| Indication | For treatment of moderate to severe vasomotor symptoms associated with the menopause, female hypogonadism, prostatic carcinoma-palliative therapy of advanced disease, breast cancer, as an oral contraceptive, and as emergency contraceptive. |
| Pharmacodynamics | Ethinyl estradiol is a synthetic derivative of the natural estrogen estradiol. It is one of two estrogens currently used in oral contraceptive pills. The other, mestranol, is converted to ethinyl estradiol before it is biologically active. Ethinyl estradiol and norethindrone are used together as an oral contraceptive agent. |
| Mechanism of action | Estrogens diffuse into their target cells and interact with a protein receptor. Target cells include the female reproductive tract, the mammary gland, the hypothalamus, and the pituitary. Estrogens increase the hepatic synthesis of sex hormone binding globulin (SHBG), thyroid-binding globulin (TBG), and other serum proteins and suppress follicle-stimulating hormone (FSH) from the anterior pituitary. This cascade is initiated by initially binding to the estrogen receptors. The combination of an estrogen with a progestin suppresses the hypothalamic-pituitary system, decreasing the secretion of gonadotropin-releasing hormone (GnRH). |
| Absorption | Rapid and complete absorption follows oral intake of ethinyl estradiol (bioavailability 43%). |
| Volume of distribution | Not Available |
| Protein binding | 97% |
| Metabolism | Hepatic. Quantitatively, the major metabolic pathway for ethinyl estradiol, both in rats and in humans, is aromatic hydroxylation, as it is for the natural estrogens. |
| Route of elimination | Not Available |
| Half life | 36 +/- 13 hours |
| Clearance | Not Available |
| Toxicity | Oral, mouse LD50: 1737 mg/kg. Symptoms of overdose include nausea and vomiting, and withdrawal bleeding may occur in females. |