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Originally derived from Gonadotropin-releasing hormone (GnRH) – a peptide containing 10 amino acids that is produced by GnRH neurons in the hypothalamus, Degarelix was made by modification of the native sequence of GnRH. Although Degarelix essentially is a changed sequence of amino acids of a natural hormone, it acts as a GnRH antagonist by competitively binding to the GnRH receptor without causing the surge in testosterone.
Degarelix’s main medical usage is as therapy for inducing and maintaining androgen deprivation in patients with prostate cancer, primarily ‘hormone-dependent’ type.
Degarelix is a synthetic GnRH blocker that inhibits the production of testosterone in men by directly blocking pituitary GnRH receptors. As a new class of hormonal agents that occupy GnRH receptor sites without activation, GnRH blockers are used for immediate and pronounced suppression of testosterone and are vital in ADT (Androgen Deprivation Therapy) in advanced stages of prostate cancer. This blockade directly suppresses the secretion of LH (Luteinising Hormone) and FSH (Follicle-Stimulating Hormone) and thereby reduces the production of testosterone by the testes, which stimulates prostate cancer cell growth.
Its application should be done in clinical conditions, and once administered, Degarelix forms a sustained-release gel under the skin that allows a steady and controlled release of the drug into the circulation, ensuring a long-lasting effect.
Previous treatments for prostate cancer involved surgical castration (orchidectomy) to prevent the disease from spreading, yet in recent studies, Degarelix was proven as effective at reducing the amount of testosterone as the actual procedure, being fully reversible, unlike the surgery.
From the 1990s onwards, several clinical studies have been conducted both on animals and volunteers, and they all show that Degarelix suppressed testosterone to castrate levels within two days and maintained such levels throughout the study.
Early experimental studies demonstrated that subcutaneous administration of Degarelix produced a rapid, reversible, and dose-dependent suppression of the pituitary-gonadal axis, as indicated by a reduction in LH and testosterone in preclinical models.
Even some animal studies done on rats and rhesus monkeys showed that Degarelix managed to maintain similar control of tumor volume compared to surgical castration.
In human trials, in addition to being compared to leuprolide, another GnRH blocker, it was monitored how Degarelix reduces levels of LH over time and up to castrate levels. Similarly to the decrease in testosterone, PSA suppression was also significantly faster in the Degarelix 240/80 mg and 240/160 mg compared to the leuprolide group: at day 14 (64% and 65% versus 18%, respectively) and at day 28 (85% and 83% versus 68%, respectively).
The studies also show that Degarelix causes a rapid and sustained reduction in serum testosterone and PSA (Prostate-Specific Antigen) without the initial stimulation seen with GnRH blockers and with no evidence of systemic allergic reactions, testosterone surge, or clinical flare.
When it comes to the side effects, Degarelix is generally speaking well-tolerated. The most frequently reported side effect associated with Degarelix therapy was hot flushes, a very common and expected androgen withdrawal symptom.
Other common side effects reported in the clinical trials that were conducted from 1996 onwards on over 2000 patients using Degarelix included fatigue, back pain, arthralgia, and urinary tract infection.
Based on the efficacy demonstrated at the clinical trials, the Degarelix dosage of 240/80 mg was approved by the US Food and Drug Administration in 2008 and the European Medicines Agency in 2009 for treatment of androgen-dependent advanced PCa.
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