Degarelix Acetate is a long-acting, synthetic peptide of the acetate class. It has
gonadotrophin-releasing hormone antagonistic properties. It is also a potent GnRH receptor
antagonist, that is used for the treatment of patients with advanced prostate cancer. Degarelix
actions block gonadotrophin-releasing hormone receptors, which are situated on the
surfaces of gonadotroph cells in the anterior pituitary. The blocking results in a reduction in
the secretion of luteinizing hormone (LH) by pituitary gonadotroph cells and so decreasing
testosterone production by interstitial cells in the testes.
Degarelix Acetate is sold under the brand name Firmagon among others.
The US Food and Drug Administration approved Degarelix in 2008, for the treatment of
patients with advanced prostate cancer in the United States. By 2009, It was subsequently
approved by the European Commission in 2009, for use in adult males with advanced,
hormone-dependent prostate cancer.
Dosage and administration
Degarelix Acetate is available as in injection in 80gm and 120gm in a single vial. It is to be
administered only subcutaneously and must not be administered intravenously. The usual
adult dose, on which the treatment begins is set at a 240 mg given as two injections of 120
mg each. This is then followed by a maintenance doses of 80 mg, administered as a single
injection every 28 days.
The cost of Degarelix Acetate
In the USA, the consumers have to pay around $519, for subcutaneous powder for injection
of 80 mg for a supply of one powder for injection. This medicine is much cheaper in UK,
whereht consumers have to pay an average retial price of £129.37, for subcutaneous
powder for injection of 80 mg for a supply of one powder for injection.
How does Degarelix Acetate Work?
GnRH receptor blockers also called antagonists are synthetic peptide derivatives of the
natural GnRH decapeptide. GnRH decapeptide is a hormone made by neurons in the
hypothalamus. Degarelix Acetate competes with natural GnRH for binding to GnRH
receptors in the pituitary gland. This binding blocks the release of LH and FSH from the
pituitary and the blocking is reversible. LH reduction leads to a rapid and sustained
suppression of testosterone release from the testicles. It also subsequently decreases the
growth of the prostate cancer. The final result is a This reduction in prostate-specific antigen
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