Propranolol hydrochloride is a nonselective β-adrenergic receptor (βAR) antagonist, has high affinity for the β1AR and β2AR with K_i 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].
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].