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Home / Drugs / Starting with C / Chlorotrianisene
 
Chlorotrianisene
 

A powerful synthetic, non-steroidal estrogen. [PubChem]
BrandsAnisene
Chlorotrisin
Clorestrolo
Clorotrisin
Hormonisene
Khlortrianizen
Merbentul
Metace
Rianil
Tace
Tace-Fn
Trianisestrol
CategoriesAntineoplastic Agents
Antineoplastic Agents, Hormonal
Estrogens, Non-Steroidal
ManufacturersBanner pharmacaps inc
Sanofi aventis us llc
SynonymsChloortrianisestrol
Chlorestrolo
Chlorotrianisenum [INN-Latin]
Chlorotrianisine
Chlorotrianizen
Chlortrianisen
Chlortrianisene
Chlortrianisenum
Chlortrianisestrol
Chlortrianisoestrolum
Chlortrianizen
Clorotrianiseno [INN-Spanish]

indication

Used to treat symptoms of menopause, deficiencies in ovary function (including underdevelopment of female sexual characteristics and some types of infertility), and in rare cases, prostate cancer. Chlorotrianisene may also be used to prevent breast engorgement following childbirth.

pharmacology

Chlorotrianisene is a nonsteroidal synthetic estrogen. After menopause, when the body no longer produces estrogen, chlorotrianisene is used as a simple replacement of estrogen. The estrogen-stimulated endometrium may bleed within 48-72 hours after discontinuance of estrogen therapy. Paradoxically, prolonged estrogen therapy may cause shrinkage of the endometrium and an increase in size of the myometrium. Estrogens have a weak anabolic effect and may cause sodium retention with associated fluid retention and edema. Estrogens may also decrease elevated blood cholesterol and phospholipid concentrations. Estrogens affect bone by increasing calcium deposition and accelerating epiphyseal closure, following initial growth stimulation. During the preovulatory or nonovulatory phase of the menstrual cycle, estrogen is the principal determinant in the onset of menstruation. A decline of estrogenic activity at the end of the menstrual cycle also may induce menstruation; however, the cessation of progesterone secretion is the most important factor during the mature ovulatory phase of the menstrual cycle. The benefit derived from estrogen therapy in the prevention of postpartum breast engorgement must be carefully weighed against the potential increased risk of puerperal thromboembolism associated with the use of large doses of estrogens.

mechanism of action

Chlorotrianisene binds to the estrogen receptor on various estrogen receptor bearing cells. Target cells include cells in 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.

toxicity

Acute overdosage of large doses of oral contraceptives in chidren reportedly produces almost no toxicity except nausea and vomiting. Acute overdosage of estrogens may cause nausea, and withdrawal bleeding may occur in females.

biotransformation

Metabolized principally in the liver, although the kidneys, gonads, and muscle tissues may be involved to some extent. The metabolic fate of the synthetic estrogens has not been fully elucidated.

absorption

Absorption following oral administration is rapid.

drug interactions

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

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

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

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

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

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

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

Raloxifene: Association not recommended