139755-83-2 Sildenafil Aphrodisiac Male Enhancement Powder For The Treatment Of Male Erectile Dysfunction API
1. Product title: Sildenafil
Sildenafil, a phosphodiesterase 5 (PDE-5) inhibitor with an IC50 of 5.22 nM, is probably the best compound for erectile dysfunction.
2. Sildenafil description:
Sildenafil was the world's first oral PDE5 inhibitor (phosphodiesterase type 5 inhibitor) for the treatment of erectile dysfunction (also known as impotence or ED), revolutionizing the treatment of ED and effectively improving penile erection hardness.
Sildenafil has been on the market for more than 10 years. Oral drugs represented by sildenafil have been recommended as first-line treatment for ED by medical guidelines in many countries and regions (such as the United States, Europe, China, Japan, etc.).
3. Product parameter table:
|Appearance||White or light white power||Main Effect||viagra|
|Brand Name||Kan Ying||Store-method||Cool Dry Place|
|Shelf Life||2 Years When
4.Sildena is not a physiological mechanism:
Mechanism of action The physiological mechanism of penile erection involves the release of nitric oxide (NO) in the sponges of the penis during sexual stimulation. NO activates guanylate cyclase to increase cGMP levels, which relaxes the smooth muscle and fills the blood.
5.Pharmacological effects of sildenafil:
(1) Effect of sildenafil on penile erectile response. Sildenafil is a highly selective phosphodiesterase 5(PDE5) inhibitor, which is highly expressed in the cavernous body of the penis and is low expressed in other tissues, including platelets, blood vessels and visceral smooth muscle, and skeletal muscle. Sildenafil can selectively inhibit PDE5, enhance the nitric oxide (NO)-cGMP pathway, and increase the level of cGMP, resulting in the relaxation of the cavernosial smooth muscle of the penis, so that patients with erectile dysfunction can produce a natural erectile response to sexual stimulation. Erectile response is generally enhanced with increasing sildenafil dose and plasma concentration. Experiments showed that the effect lasted up to 4 hours, but the response was weaker than that at 2 hours.
(2) Response of sildenafil to myocardium. PDE5 does not exist in normal or pathological cardiac conduction tissues, cardiomyocytes, endothelial cells, and lymphoid tissues. Therefore, sildenafil (PDE5 inhibitor) has no positive inotropic effect and cannot directly affect myocardial systolic function.
(3) The effect of sildenafil on cardiac parameters. No clinically significant ECG changes were observed in normal male volunteers with a single dose of sildenafil 100mg. Eight patients with stable ischemic heart disease received a total of 40mg of sildenafil in four intravenous doses monitored by a Swan-Ganz catheter. Systolic and diastolic blood pressure at rest decreased by 7% and 10%, respectively, from baseline. Rest right atrium, pulmonary artery pressure, pulmonary wedge pressure, and cardiac output decreased by an average of 28%, 28%, 20%, and 7%, respectively. Although this intravenous dose was 2 to 5 times higher than the average peak plasma concentration of 100mg of sildenafil in a single dose of oral sildenafil in healthy male volunteers, these hemodynamic responses remained during exercise.
6. Effect of sildenafil on erectile response:
In eight double-blind, placebo-controlled cross-trials of patients with organic or cardiac erectile dysfunction, sildenafil improved sexual stimulation-induced erections compared with placebo as measured by a durotester for erectile hardness and duration. Most trials assess the efficacy of sildenafil about 60 minutes after taking the drug. Erectile response generally increased with sildenafil dose and plasma concentration as measured by durometer. A trial to determine the duration of the effect showed that it lasted up to four hours, but the response was weaker than at two hours.