Silden afil Citrate Powder Male Sex Enhancement CAS 171599-83-0

What is Silden afil ?

1. Product title: Silden afil citrate

Silden afil citrate is a drug, chemically named 1-[4-ethoxy-3 -[5-(6, 7-dihydro1-methyl-7-oxy-3-propyl - 1h-pyrazolo-[4, 3D] pyrimidine)] benzenesulfonyl] -4-methylpiperazine citrate, white powder.

2. Product parameter table:

3. Description of silden afil citrate:

Pharmacological effects

This product is an oral medication for erectile dysfunction (ED). It is the citrate of silden afil, a selective inhibitor of type 5 phosphodiesterase (PDE5) specific to cyclic guanosine phosphate (cGMP). Mechanism of action: The physiological mechanism of penile erection involves the release of nitric oxide (NO) in the penile sponge during sex ual stimulation. NO activation of guanosine cyclase leads to increased levels of cyclic guanosine phosphate (cGMP), which relaxes smooth muscle and fills blood in sponges.

Effect of silden afil on penile erection response: Silden afil is a highly selective phosphatidiesterase 5(PDE5) inhibitor, which is highly expressed in the cavernosa of the pen is and low in other tissues, including platelets, vascular and visceral smooth muscle, and skeletal muscle. Silden afil leads to relaxation of the smooth muscle of the cavernose by selectively inhibiting PDE5, enhancing the nitric oxide (NO) -CGMP pathway, and elevating the level of cGMP, leading to a natural erectile response to sex ual stimulation in erectile dysfunction patients. Erectile response generally increases with silden afil dose and plasma concentration. Experiments showed that the effect lasted up to 4 hours, but the reaction was weaker than 2 hours. Silden afil response to myocardium: PDE5 does not exist in normal or pathological cardiac conduction tissues, myocardium cells, endothelial cells, and lymphatic tissues, so silden afil (PDE5 inhibitor) has no positive inotropic effect and cannot directly affect myocardial systolic function.

Effect of silden afil on cardiac parameters: a single dose of silden afil 100mg in normal male volunteers showed no clinically significant ecg changes. Eight patients with stable ischemic heart disease received silden afil 40mg intravenously in 4 doses monitored by a swan-ganz catheter. Systolic and diastolic blood pressure at rest decreased by 7% and 10%, respectively, from baseline. Resting right atrium, pulmonary artery pressure, pulmonary wedge pressure and cardiac output decreased by 28%, 28%, 20% and 7%, respectively. Although this intravenous dose was two to five times higher than the average peak plasma concentration of 100mg for a single oral dose of silden afil in healthy male volunteers, these hemodynamic responses persisted during exercise.