Monlastik Mechanism of Action

Leukotriene Receptor Antagonist.
Pharmacology: Mechanism of Action: Montelukast is an orally active compound that binds with high affinity and selectively to the cysteinyl leukotrienes type-1 (CysLT1) receptor (in preference to other pharmacologically important airway receptors, such as the prostanoid, cholinergic, or beta-adrenergic receptor) is found in the human airway (including airway smooth muscle cells and airway macrophages) and on other pro-inflammatory cells (including eosinophils and certain myeloid stem cells). CysLTs have been correlated with the pathophysiology of asthma and allergic rhinitis. In asthma, leukotriene-mediated effects include airway edema, smooth muscle contraction, and altered cellular activity associated with the inflammatory process. In allergic rhinitis, CysLTs are released from the nasal mucosa after allergen exposure during both early and late phase reactions and are associated with symptoms of allergic rhinitis. Intranasal challenge with CysLTs has been shown to increase nasal airway resistance and symptoms of nasal obstruction. Montelukast inhibits physiologic actions of LTD4 at the CysLT1 receptor without any agonist activity.
Pharmacokinetics: Peak plasma concentrations of Montelukast are achieved in 3 to 4 hours after oral doses. The mean oral bioavailability is 64%. Montelukast is more than 99% bound to plasma proteins. It is extensively metabolized in the liver by cytochrome P450 isoenzymes CYP3A4, CYP2A6, and CYP2C9, and is excreted principally in the feces via the bile.