product name Bosentan Hydrate
Description: Bosentan (also known as Ro 47-0203) is an endothelin (ET) receptor antagonist for ET-A and ET-B with Ki of 4.7 nM and 95 nM, respectively. Bosentan is used as a vasodilator. Bosentan is an inhibitor of ETAR and ETBR. It is used for the treatment of pulmonary artery hypertension (PAH). Bosentan blocks the action of endothelin molecules that would otherwise promote narrowing of the blood vessels and lead to high blood pressure.
References: Pathophysiology. 2003 Sep;9(4):249-256; J Pharmacol Exp Ther. 1994 Jul;270(1):228-35.
569.63
Formula
C27H29N5O6S.H2O
CAS No.
157212-55-0
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 100 mg/mL (175.6 mM)
Water: <1 mg/mL
Ethanol: 2 mg/mL (3.5 mM)
Solubility (In vivo)
Synonyms
Ro 47-0203
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19417166
| In Vitro |
In vitro activity: Bosentan competitively antagonizes the specific binding of [125 I]-labeled ET-1 on human smooth muscle cells (ET-A receptors)human placenta (ET-B receptors). Bosentan also inhibits the binding of selective ET-B ligands on porcine trachea. Contractions induced by ET-1 in isolated rat aorta (ET-A) and by the selective ET-B agonist sarafotoxin S6C in rat trachea are competitively inhibited by Bosentan (pA2= 7.2 and 6.0, respectively), as is the endothelium-dependent relaxation to sarafotoxin S6C in rabbit superior mesenteric artery (pA2= 6.7). The binding of 40 other peptides, prostaglandins, ions and neurotransmitters is not significantly affected by Bosentan, which shows its specificity for ET receptors. Kinase Assay: Cell Assay: A study was performed in vitro to measure the influence of Bosentan on the angiogenic performance of dermal microvascular endothelial cells (MVECs) and to detect the capacity of Bosentan in offsetting the antiangiogenic effects of systemic sclerosis sera. It was found that Bosentan significantly increased cell viability and offset the antiangiogenic effects of systemic sclerosis sera on dermal MVECs. |
|---|---|
| In Vivo | Bosentan inhibits the presser response to big ET-1 both after i.v. and oral administration, with a long duration of action and no intrinsic agonist activity. Bosentan also inhibits the depressor and presser effect of ET-1 and sarafotoxin S6C. Its pharmacological profile makes Bosentan a potentially useful drug in the management of clinical disorders associated with vasoconstriction. Bosentan is the first oral non-peptide mixed ETA/B-receptor antagonist. Long-term treatment with Bosentan has markedly increased the survival, hemodynamics, and cardiac remodeling in rats with CHF. Bosentan decreases arterial BP to a similar degree as an angiotensin-converting enzyme (ACE) inhibitor. Administration of Bosentan in rats with CHF after acute MI significantly decreases arterial BP and has additive effect to that of an ACE inhibitor. Acute and chronical treatment with Bosentan also improves the systemic and pulmonary hemodynamics by a decrease in peripheral and pulmonary vascular resistance, and increase of cardiac output in patients with CHF. |
| Animal model | Male Wistar rats with CHF |
| Formulation & Dosage | Dissolved in 5% gum arabic and prepared freshly every day; 30, or 100 mg/kg; oral gavage |
| References | Pathophysiology. 2003 Sep;9(4):249-256; J Pharmacol Exp Ther. 1994 Jul;270(1):228-35. |
