Drug/Small Molecule:

ethinyl estradiol

A semisynthetic alkylated estradiol with a 17-alpha-ethinyl substitution. It has high estrogenic potency when administered orally, and is often used as the estrogenic component in oral contraceptives. PubChem (source: Drug Bank)

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. (source: Drug Bank)

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. The combination of an estrogen with a progestin suppresses the hypothalamic-pituitary system, decreasing the secretion of gonadotropin-releasing hormone (GnRH). (source: Drug Bank)

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. (source: Drug Bank)

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. (source: Drug Bank)

97% (source: Drug Bank)

Rapid and complete absorption follows oral intake of ethinyl estradiol (bioavailability 43%). (source: Drug Bank)

Oral, mouse LD₅₀: 1737 mg/kg. Symptoms of overdose include nausea and vomiting, and withdrawal bleeding may occur in females. (source: Drug Bank)

C[C@]12CC[C@@H]3c4ccc(cc4CC[C@H]3[C@@H]1CC[C@]2(C#C)O)O (source: Drug Bank)