Adeflo Mechanism of Action

Pharmacology: The combination previously-mentioned represents 2 classes of medications (a synthetic corticosteroid and a selective, long-acting beta-adrenergic receptor agonist) that have different effects on clinical and physiological indices.
Fluticasone Propionate: It is a synthetic trifluorinated corticosteroid with potent anti-inflammatory activity. In vitro assays using human lung cytosol preparations have established fluticasone propionate as a human glucocorticosteriod receptor agonist with an affinity 18 times greater than dexamethasone, almost twice that of beclomethasone - 17-monopropionate (BMP), the active metabolite of beclomethasone dipropionate and over 3 times that of budesonide. Inflammation is an important component in the pathogenesis of asthma. Corticosteroids have been shown to inhibit multiple cell types (eg, mast cells, eosinophils, basophils, lymphocytes, macrophages and neutrophils) and mediator production or secretion (eg, histamine, eicosanoids, leukotrienes and cytokines) involved in the asthmatic response. These anti-inflammatory actions of corticosteroids contribute to their efficacy in asthma. Inflammation is also a component in the pathogenesis of chronic obstructive pulmonary disease (COPD).
Salmeterol Xinafoate: It is a long-acting beta-2 adrenergic agonist. The pharmacologic effect of Salmeterol Xinafoate is part attributable to stimulation of intracellular adenyl cyclase, the enzyme that catalyzes the conversion of adenosine triphosphate (ATP) to cyclic-3',5'-adenosine monophosphate (cyclic AMP). Increased cyclic AMP levels caused relaxation of bronchial smooth muscle and inhibition of release mediators of immediate hypersensitivity from cells, especially from mast cells. In vitro tests show that salmeterol is a potent and long-lasting inhibitor of the release of mast cell mediator, such as histamine, leukotrienes and prostaglandin D2, from human lung. Salmeterol inhibits histamine-induced plasma protein extravasation and inhibits platelet-activating factor-induced eosinophil accumulation in the lungs of guinea pigs when administered by the inhaled route.