Montair Mechanism of Action

Pharmacology: Pharmacodynamics: Montelukast causes potent inhibition of airway cysteinyl leukotriene receptors as demonstrated by the ability to inhibit bronchoconstriction due to inhaled LTD4 in asthmatic patients. Doses as low as 5 mg cause substantial blockage of LTD4-induced bronchoconstriction.
Montelukast is a selective leukotriene-receptor antagonist that specifically inhibits the cysteinyl leukotriene CysLT1 receptor. The cysteinyl leukotrienes [CysLT (LTC4, LTD4, and LTE4)] are potent inflammatory eicosanoids released from various cells including mast cell and eosinophils that bind to CysLT receptors. The CysLT type 1 (CysLT1) receptor is present in the human airway (including airway smooth muscle cells and airway macrophages). CysLT contribute to the pathophysiology of asthma and allergic rhinitis. In asthma, CysLT are found to increase mucus secretion, vascular permeability, and bronchoconstriction. In allergic rhinitis, CysLT are released from the nasal mucosa after exposure to allergens and are associated with symptoms of allergic rhinitis. Montelukast inhibits bronchoconstriction and reduces inflammation of the nasal mucosa induced by exposure to known precipitants.
Pharmacokinetics: Peak plasma concentrations of Montelukast are achieved in 2 to 4 hours after oral administrations. 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 excreted principally in the feces via the bile. Metabolism was reduced and the elimination half-life prolonged in patients with mild to moderate hepatic impairment.