1. GPCR/G Protein
    Neuronal Signaling
  2. Adrenergic Receptor
  3. Propranolol hydrochloride

Propranolol hydrochloride 

Cat. No.: HY-B0573 Purity: 99.79%
Handling Instructions

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 to control hypertension, pheochromocytoma, myocardial infarction, cardiac arrhythmias, angina pectoris, and hypertrophic cardiomyopathy.

For research use only. We do not sell to patients.

Propranolol hydrochloride Chemical Structure

Propranolol hydrochloride Chemical Structure

CAS No. : 318-98-9

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Based on 3 publication(s) in Google Scholar

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Description

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[1]. Propranolol hydrochloride inhibits [3H]-DHA binding to rat brain membrane preparation with an IC50 of 12 nM[2]. Propranolol hydrochloride is used to control hypertension, pheochromocytoma, myocardial infarction, cardiac arrhythmias, angina pectoris, and hypertrophic cardiomyopathy[3].

IC50 & Target

IC50: 12 nM (βAR)[1]

In Vitro

Propranolol hydrochloride (10-7 M-10-3 M; 24 and 48 hours) increases the total ERK1/2 levels in a dose-dependent manner, and ERK1/2 activation is observed specifically at 10-5 M in HemSCs[4].
Propranolol hydrochloride (10-9 M-10-3 M; 24 and 48 hours) significant decreases cell proliferation at 10-4 M propranolol after 24 hours and 10-9 M propranolol after 48 hours in HemSCs[4].
Propranolol hydrochloride (50 μM-200 μM; 24 hours) increases Annexin V positivity and caspase-3 activation, rapidly induces HemSC apoptosis[4].

Western Blot Analysis[4]

Cell Line: HemSC cells
Concentration: 10-7 M-10-3 M
Incubation Time: 24 and 48 hours
Result: Increased the total ERK1/2 levels in a dose-dependent manner.

Cell Viability Assay[4]

Cell Line: HemSC cells
Concentration: 10-9 M-10-3 M
Incubation Time: 24 and 48 hours
Result: Suppressed HemSC Proliferation.

Apoptosis Analysis[4]

Cell Line: HemSC cells
Concentration: 50 μM, 100 μM, or 200 μM
Incubation Time: 24 hours
Result: Induced HemSC cell death occurred via an apoptotic pathway.
In Vivo

Propranolol hydrochloride (orally administration; 40 mg/kg; daily) significantly reduces the vessel diameter relative to the vehicle-treated implants, and increases the number of cells that expressed phosphorylated ERK1/2 within the IH Matrigel implant[4].

Animal Model: A xenograft mouse model of IH (infantile hemangiomas) with HemSC cells[4]
Dosage: 40 mg/kg
Administration: Orally administration; 40 mg/kg; daily
Result: Improved vessel development in the IH mouse model that correlated with MAPK pathway activation.
Clinical Trial
Molecular Weight

295.80

Formula

C₁₆H₂₂ClNO₂

CAS No.

318-98-9

SMILES

OC(CNC(C)C)COC1=CC=CC2=CC=CC=C12.Cl

Shipping

Room temperature in continental US; may vary elsewhere.

Storage
Powder -20°C 3 years
  4°C 2 years
In solvent -80°C 6 months
  -20°C 1 month
Solvent & Solubility
In Vitro: 

DMSO : ≥ 150 mg/mL (507.10 mM)

H2O : 33.33 mg/mL (112.68 mM; Need ultrasonic)

*"≥" means soluble, but saturation unknown.

Preparing
Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 3.3807 mL 16.9033 mL 33.8066 mL
5 mM 0.6761 mL 3.3807 mL 6.7613 mL
10 mM 0.3381 mL 1.6903 mL 3.3807 mL
*Please refer to the solubility information to select the appropriate solvent.
References
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Keywords:

PropranololAdrenergic ReceptorBeta ReceptorInhibitorinhibitorinhibit

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Propranolol hydrochloride
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HY-B0573
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