Browse Prescribing Notes by Therapeutic Subcategory

Gonadotropin releasing hormone (GnRH) agonists cause an initial surge of luteinizing hormone and follicle-stimulating hormone followed by inhibition of gonadotropin release which decreases testosterone production. Transient disease flare may occur due to an initial hormone surge and can be prevented with a 2 to 4 week course of an androgen receptor blocker or GnRH antagonist.
Aromatase inhibitors block the conversion of androgens to estrogens via the aromatase enzyme system by competitively binding to the heme of the cytochrome P450 subunit of the enzyme, resulting in a reduction of estrogen biosynthesis in all tissues.
Selective Estrogen-Receptor Modulators (SERMs) bind to estrogen receptors which results in activation of estrogenic pathways in some tissues and blockade of estrogenic pathways in others.
Estrogen receptor antagonists competitively bind to estrogen receptors (ER) and downregulate the ER protein in human breast cancer cells. Estrogen receptor antagonists are considered "pure anti-estrogens" because they show no agonist-type effects.
Aromatase inactivators act as a false substrate for the aromatase enzyme. They bind irreversibly to the active site of the enzyme causing its inactivation, an effect known as "suicide inhibition."
Antiandrogens competitively inhibit the action of androgens by binding to cytosol androgen receptors in the target tissue.
Progestins produce antineoplastic effects on breast carcinoma by modifying the action of other steroid hormones and by exerting a direct cytotoxic effect on tumor cells. They may also stimulate appetite and restore a sense of well-being in cachectic patients with advanced cancer.
Lysodren is chemically similar to the insecticides DDT and DDD and it selectively attacks normal or neoplastic adrenocortical cells and causes a rapid reduction in the levels of adrenocorticosteroids and their metabolites.