Mechanism of action<unk>  has well-established antifibrotic and anti-inflammatory properties in various in vitro systems and animal models of fibrosis. A number of cell-based studies have shown that<unk>  reduces fibroblast proliferation, inhibits transforming growth factor beta stimulated collagen production and reduces the production of fibrogenic mediators such as transforming growth factor beta.<unk>  has also been shown to reduce production of inflammatory mediators such as tumor necrosis factor alpha and IL-1β in both cultured cells and isolated human peripheral blood mononuclear cells. These activities are consistent with the broader antifibrotic and anti-inflammatory activities observed in animal models of fibrosis. Pharmacokinetics<unk>  is administered orally. Though the presence of food significantly reduces the extent of absorption, the drug is to be taken after food, to reduce the nausea and dizziness associated with the drug. The drug is around 60% bound to plasma proteins, especially to albumin. Up to 50% of the drug is metabolized by hepatic CYP1A2 enzyme system to yield 5-carboxypirfenidone, the inactive metabolite. Almost 80% of the administered dose is excreted in the urine within 24 hours of intake.
Pirfenidone
Lurasidone
Chlortalidone
Methylphenidate
Dexmethylphenidate
Rimonabant
Ethylphenidate
Pirlindole