product name Valsartan
Description: Valsartan (also known as CGP-48933) is a potent and selective angiotensin II receptor antagonist that is used for the treatment of high blood pressure and congestive heart failure. Valsartan is selective for the type I (AT1) angiotensin receptor. Valsartan dose-dependently inhibits the vasoconstriction induced by angiotensin II and lowers blood pressure in renin-dependent models of hypertension.
References: Expert Opin Investig Drugs. 1998 Nov;7(11):1915-25; Hypertension. 2010 Mar;55(3):715-21.
435.52
Formula
C24H29N5O3
CAS No.
137862-53-4
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 87 mg/mL (199.8 mM)
Water:<1 mg/mL
Ethanol: 87 mg/mL (199.8 mM)
Solubility (In vivo)
Synonyms
CGP-48933
other peoduct :
| In Vitro |
In vitro activity: Valsartan dose-dependently inhibits the vasoconstriction induced by angiotensin II and lowers blood pressure in renin-dependent models of hypertension. Valsartan is at least as effective as ACE inhibitors, diuretics, beta-blockers and calcium antagonists. Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | Valsartan results in improved glucose tolerance, reduced fasting blood glucose levels, and reduced serum insulin levels in mice fed a Western diet. Valsartan treatment also blocks Western diet-induced increases in serum levels of the proinflammatory cytokines interferon-gamma and monocyte chemotactic protein 1. Valsartan enhances mitochondrial function and prevents Western diet-induced decreases in glucose-stimulated insulin secretion in the pancreatic islets of mice. Valsartan treatment blocks or attenuates Western diet-induced changes in expression of several key inflammatory signals: interleukin 12p40, interleukin 12p35, tumor necrosis factor-alpha, interferon-gamma, adiponectin, platelet 12-lipoxygenase, collagen 6, inducible NO synthase, and AT1R in isolated adipocytes. Valsartan significantly increases insulin-mediated 2-[3H]deoxy-d-glucose (2-[3H]DG) uptake into skeletal muscle and attenuates the increase in plasma glucose concentration after a glucose load and plasma concentrations of glucose and insulin. Valsartan treatment exaggerates the insulin-induced phosphorylation of IRS-1, the association of IRS-1 with the p85 regulatory subunit of phosphoinositide 3 kinase (PI 3-K), PI 3-K activity, and translocation of GLUT4 to the plasma membrane. Valsartan also reduces tumor necrosis factor-alpha (TNF-alpha) expression and superoxide production in skeletal muscle of KK-Ay mice. |
| Animal model | |
| Formulation & Dosage | |
| References | Expert Opin Investig Drugs. 1998 Nov;7(11):1915-25; Hypertension. 2010 Mar;55(3):715-21. |
