Moxisylyte

279.3746

279.37

200-204-1

PW8QYA7KI0

759308

DTXSID4023339

C - Cardiovascular system|G - Genito urinary system and sex hormones

2922509090

38.8

3.17

1.018g/cm3

144.5 °C

371ºC at 760 mmHg

178.2ºC

1.501

H2O: >47.4 ug/ml

8.71None

8.71

Moxisylyte is very well accepted by the patients and it presents very few adverse effects. The side effects are usually related to a profound alpha blockade than to a toxic response.

By the WHO, moxisylyte is indicated for the symptomatic management of sequelae of cerebral infarction or hemorrhage. The cerebral infarction is characterized by the blockage of the artery either by the formation of a thrombus or an embolus. On the other hand, the FDA classified moxisylyte for the reversal of phenylephrine-induced mydriasis in patients who have narrow anterior angles and are at risk of developing an acute attack of angle-closure glaucoma. Closed-angle glaucoma is caused by the contact between the iris and the trabecular meshwork. This contact will damage the aqueous outflow by the meshwork thus, increasing eye pressure and producing the symptoms of glaucoma. Mydriasis is referred to the dilatation of the pupils and this standard body function is known to be a trigger factor for the development of acute closed-angle glaucoma.This risk is explained by the generation of a pupillary block, which is the contact between the pupillary margins and the lens, thus preventing flow from the aqueous humor to the anterior chamber and followed by an increased pressure gradient. Moxisylyte is also approved in France as the first drug for the treatment of impotence.

Administration of moxisylyte has shown to improve peripheral flow in occlusive arterial disease with little effect in blood pressure. There are reports of increases in cutaneous blood flow and skin temperature after local application of moxisylyte.

Agents causing contraction of the pupil of the eye. Some sources use the term miotics only for the parasympathomimetics but any drug used to induce miosis is included here. (See all compounds classified as Miotics.)|Drugs that inhibit the actions of the sympathetic nervous system by any mechanism. The most common of these are the ADRENERGIC ANTAGONISTS and drugs that deplete norepinephrine or reduce the release of transmitters from adrenergic postganglionic terminals (see ADRENERGIC AGENTS). Drugs that act in the central nervous system to reduce sympathetic activity (e.g., centrally acting alpha-2 adrenergic agonists, see ADRENERGIC ALPHA-AGONISTS) are included here. (See all compounds classified as Sympatholytics.)|Drugs that bind to but do not activate alpha-adrenergic receptors thereby blocking the actions of endogenous or exogenous adrenergic agonists. Adrenergic alpha-antagonists are used in the treatment of hypertension, vasospasm, peripheral vascular disease, shock, and pheochromocytoma. (See all compounds classified as Adrenergic alpha-Antagonists.)|Drugs used to cause dilation of the blood vessels. (See all compounds classified as Vasodilator Agents.)

Moxisylyte is rapidly absorbed after oral administration. Its pharmacokinetic profile is linear in the dose range from 10 to 30 mg for the values of Cmax and AUC. After intravenous administration, the maximal plasma concentration was of 352.8 ng/ml with an AUC of 152.6 mcg h/L. In preclinical trials, the bioavailability was always presented in approximately 10%.|The major elimination route of moxisylyte is via the kidneys. The complete elimination of all the metabolites by urine is of 75% when administered intravenously and 69% when administered orally. From the elimination profile, The specific ranges of the two major metabolites of moxisylyte in the urine are of 50% and 10% for desacetyl-thymoxamine and N-monodemethyl-desacetyl-thymoxamine respectively. The fecal elimination corresponded only to the 14% of the administered dose.|In preclinical trials, the volume of distribution presented for beagle dogs is in the range of 0.83-0.98 L/kg.|In preclinical trials, the plasma clearance was of 7.17 ml min/kg for beagle dogs.

The pharmacokinetic profile of moxisylyte can make this drug to be considered as a prodrug as its biotransformation is very rapid. This drug gets rapidly hydrolyzed by pseudocholinesterase in plasma and tissues to give the major metabolite deacetyl-thymoxamine. This first metabolite is later demethylated by the cytochrome P450 monooxygenase system to form deacetyl-demethyl-thymoxamine. Both of this major metabolites are pharmacologically active. The pharmacokinetic studies with moxisylyte in urine and feces have shown the presence of 8 different metabolites, where two of them are highly polar and resistant to enzymatic hydrolysis. From this metabolites, it has been detected the sulfate and glucuronide conjugates of the major metabolites.

The half-life of moxisylyte was of 1-2 hours.

Moxisylyte is vasodilator that works as a specific alpha-adrenergic blocking agent. Its action is known to be competitive against norepinephrine without beta-receptor blocking, anti-angiotensin or anti-serotonin activity.

Acetoxythymoxamine