2-Ethoxybenzoic acid 134-11-2 Factory 99%

The product is mainly used in the preparation of sildenafil.

CAS No. 134-11-2

Name: 2-Ethoxybenzoic acid

CBNumber: CB8417190

Appearance: Colorless oily liquid.

Melting point: 20.7℃
Boiling point: 174-176℃ (2.0 kPa).
The relative density: 1.105.
The refractive index: 1.5400.
Soluble in hot water, slightly soluble in alcohol and cold water.

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Sildenafil is a selective inhibitor of cyclic guanosine phosphate (cGMP) specific phosphodiesterase type 5 (PDE5), and is an oral drug for ED. The physiological mechanism of penile erection in normal people involves the release of nitric oxide (NO) during sexual stimulation. Nitric oxide activates guanylate cyclase in the smooth muscle cells of the corpus cavernosum, which leads to the increase of cGMP level, relaxation of smooth muscle in the corpus cavernosum, expansion of the cavernous sinus, and inflow of blood to make the penis erect. The main cause of erectile dysfunction is the relaxation of smooth muscle in the corpus cavernosum of the penis. Sildenafil has no direct relaxation effect on human cavernosum in vitro, but it can enhance the role of nitric oxide by inhibiting the decomposition of cGMP by PDE5 in cavernosum. Sildenafil inhibits PDE5 and increases the level of cGMP, relaxes the smooth muscle of the cavernous body, and blood flows into the cavernous body. Studies have shown that the erectile response increases with the increase of dose and plasma concentration, and the efficacy lasts for 4 hours (but is weaker than that at 2 hours). In vitro experiments showed that sildenafil had a high selectivity for PDE5, which was more than 80 times higher than that of PDE1, 700 times higher than that of PDE2 and PDE4, and 4000 times higher than that of PDE3. Because PDE3 is related to the control of myocardial contractility, there is no PDE5 in myocardium, so sildenafil has no positive inotropic effect and does not directly affect myocardial contractile function. However, Sildenafil can relax the systemic circulation vessels. Oral administration of high dose (100mg) can lead to a decrease in blood pressure in recumbent position [with an average maximum decrease of 1.12/0.73kPa (8.4/5.5mmHg)]. The most significant decrease in blood pressure is 1-2 hours after taking sildenafil, so sexual activity may induce cardiac events at peak blood concentration. The selectivity of sildenafil to PDE5 is only 10 times higher than that of PDE6. PDE6 is an enzyme in the retina, so sildenafil may cause color vision abnormalities at high dose or high blood concentration. In addition to human cavernous smooth muscle, low concentration of PDE5 was also found in platelets, blood vessels, visceral smooth muscle and skeletal muscle. Sildenafil may enhance the effects of anti-platelet aggregation (in vitro), inhibition of platelet thrombosis (in vivo) and relaxation of peripheral blood vessels (in vivo) by inhibiting PDE5 in these tissues.