indication

Used in hormone replacement therapy, treating symptoms of menopause such as hot flashes. Also used to treat breast and prostate cancer.

pharmacology

Quinestrol is the 3-cyclopentyl ether of ethinyl estradiol (the active metabolite). After gastrointestinal absorption, it is stored in adipose tissue where it is slowly released and metabolized principally to the parent compound, ethinyl estradiol. Ethinyl estradiol is a synthetic derivative of the natural estrogen estradiol.

mechanism of action

Estrogens diffuse into their target cells and interact with a protein receptor (the estrogen receptor). Estrogen interacts with a target cell receptor. When the estrogen receptor has bound its ligand it can enter the nucleus of the target cell, and regulate gene transcription which leads to formation of messenger RNA. The mRNA interacts with ribosomes to produce specific proteins that express the effect of estradiol upon the target cell. 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. 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).

toxicity

Symptoms of overdose include nausea and vomiting, and withdrawal bleeding may occur in females.

biotransformation

Metabolized principally to the parent compound, ethinyl estradiol. Ethinyl estradiol is metabolized in the liver. Quantitatively, the major metabolic pathway for ethinyl estradiol, both in rats and in humans, is aromatic hydroxylation, as it is for the natural estrogens.

absorption

Absorbed following oral administration.

drug interactions

Fosphenytoin: The enzyme inducer, fosphenytoin, decreases the effect of the hormone agent, quinestrol.

Griseofulvin: The enzyme inducer, griseofulvin, decreases the effect of the hormone agent, quinestrol.

Phenobarbital: The enzyme inducer, phenobarbital, decreases the effect of the hormone agent, quinestrol.

Phenytoin: The enzyme inducer, phenytoin, decreases the effect of the hormone agent, quinestrol.

Prednisolone: The estrogenic agent, quinestrol, may increase the effect of the corticosteroid, prednisolone.

Prednisone: The estrogenic agent, quinestrol, may increase the effect of corticosteroid, prednisone.

Primidone: The enzyme inducer, primidone, decreases the effect of the hormone agent, quinestrol.