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Carvedilol(BM14190), an antagonist ofα1- and β-adrenergic receptors (ARs), is used to treat congestive heart failure (CHF) and high blood pressure [1].

Adrenergic receptors, a class of G protein-coupled receptors, are targets of thenorepinephrine and epinephrine which have been involved in sympathetic nervous system[2]..

In vitro: Carvedilol potently inhibited Fe2+-initiated lipid peroxidation in rat brain homogenate with an IC50 of 8.1 μM. In rat brain homogenate, carvedilol protected against Fe2+-induced α-tocopherol depletion with an IC50 of 17.6 μM. Carvedilol dose-dependently decreased the intensity of the DMPO-OH signal, with an IC50 of 25 μM [1]. Carvedilol prevented vascular smooth muscle cell migration, proliferation, and neointimal formation following vascular injury. In human cultured pulmonary artery vascular smooth muscle cells, carvedilol (0.1-10 μM) concentration-dependently inhibited the mitogenesis stimulated by platelet-derived growth factor, epidermal growth factor, thrombin, and serum, with IC50 values ranging from 0.3 to 2.0 μM. Carvedilol concentration-dependently inhibited vascular smooth muscle cell migration induced by platelet-derived growth factor with an IC50 value of 3 μM [3].

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