antiinflammatory; Glucocorticoid; antipsoriatic.
Flurandrenolide (Cordran, Cordran SP) is a synthetic fluorinated corticosteroid.
ChEBI: Flurandrenolide is a 21-hydroxy steroid.
Flurandrenolide (Cordran, Cordran SP) is a synthetic fluorinated corticosteroid.
Cordran (Oclassen); Cordran (Watson).
Glucocorticoid, Antiinflammatory
Corticosteroids influence all tissues of the body and produce numerous and varying effects in cells.
These steroids regulate carbohydrate, lipid, and protein biosynthesis and metabolism (glucocorticoid effects),
and they influence water and electrolyte balance (mineralocorticoid effects). Cortisol is the most potent
glucocorticoid secreted by the adrenal gland, and aldosterone is the most potent endogenous mineralocorticoid.
Both naturally occurring glucocorticoids and related, semisynthetic analogues can be evaluated in terms of their
ability to sustain life, to stimulate an increase in blood glucose concentrations and a deposition of liver
glycogen, to decrease circulating eosinophils, and to cause thymus involution in adrenalectomized
animals. In addition, corticosteroids can affect immune system functions, inflammatory responses,
and cell growth.
The primary physiologic function of glucocorticoids is to maintain blood glucose levels and, thus, ensure
glucose-dependent processes critical to life, particularly brain functions. Cortisol and related steroids
accomplish this by stimulating the formation of glucose, by diminishing glucose use by peripheral tissues, and
by promoting glycogen synthesis in the liver to increase carbohydrate stores for later release of glucose.
Flurandrenolide, 6α-fluoro-11β,21-dihydroxy-16α,17-[(1-methylethylidene)bis(oxy)]pregn-4-ene-3,20-dione, although available as a tape product,can stick to and remove damaged skin, so it should beavoided with vesicular or weeping dermatoses.
Glucocorticoid action is mediated through the glucocorticoid receptor, which is found primarily in the cytosol of
the cell when not bound to glucocorticoids. The GR is stabilized in the cytosol by complexation with
phosphorylated proteins, including a 90-kDa protein referred to as a heat shock protein 90. The steroid
molecule binds to the GR, resulting in a conformational change of the receptor to dissociate the other proteins
and initiate translocation of the steroid–receptor complex into the nucleus. The steroid–nuclear GR complex
interacts with particular HRE regions of the cellular DNA, referred to as glucocorticoid-responsive elements and
initiates transcription of the DNA sequence to produce mRNA. Finally, the elevated levels of mRNA lead to
increased protein synthesis in the endoplasmic reticulum. These proteins then mediate glucocorticoid effects on
carbohydrate, lipid, and protein metabolism. An alternative isoform of the GR has been identified. This isoform
of the receptor does not bind known glucocorticoids, and its function remains to be determined.
Two major uses of glucocorticoids are in the treatment of rheumatoid diseases and allergic manifestations.
Their use in the treatment of severe asthma is well documented, as is the utility of glucocorticoids in sepsis and
acute respiratory distress syndrome. They are effective in the treatment of rheumatoid arthritis, acute
rheumatic fever, bursitis, spontaneous hypoglycemia in children, gout, rheumatoid carditis, sprue, allergy
(including contact dermatitis), and other conditions. The treatment of chronic rheumatic diseases and allergic
conditions with glucocorticoids is symptomatic and continuous. Symptoms return after withdrawal of the drug.
Although side effects and toxicities vary with the drug and, sometimes, with the patient, facial mooning,
flushing, sweating, acne, thinning of the scalp hair, abdominal distention, and weight gain are observed with
most glucocorticoids. Protein depletion (with osteoporosis and spontaneous fractures), myopathy (with
weakness of muscles of the thighs, pelvis, and lower back), and aseptic necrosis of the hip and humerus are
other side effects.
