Cyclocort is a synthetic corticosteroid created to imitate natural glucocorticoids. In order to do so,<unk>  acts as an agonist to target glucocorticoid receptors. After interacting with the receptor, endocytosis occurs at which point the drug can bind to DNA within the cell. Gene expression is subsequently modified to produce anti-inflammatory mediators while preventing the formation of inflammatory agents thus reducing overall inflammation and immune system response. Mechanism of Action The mechanism by which<unk>  causes anti-inflammatory responses is unclear with current research focused on similar topical steroids that may possess the same mechanism. This is thought to occur via the induction of lipocortin (phospholipase A2 inhibitor proteins). Ongoing research predicts that<unk>  prevents the release of arachidonic acid which, in turn, stops the synthesis of the inflammation mediators prostaglandins and leukotrienes. Phospholipase A2 normally causes membrane phospholipids to release arachidonic acid, therefore causing a cascade of reactions leading to inflammation of the skin. Due to<unk> 's high affinity for the glucocorticoid receptor, a neuroactive ligand-receptor interaction occurs and the initial acid release is inhibited, thus helping to alleviate any itching/ burning symptoms. Metabolism & Elimination<unk>  undergoes transdermal absorption with pharmacokinetic profiles similar to that of other corticosteroids administered systematically. Metabolism occurs mainly in the liver and its hepatic cells. The metabolized compound is predominately filtered through the kidneys and excreted in urine although a small amount is excreted in the bile.
Amcinonide
Fluocinonide
Ciclesonide
Fluocinolone acetonide
Triamcinolone acetonide
Triamcinolone benetonide
Triamcinolone
Mometasone