Molecular Formula | C23H39ClN6O7S |
Molar Mass | 579.10976 |
Solubility | ≥13.3 mg/mL in DMSO; ≥3.42 mg/mL in EtOH with gentle warming and ultrasonic; ≥95 mg/mL in H2O |
Appearance | neat |
Storage Condition | under inert gas (nitrogen or Argon) at 2-8°C |
In vitro study | Vadenine hydrochloride non-specifically inhibits PDE5 Mediated Hydrolysis of cGMP with an IC50 of 0.7 nM(6.6 nM). Vardenafi significantly enhanced SNP-induced relaxation of human trabecular smooth muscle at 3 nM(10 nM). Vardenafi significantly induced acetylcholine and electrical stimulation-induced relaxation of trabecular smooth muscle. Vardenafil(100 mM) increased the level of hippocampal cGMP in rats. Vardenafil, tadalafil, and Sildenafil competitively inhibit the hydrolyzing phosphodiesterase 5(PDE5) of cGMP, thereby promoting the accumulation and relaxation of cGMP in vascular smooth muscle. |
In vivo study | Vadinafil hydrochloride trihydrate dose-dependently induced the erectile response induced by intravenous injection of Nitroprusside Sodium salt in rabbits. Vardenafil(3 mg/kg, P. O.) caused alterations in object recognition ability in rats. Vardenafil(30 mg / L,p.o.) A simultaneous increase in the expression of iNOS and proliferating cell nuclear antigen (replication of SM cells) in rats was accompanied by a normalization of the rate of decline of dynamic corpus cavernosum fusion and the SM/collagen ratio. In rabbit hearts, Vardenafil induces a powerful preconditioning-like cardioprotective effect against ischemia/reperfusion injury by opening mitochondrial K(ATP) channels. Vardenafil protects against myocardial ischemia in reperfusion injury by relying on a mitochondrial K(ATP) channel opening mechanism. |
UN IDs | UN 2811 6.1 / PGIII |
HS Code | 2933595960 |