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Pharmacology: Pharmacodynamics: 4 mg: 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 causes bronchodilation within 2 hours of oral administration; these effects were additive to the bronchodilation caused by β-agonist.
Pharmacokinetics: Peak plasma concentrations of montelukast are achieved in 3 to 4 hours after oral administration. The mean oral bioavailability is 64%. Montelukast is more than 99% bound to plasma proteins. It is extensively metabolised in the liver by cytochrome P450 isoenzyme CYP3A4, CYP2A6, and CYP2C9, and is excreted principally in the faeces via the bile. Metabolism was reduced and the elimination half-life prolonged in patients with mild to moderate hepatic impairment.
