318-98-9
Chemical Structure
Propranolol hydrochloride
- CAS No.: 318-98-9
- Formula:C16H22ClNO2
- Molecular Weight:295.80
IUPAC Name: 1-(isopropylamino)-3-(naphthalen-1-yloxy)propan-2-ol hydrochloride
InChIKey: ZMRUPTIKESYGQW-UHFFFAOYSA-N
SMILES: OC(CNC(C)C)COC1=CC=CC2=CC=CC=C12.Cl
Biological Activity: Propranolol hydrochloride is a nonselective and BBB-permeableβ-adrenergic receptor (βAR) antagonist, has high affinity for the β1AR and β2AR with Ki values of 1.8 nM and 0.8 nM, respectively. Propranolol hydrochloride inhibits [3H]-DHA binding to rat brain membrane preparation with an IC50 of 12 nM. Propranolol hydrochloride is used for study of hypertension, pheochromocytoma, myocardial infarction, cardiac arrhythmias, angina pectoris, and hypertrophic cardiomyopathy[1][2][3][4][5].
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Propranolol hydrochloride | 99.95% | Propranolol hydrochloride is a nonselective and BBB-permeableβ-adrenergic receptor (βAR) antagonist, has high affinity for the β1AR and β2AR with Ki values of 1.8 nM and 0.8 nM, respectively. Propranolol hydrochloride inhibits [3H]-DHA binding to rat brain membrane preparation with an IC50 of 12 nM. Propranolol hydrochloride is used for study of hypertension, pheochromocytoma, myocardial infarction, cardiac arrhythmias, angina pectoris, and hypertrophic cardiomyopathy. | ||||||||||||||||||||
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Propranolol hydrochloride (Standard) | 99.93% | Propranolol (hydrochloride) (Standard) is the analytical standard of Propranolol (hydrochloride). This product is intended for research and analytical applications. Propranolol hydrochloride is a nonselective β-adrenergic receptor (βAR) antagonist, has high affinity for the β1AR and β2AR with Ki values of 1.8 nM and 0.8 nM, respectively. Propranolol hydrochloride inhibits [3H]-DHA binding to rat brain membrane preparation with an IC50 of 12 nM. Propranolol hydrochloride is used for study of hypertension, pheochromocytoma, myocardial infarction, cardiac arrhythmias, angina pectoris, and hypertrophic cardiomyopathy. | ||||||||||||||||||||
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Propranolol-d7 (ring-d7) | 99.71% | Propranolol-d7 (ring-d7) is the deuterium labeled Propranolol hydrochloride. Propranolol hydrochloride is a nonselective β-adrenergic receptor (βAR) antagonist, has high affinity for the β1AR and β2AR with Ki values of 1.8 nM and 0.8 nM, respectively. Propranolol hydrochloride inhibits [3H]-DHA binding to rat brain membrane preparation with an IC50 of 12 nM. Propranolol hydrochloride is used for study of hypertension, pheochromocytoma, myocardial infarction, cardiac arrhythmias, angina pectoris, and hypertrophic cardiomyopathy. | ||||||||||||||||||||
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Propranolol-d7 hydrochloride | 98.47% | Propranolol-d7 (hydrochloride) is a deuterium labeled Propranolol hydrochloride. Propranolol hydrochloride is a nonselective β-adrenergic receptor (βAR) antagonist, has high affinity for the β1AR and β2AR with Ki values of 1.8 nM and 0.8 nM, respectively. Propranolol hydrochloride inhibits [3H]-DHA binding to rat brain membrane preparation with an IC50 of 12 nM. Propranolol hydrochloride is used for the study of hypertension, pheochromocytoma, myocardial infarction, cardiac arrhythmias, angina pectoris, and hypertrophic cardiomyopathy. | ||||||||||||||||||||
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- [1]. Galandrin S, et al. Distinct signaling profiles of beta1 and beta2 adrenergic receptor ligands toward adenylyl cyclase and mitogen-activated protein kinase reveals the pluridimensionality of efficacy. Mol Pharmacol. 2006 Nov;70(5):1575-84. Epub 2006 Aug 1 [Content Brief]
- [2]. Briley M, et al. Evidence against beta-adrenoceptor blocking activity of diltiazem, a drug with calcium antagonist properties. Br J Pharmacol. 1980 Aug;69(4):669-73. [Content Brief]
- [3]. Al-Majed AA, et al. Propranolol. Profiles Drug Subst Excip Relat Methodol. 2017;42:287-338. [Content Brief]
- [4]. Munabi NC, et al. Propranolol Targets Hemangioma Stem Cells via cAMP and Mitogen-Activated Protein Kinase Regulation. Stem Cells Transl Med. 2016 Jan;5(1):45-55. [Content Brief]
- [5]. Neil-Dwyer G, et al. Beta-adrenoceptor blockers and the blood-brian barrier. Br J Clin Pharmacol. 1981 Jun;11(6):549-53. [Content Brief]