Fluticasone propionate is an artificial trifluorinated corticosteroid with anti-inflammatory task. Fluticasone propionate has actually been received vitro to exhibit a binding fondness for the human glucocorticoid receptor that is 18 times that of dexamethasone, virtually two times that of beclomethasone-17-monopropionate (BMP), the active metabolite of beclomethasone dipropionate, as well as over 3 times that of budesonide. Data from the McKenzie vasoconstrictor assay in guy follow these results. The medical importance of these findings is unknown.
Systemic corticosteroids can reactivate tuberculosis and should not be used in patients with a history of active tuberculosis, except when chemoprophylaxis is instituted concomitantly. The incidence or course of acute bacterial infection are probably minimally affected by inhaled triamcinolone. Application of topical corticosteroids to areas of infection, including tuberculosis of the skin, should be initiated or continued only if the appropriate antiinfective treatment is instituted. If the infection does not respond to the antimicrobial therapy, the concurrent use of the topical corticosteroid should be discontinued until the infection is controlled.
In 1952, . Peterson and . Murray of Upjohn developed a process that used Rhizopus mold to oxidize progesterone into a compound that was readily converted to cortisone.  The ability to cheaply synthesize large quantities of cortisone from the diosgenin in yams resulted in a rapid drop in price to US $6 per gram, falling to $ per gram by 1980. Percy Julian's research also aided progress in the field.  The exact nature of cortisone's anti-inflammatory action remained a mystery for years after, however, until the leukocyte adhesion cascade and the role of phospholipase A2 in the production of prostaglandins and leukotrienes was fully understood in the early 1980s.