Tanaka, et al. Hypotensive effect of bopindolol in pithed rats. Gen Pharmacol. 1993 Mar;24(2):373-5. [Content Brief]
[3]. Y Hosohata, et al. Bopindolol is a slowly dissociating beta 1-adrenoceptor antagonist when compared to other beta-blockers. Biol Pharm Bull. 1995 Aug;18(8):1066-71. [Content Brief]
[4]. Nagatomo T, et al. Bopindolol: pharmacological basis and clinical implications. Cardiovasc Drug Rev. 2001 Spring;19(1):9-24. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Bopindolol Related Classifications
HY-B1562 Related Classifications
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