Abarelix

Superiority:

treatment of advanced symptomatic prostate cancer. Hormonal therapy of prostate cancer is based on the modulation of testosterone to achieve medical castration levels. The inhibition of GnRH activity causes the suppression of luteinizing hormone (LH) and follicle stimulating hormone (FSH) secretion, thereby reducing the secretion of testosterone by the testes. Abarelix is the first GnRH antagonist to reach its market. Hormonal therapy with GnRH agonists such as leuprolide, buserelin, and goserelin has been in use for over two decades. Drugs of this type achieve the suppression of LH and FSH by a feedback inhibition mechanism, which involves an initial rise in the LH and FSH levels and, consequently, in the levels of testosterone. A testosterone surge may induce a clinical tumor flare that worsens cancer-related symptoms. This phenomenon is observed in 4–33% of patients receiving a GnRH agonist. A GnRH antagonist such as abarelix acts by direct inhibition of LH and FSH secretion, which avoids the initial surge in serum testosterone concentrations. Abarelix is a decapeptide, and it is prepared by a typical coupling cycle for peptide synthesis using Boc-amino acids and a methylbenzhydrylamine (MBHA) resin. Abarelix has high binding affinittreatment of advanced symptomatic prostate cancer. Hormonal therapy of prostate cancer is based on the modulation of testosterone to achieve medical castration levels. The inhibition of GnRH activity causes the suppression of luteinizing hormone (LH) and follicle stimulating hormone (FSH) secretion, thereby reducing the secretion of testosterone by the testes. Abarelix is the first GnRH antagonist to reach its market. Hormonal therapy with GnRH agonists such as leuprolide, buserelin, and goserelin has been in use for over two decades. Drugs of this type achieve the suppression of LH and FSH by a feedback inhibition mechanism, which involves an initial rise in the LH and FSH levels and, consequently, in the levels of testosterone. A testosterone surge may induce a clinical tumor flare that worsens cancer-related symptoms. This phenomenon is observed in 4–33% of patients receiving a GnRH agonist. A GnRH antagonist such as abarelix acts by direct inhibition of LH and FSH secretion, which avoids the initial surge in serum testosterone concentrations. Abarelix is a decapeptide, and it is prepared by a typical coupling cycle for peptide synthesis using Boc-amino acids and a methylbenzhydrylamine (MBHA) resin. Abarelix has high binding affinittreatment of advanced symptomatic prostate cancer. Hormonal therapy of prostate cancer is based on the modulation of testosterone to achieve medical castration levels. The inhibition of GnRH activity causes the suppression of luteinizing hormone (LH) and follicle stimulating hormone (FSH) secretion, thereby reducing the secretion of testosterone by the testes. Abarelix is the first GnRH antagonist to reach its market. Hormonal therapy with GnRH agonists such as leuprolide, buserelin, and goserelin has been in use for over two decades. Drugs of this type achieve the suppression of LH and FSH by a feedback inhibition mechanism, which involves an initial rise in the LH and FSH levels and, consequently, in the levels of testosterone. A testosterone surge may induce a clinical tumor flare that worsens cancer-related symptoms. This phenomenon is observed in 4–33% of patients receiving a GnRH agonist. A GnRH antagonist such as abarelix acts by direct inhibition of LH and FSH secretion, which avoids the initial surge in serum testosterone concentrations. Abarelix is a decapeptide, and it is prepared by a typical coupling cycle for peptide synthesis using Boc-amino acids and a methylbenzhydrylamine (MBHA) resin. Abarelix has high binding affinittreatment of advanced symptomatic prostate cancer. Hormonal therapy of prostate cancer is based on the modulation of testosterone to achieve medical castration levels. The inhibition of GnRH activity causes the suppression of luteinizing hormone (LH) and follicle stimulating hormone (FSH) secretion, thereby reducing the secretion of testosterone by the testes. Abarelix is the first GnRH antagonist to reach its market. Hormonal therapy with GnRH agonists such as leuprolide, buserelin, and goserelin has been in use for over two decades. Drugs of this type achieve the suppression of LH and FSH by a feedback inhibition mechanism, which involves an initial rise in the LH and FSH levels and, consequently, in the levels of testosterone. A testosterone surge may induce a clinical tumor flare that worsens cancer-related symptoms. This phenomenon is observed in 4–33% of patients receiving a GnRH agonist. A GnRH antagonist such as abarelix acts by direct inhibition of LH and FSH secretion, which avoids the initial surge in serum testosterone concentrations. Abarelix is a decapeptide, and it is prepared by a typical coupling cycle for peptide synthesis using Boc-amino acids and a methylbenzhydrylamine (MBHA) resin. Abarelix has high binding affinit