product name Carvedilol
Description: Carvedilol (also known as BM-14190, SKF 105517) is a non-selective beta blocker/alpha-1 blocker, used to treat congestive heart failure (CHF) and high blood pressure. Carvedilol rapidly inhibits Fe(++)-initiated lipid peroxidation, measured as thiobarbituric acid reactive substance (TBARS), in rat brain homogenate with an IC50 of 8.1 mM. Carvedilol protects against Fe(++)-induced alpha-tocopherol depletion in rat brain homogenate with an IC50 of 17.6 mM. Carvedilol dose-dependently decreases the intensity of the DMPO-OH signal with an IC50 of 25 mM.
References: J Pharmacol Exp Ther. 1992 Oct;263(1):92-8; Proc Natl Acad Sci U S A. 2007 Oct 16;104(42):16657-62.
406.47
Formula
C24H26N2O4
CAS No.
72956-09-3
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 81 mg/mL (199.3 mM)
Water: <1 mg/mL
Ethanol: 4 mg/mL (9.8 mM)
Solubility (In vivo)
Synonyms
BM-14190, SKF 105517
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19398089
| In Vitro |
In vitro activity: Carvedilol rapidly inhibits Fe(++)-initiated lipid peroxidation, measured as thiobarbituric acid reactive substance (TBARS), in rat brain homogenate with an IC50 of 8.1 mM. Carvedilol protects against Fe(++)-induced alpha-tocopherol depletion in rat brain homogenate with an IC50 of 17.6 mM. Carvedilol dose-dependently decreases the intensity of the DMPO-OH signal with an IC50 of 25 mM. Carvedilol has inverse efficacy for stimulating G(s)-dependent adenylyl cyclase but stimulates phosphorylation of the receptors cytoplasmic tail on previously documented G protein-coupled receptor kinase sites in beta2 adrenergic receptor (beta2AR)-expressing HEK-293 cells. Carvedilol (0.1-10 mM) produces a concentration-dependent inhibition of the mitogenesis stimulated by platelet-derived growth factor, epidermal growth factor, thrombin, and serum in human cultured pulmonary artery vascular smooth muscle cells, with IC50 values ranging from 0.3 mM to 2.0 mM. Carvedilol also produces a concentration-dependent inhibition of vascular smooth muscle cell migration induced by platelet-derived growth factor, with an IC50 value of 3 mM. Carvedilol decreases the extent of cellular vacuolization in cardiac myocytes and prevents the inhibitory effect of doxorubicin on mitochondrial respiration in both heart and liver. Carvedilol also prevents the decrease in mitochondrial Ca(2+) loading capacity and the inhibition of the respiratory complexes of heart mitochondria caused by doxorubicin. Kinase Assay: Cell Assay: 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. 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. |
|---|---|
| In Vivo | |
| Animal model | |
| Formulation & Dosage | |
| References | J Pharmacol Exp Ther. 1992 Oct;263(1):92-8; Proc Natl Acad Sci U S A. 2007 Oct 16;104(42):16657-62. |
Related Posts
product name Carvedilol
Description: Carvedilol (also known as BM-14190, SKF 105517) is a non-selective beta blocker/alpha-1 blocker, used to treat congestive heart failure (CHF) and high blood pressure. Carvedilol rapidly inhibits Fe(++)-initiated lipid peroxidation, measured as thiobarbituric acid reactive substance (TBARS), in rat brain homogenate with an IC50 of 8.1 mM. Carvedilol protects against Fe(++)-induced alpha-tocopherol depletion in rat brain homogenate with an IC50 of 17.6 mM. Carvedilol dose-dependently decreases the intensity of the DMPO-OH signal with an IC50 of 25 mM.
References: J Pharmacol Exp Ther. 1992 Oct;263(1):92-8; Proc Natl Acad Sci U S A. 2007 Oct 16;104(42):16657-62.
406.47
Formula
C24H26N2O4
CAS No.
72956-09-3
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 81 mg/mL (199.3 mM)
Water: <1 mg/mL
Ethanol: 4 mg/mL (9.8 mM)
Solubility (In vivo)
Synonyms
BM-14190, SKF 105517
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19398089
| In Vitro |
In vitro activity: Carvedilol rapidly inhibits Fe(++)-initiated lipid peroxidation, measured as thiobarbituric acid reactive substance (TBARS), in rat brain homogenate with an IC50 of 8.1 mM. Carvedilol protects against Fe(++)-induced alpha-tocopherol depletion in rat brain homogenate with an IC50 of 17.6 mM. Carvedilol dose-dependently decreases the intensity of the DMPO-OH signal with an IC50 of 25 mM. Carvedilol has inverse efficacy for stimulating G(s)-dependent adenylyl cyclase but stimulates phosphorylation of the receptors cytoplasmic tail on previously documented G protein-coupled receptor kinase sites in beta2 adrenergic receptor (beta2AR)-expressing HEK-293 cells. Carvedilol (0.1-10 mM) produces a concentration-dependent inhibition of the mitogenesis stimulated by platelet-derived growth factor, epidermal growth factor, thrombin, and serum in human cultured pulmonary artery vascular smooth muscle cells, with IC50 values ranging from 0.3 mM to 2.0 mM. Carvedilol also produces a concentration-dependent inhibition of vascular smooth muscle cell migration induced by platelet-derived growth factor, with an IC50 value of 3 mM. Carvedilol decreases the extent of cellular vacuolization in cardiac myocytes and prevents the inhibitory effect of doxorubicin on mitochondrial respiration in both heart and liver. Carvedilol also prevents the decrease in mitochondrial Ca(2+) loading capacity and the inhibition of the respiratory complexes of heart mitochondria caused by doxorubicin. Kinase Assay: Cell Assay: 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. 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. |
|---|---|
| In Vivo | |
| Animal model | |
| Formulation & Dosage | |
| References | J Pharmacol Exp Ther. 1992 Oct;263(1):92-8; Proc Natl Acad Sci U S A. 2007 Oct 16;104(42):16657-62. |