Pharmacodynamics<unk>  is an antagonist of cysteinyl leukotriene receptor 1 (CysLT1), a receptor found throughout the smooth muscle of the lungs, within interstitial lung macrophages (white blood cells that operate in the interstitial space of the lungs), and rarely in epithelial cells. CystLT1 is a receptor for a specific class of leukotrienes that contain the amino acid cysteine. These cysteinyl leukotrienes include leukotriene C4, leukotriene D4, and leukotriene E4, all of which are produced by inflammatory cells like eosinophils, basophils, and macrophages in the lungs. Through their action on CysLT1 these leukotrienes can trigger bronchoconstriction, a state in which the bronchial passages of the lungs constrict, leading to the characteristic, reactive airway symptoms associated with bronchial asthma. The other pro-inflammatory effects of leukotrienes, such as their inhibition of mucus clearance and their stimulation of mucus secretion and edema, are thought to play a role in the characteristic symptoms of allergic rhinitis (also called hay fever). By inhibiting the action of these specific leukotrienes,<unk>  is thought to exert an anti-inflammatory effect against leukotriene-mediated inflammatory conditions. Pharmacokinetics Absorption<unk>  is rapidly absorbed into the bloodstream following oral administration, reaching peak plasma levels within 3 hours of taking the dose. The peak plasma level is the maximum concentration of<unk>  in the blood. Distribution<unk>  is moderately distributed into the body's tissues, with an apparent steady state volume of distribution of 70 liters.<unk>  is highly plasma protein bound, 99% bound to albumin. Albumin is the most abundant protein found in human plasma and is capable of carrying and transporting drugs (like<unk>  throughout the body. In vivo research indicates that<unk>  has low blood-brain barrier penetration. The blood-brain barrier is a protective system that prevents many chemicals from entering the brain. Metabolism<unk>  undergoes extensive hepatic metabolism into inactive metabolites.<unk>  is primarily metabolized by the enzyme CYP2C9 to a hydroxylated metabolite. Elimination<unk>  is primarily cleared through biliary excretion at a rate of 20 liters/hour.<unk>  is undetectable in urine. The mean terminal half-life ranges 8–16 hours, following linear kinetics up to doses of 80 mg. Pharmacogenomics LTC4 synthase Genetic polymorphisms in the LTC4 synthase promoter may predict response to<unk> . The single-nucleotide polymorphism (SNP) A444C (the wild-type DNA base adenine, at the 444th position on the gene, is mutated; cytosine is there instead), which is associated with a severe asthma phenotype, has been shown to decrease the clinical response to<unk>  (both when the genetic alteration was heterozygous or homozygous). CYP2C9<unk>  is metabolized through the hepatic enzyme CYP2C9. SNPs that decrease the function of CYP2C9 (such as CYP2C9*3 and CYP2C9*13) may decrease the hepatic clearance of<unk> , leading to increased exposure of<unk> . Notably, the CYP2C9*3 polymorphism is more commonly encountered in people of south/central Asian ancestry (10.165%) compared to people of Caucasian (7.083%), African American (1.170%), African (1.033%), middle eastern (9.312%), and east Asian (3.365%) ancestry.
Zafirlukast
Pranlukast
Seratrodast
Montelukast
Levosalbutamol
Salbutamol
Lifitegrast
Pemirolast