| Name | Vardenafil |
| Description | Vardenafil (Vivanza) is an oral therapy for the treatment of erectile dysfunction. It is a selective inhibitor of cyclic guanosine monophosphate (cGMP)-specific phosphodiesterase type 5 (PDE5). Penile erection is a hemodynamic process initiated by the relaxation of smooth muscle in the corpus cavernosum and its associated arterioles. During sexual stimulation, nitric oxide is released from nerve endings and endothelial cells in the corpus cavernosum. Nitric oxide activates the enzyme guanylate cyclase resulting in increased synthesis of cyclic guanosine monophosphate (cGMP) in the smooth muscle cells of the corpus cavernosum. The cGMP in turn triggers smooth muscle relaxation, allowing increased blood flow into the penis, resulting in erection. The tissue concentration of cGMP is regulated by both the rates of synthesis and degradation via phosphodiesterases (PDEs). The most abundant PDE in the human corpus cavernosum is the cGMPspecific phosphodiesterase type 5 (PDE5); therefore, the inhibition of PDE5 enhances erectile function by increasing the amount of cGMP. |
| In vitro | Vardenafil, through the mechanism of mitochondrial K(ATP) channel opening, protects against myocardial ischemia due to reperfusion injury. Oral administration of 3 mg/kg Vardenafil alters object recognition capability in rats. A dose of 30 mg/L orally also upregulates iNOS and proliferating cell nuclear antigen expression (replication of SM cells), leading to the normalization of the rate of dynamic corporal tissue fusion decline and the SM/collagen ratio. Furthermore, Vardenafil induces robust preconditioning-like cardioprotective effects against ischemia/reperfusion injury in rabbits by opening mitochondrial K(ATP) channels. Additionally, it dose-dependently induces an erectile response in rabbits when administered intravenously with Nitroprusside sodium. |
| In vivo | Vardenafil significantly induces relaxation of trabecular smooth muscle elicited by both acetylcholine and electrical stimulation. It competitively inhibits phosphodiesterase type 5 (PDE5), thus enhancing the accumulation and relaxation effect of cyclic guanosine monophosphate (cGMP) in vascular smooth muscle. Its IC50 for specifically inhibiting PDE5-mediated cGMP hydrolysis is 0.7 nM (6.6 nM). At 3 nM (10 nM), Vardenafil notably potentiates the relaxation of human trabecular smooth muscle induced by SNP. At 100 mM, Vardenafil significantly increases cGMP levels in rat hippocampus. |
| Storage | Shipping with blue ice/Shipping at ambient temperature. |
| Solubility Information | DMSO : 45 mg/mL (92.1 mM), Sonication is recommended.
10% DMSO+40% PEG300+5% Tween 80+45% Saline : 2 mg/mL (4.09 mM), Sonication is recommended.
|
| Keywords | Zucker diabetic fatty (ZDF) rats | Vardenafil | stimulation | phosphodiesterase | PED5 | PDE1 | impotence | hepatitis | erectile dysfunction | erectile | cGMP |
| Inhibitors Related | Sucrose | Aceglutamide | Nicotinamide riboside malate | DL-Lysine | D(+)-Raffinose pentahydrate | Guanidine hydrochloride | Malic acid | Formamide | Glycerol | Thymidine | Corn starch | Gluconate Calcium |
| Related Compound Libraries | Bioactive Compound Library | Approved Drug Library | Drug-induced Liver Injury (DILI) Compound Library | ReFRAME Related Library | EMA Approved Drug Library | Drug Repurposing Compound Library | Inhibitor Library | Anti-Cardiovascular Disease Compound Library | FDA-Approved Drug Library | Metabolism Compound Library | Orally Active Compound Library | Bioactive Compounds Library Max |
United States
