Momate Nasal Spray Mechanism of Action

Pharmacology: Pharmacodynamics: Mechanism of Action: Mometasone furoate monohydrate is a corticosteroid demonstrating potent ant-inflammatory properties.
Corticosteroids have been shown to have a wide range of effects on multiple cell types (e.g. mast cells, eosinophils, neutrophils, macrophages and lymphocytes) and mediators (e.g. histamine, eicosanoids, leukotrienes and cytokines) involved in inflammation.
In two clinical studies utilizing nasal antigen challenge, Mometasone furoate monohydrate Nasal Spray 50 mcg decreased some markers of the early- and late-phase allergic response. These observations included decreases (vs. placebo) in histamine and eosinophil cationic protein levels and reductions (vs. baseline) in eosinophils, neutrophils, and epithelial cell adhesion proteins. The clinical significance of these findings is not known.
Pharmacokinetics: Absorption: Mometasone furoate monohydrate administered as a nasal spray suspension has very low bioavailability (<1%) in plasma using a sensitive assay with a lower quantitation limit (LOQ) of 0.25 pcg/mL.
Distribution: The in vitro protein binding for mometasone furoate was reported to be 98% to 99% in concentration range of 5 to 500 ng/mL.
Metabolism: Studies have shown that any portion of mometasone furoate dose which is swallowed and absorbed undergoes extensive metabolism to multiple metabolites. There are no major metabolites detectable in plasma. Upon in vitro incubation, one of the minor metabolites formed is 6β-hydroxymometasone furoate. In human liver microsomes, the formation of the metabolite is regulated by cytochrome P450 3A4 (CYP3A4).
Elimination: Following intravenous administration the effective plasma elimination half-life of mometasone furoate is 5.8 hours. Any absorbed drug is excreted as metabolites mostly via the bile, and to a limited extent into the urine.
Special Populations: Hepatic Impairment: Administration of a single inhaled dose of 400 mcg mometasone furoate to subjects with mild, moderate, and severe hepatic impairment resulted in only 1 or 2 subjects in each group having detectable peak plasma concentrations of mometasone furoate (ranging from 50 to 105 pcg/mL). The observed peak plasma concentrations appear to increase with severity of hepatic impairment, however, the numbers of detectable levels were few.
Renal Impairment: The effects of renal impairment on mometasone furoate pharmacokinetics have not been adequately investigated.
Pediatric: Mometasone furoate pharmacokinetivs has not been investigated in the pediatric population.
Gender: The effects of gender on mometasone furoate pharmacokinetics have not been adequately investigated.
Race: The effects of race on mometasone furoate pharmacokinetics have not been adequately investigated.