Vilanterol Trifenatate

Химические свойства

Vilanterol trifenatate is a white powder with a molecular weight of 774.8, and the empirical formula is C24H33Cl2NO5.C20H16O2. It insoluble in water and slightly soluble in methanol, ethanol, acetonitrile and propan-2-ol. It is slightly hygroscopic. It is provided in a micronized form.

Использование

Vilanterol Trifenatate is a long-acting β2 adrenergic receptor Agonist with alonger than 24-hour activity in humans, and is being developed to be used in combination with FF. It is also highly selective for the β2-receptor, with over 1000-fold greater selectivity compared to β1-receptors. It demonstrates prolonged bronchodilation in subjects with asthma and COPD.

Подготовка

Vilanterol trifenatate is synthesized by incorporation of an oxygen atom at the homobenzylic position of the right-hand side phenyl ring of (R)-salmeterol and has suitable chemical properties for inhaled administration. The combination in fluticasone furoate (FF) and vilanterol trifenatate (VI) in a single inhaler is the first once daily combination available on the market for the treatment of stable COPD.

Определение

ChEBI: Vilanterol Trifenatate is a triphenylacetate salt obtained by combining vilanterol with one equivalent of triphenylacetic acid. Used in combination with fluticasone furoate for treatment of bronchospasm associated with chronic obstructive pulmonary disease. It has a role as a beta-adrenergic agonist and a bronchodilator agent. It contains a vilanterol(1+).

Дозировка

The recommended and maximum dose is one inhalation of vilanterol trifenatate 25 micrograms once daily either morning or evening but at the same time every day.

Способ действия

Vilanterol Trifenatate is a selective long-acting beta2-receptor agonist (also referred to as a LABA). The pharmacologic effects of beta2-adrenoceptor agonist drugs, including vilanterol trifenatate, are at least in part attributable to stimulation of intracellular adenylate cyclase, the enzyme that catalyses the conversion of adenosine triphosphate (ATP) to cyclic-3',5'-adenosine monophosphate (cyclic AMP). Increased cyclic AMP levels cause relaxation of bronchial smooth muscle and inhibition of release of mediators of immediate hypersensitivity from cells, especially from mast cells.