Pharmacodynamics<unk>  furoate reduces inflammation by causing several effects: * Reversing the activation of inflammatory proteins * Activating the secretion of anti-inflammatory proteins * Stabilizing cell membranes * Decreasing the influx of inflammatory cells In addition to the glucocorticoid properties of<unk>  furoate, it is a very potent agonist of the progesterone receptor as well as a partial agonist of the mineralocorticoid receptor. Mechanism of action<unk>  — the metabolite of<unk>  furoate.<unk> , like other corticosteroids, possesses anti-inflammatory, antipruritic, and vasoconstrictive properties. For allergies, corticosteroids reduce the allergic reactions in various types of cells (mastocytes and eosinophils) that are responsible for allergic reactions.<unk>  and other corticosteroids circulate in the blood easily, crossing cellular membranes and binding with cytoplasmic receptors, resulting in the transcription and synthesis of proteins. It also inhibits the actions of the enzyme cytochrome P450 2C8 which participates in the activity of monooxygenase. The inflammation is reduced in decreasing the liberation of hydrolase acids of leukocytes, the prevention of the accumulation macrophages in the sites of inflammation, the interference with adhesion of leukocytes to capillary walls, the reduction of the permeability of the capillary membranes and consequently edema, the reduction of complementary components, inhibition of histamine and kinin liberation, and interference with scar tissue formation. The proliferation of fibroblasts and collagen deposits is also reduced. It is believed that the action of corticosteroid anti-inflammatory agents is bound to inhibitive proteins of phospholipase A2, collectively called lipocortins. The lipocortins, in turn, control the biosynthesis of potent mediators of inflammation as the prostaglandins and leukotrienes, inhibiting the liberation of the molecular precursors of arachidonic acid. Intranasal<unk>  alleviates symptoms such as rhinorrhea aquosa, nasal congestion, nasal drip, sneezing, and pharyngeal itching. Topical administration applied to skin reduces the inflammation associated with chronic or acute dermatosis. Although<unk>  furoate does not have significant systemic immunomodulatory effects, it can be considered a local immunosuppressive drug because clinical studies have shown reductions (vs. baseline ) in neutrophils (a white blood cell) in the nasal mucosa. It could be also considered an antihistamine along with its glucocorticoid effects because it significantly reduces histamine and eosinophil cationic protein levels. Pharmacokinetics Metabolism Extensive metabolic hepatic metabolism of<unk>  furoate to multiple metabolites occurs. No principal metabolites are detectable in plasma. After in vitro incubation, one of the minor metabolites formed is furoate 6β-hydroxymometasone. In human hepatic microsomes, the formation of these metabolites is regulated by CYP3A4.<unk> <unk>  by itself is a synthetic, steroidal glucocorticoid or corticosteroid that was never marketed. The C17α furoate ester of<unk> , is the marketed medication.<unk>  furoate acts as a prodrug of<unk> . In addition to its glucocorticoid activity,<unk>  also has very potent progestogenic activity and acts as a partial agonist of the mineralocorticoid receptor.
Mometasone
Beclometasone
Alclometasone
Clobetasone
Flumetasone
Fluticasone furoate
Eszopiclone
Zopiclone