Application of GnRH analogs is also known as “chemical castration”. Both can suppress Gn secretion and thus block the production of testicular androgens. As for agonists, initial application leads to a surge of FSH and LH secretion after their binding to GnRH receptors in gonadotrope cells in the pituitary. This surge causes a large amount of testosterone and DHT to be produced in the testes, and thus leads to a tumor growth spurt (termed “tumor flare”). Nevertheless, after around 10 days, these gonadotrope cells are no longer sensitive to endogenous GnRH or GnRH agonists, leading to a major reduction in Gn concentration and consequently to the decline of androgen levels comparable to that after castration. This suppression of androgen production lasts as long as GnRH are consecutively administered. On the other hand, GnRH competitively bind to the GnRH receptor and consequently block Gn release directly. Although GnRH analogs, such as leuprolide, goserelin, and buserelin, annihilate the androgen production in testes, they have no effect on adrenals. Despite the fact that the plasma testosterone concentration is reduced to less than 50 ng/dL, the androgens inside the prostate, which either originate from adrenals or are synthesized de novo in the tumor, are still in concentrations high enough to promote cancer cell growth. Moreover, side effects such as testicular atrophy and loss of bone mineral density are also observed as the consequences of the application of GnRH