Antagonists such as degarelix, m Possible Bortezomib PS-341 therapeutic alternatives to traditional GnRH agonist as described above. Androgen concentrations by these agents are blocking the GnRH receptor, and directly reduced as such, they do not cause that an increase of LH and testosterone increased Ht initial reactions associated with GnRH analogues. Anti-androgen supplementation before and may need during the beginning of the treatment is not necessary with this drug class. Abarelix was the first GnRH antagonist to be approved by the Food and Drug Administration, but was withdrawn from the U.S. market because of an unacceptable rate of systemic allergic reactions. Subsequently End, the FDA approved degarelix for the treatment of advanced prostate cancer in 2008 at a dose of 80 mg per month after a subcutaneous injection of 240 mg loading dose.52 In a phase III randomized 610 patients to degarelix or leuprolide for prostate cancer with a prime Ren endpoint of testosterone suppression in ML21 F0.5 ng was degarelix induced no worse than in maintaining low testosterone levels over a period of one year and leuprolide testosteroneand PSA suppression significantly faster than leuprolide.53 An updated analysis reports that 504 patients who completed zweij hrige study, 384 up to a Loss EXTENSIONS continue to vigorously study in which recipients were rerandomized leuprolide to degarelix 240/80 mg or 240/160 mg. W During the first year of treatment, the risk of PSA-PFS was found to be significantly lower with degarelix 240/80 mg compared to leuprolide. After a median follow-up of 27.5 months, the hazard rate of PSA PFS was significantly higher in patients, transfer of degarelix compared with leuprolide reduced before crossover.54 short beautiful adverse effects of this agent as hot flashes, pain at the injection site, weight gain and increased hte serum transaminases.55 cytochrome P450 inhibitors were used in the treatment of advanced prostate cancer as second-line hormonal therapy and beyond, since these enzymes are required for the synthesis of androgens. These agents include ketoconazole, abiraterone acetate and aminoglutethimide. Ketoconazole, an imidazole antifungal agent, inhibits adrenal androgen synthesis by acting as a non-selective CYP17.56 ketoconazole can also be a direct cytotoxic effect on prostate cancer cells in the pr Clinical models.57 In a phase III study comparing the struggle against the withdrawal of androgens alone vs. observed the fight against the withdrawal of androgens with ketoconazole, O50% decline in PSA were observed in 11% versus 27% of patients and objective tumor responses were 2% versus 20% of people with the disease observed measurable, respectively. 58 However, median survival time was not between the groups. Because of side effects of this drug Lich nausea and vomiting in confinement as the H Half of all patients, it is often difficult to tolerate a drug. In addition, an Vismodegib Hedgehog inhibitor adrenal insufficiency occur with this therapy, so patients usually need additionally USEFUL hydrocortisone competitors. The abiraterone acetate is a novel oral selective inhibitor of androgen biosynthesis, which selectively blocks the effect of CYP17 and powerful in testes and adrenal glands, enter Ing completely Ndigen withdrawal of androgens. In addition, recent data suggest that prostate tumors are themselves able to endogenous androgens, which synthesize.