Quinestrol

364.52

364.52

205-803-1

JR0N7XD5GZ

DTXSID6046553

29.5

5.3

Solid

1.0693 (rough estimate)

107.5 °C

435.69°C (rough estimate)

218.8±24.4 °C

1.4480 (estimate)

1.57e-03 g/L

6.43E-11mmHg at 25°C

D25 +5° (c = 0.5 in dioxane)

Ⅲ

2811

3

45-61-20/21/22-46

53-22-36/37/39-45

RC8948000

T

Stable at normal temperatures and pressures.

P201-P280-P308 + P313

H302-H312-H332-H350-H360

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

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

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.

Compounds that interact with ESTROGEN RECEPTORS in target tissues to bring about the effects similar to those of ESTRADIOL. Estrogens stimulate the female reproductive organs, and the development of secondary female SEX CHARACTERISTICS. Estrogenic chemicals include natural, synthetic, steroidal, or non-steroidal compounds. (See all compounds classified as Estrogens.)

Absorbed following oral administration.

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.

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).

Estrovis

Human Drugs -> FDA Approved Drug Products with Therapeutic Equivalence Evaluations (Orange Book) -> Active Ingredients|Lipids -> Sterol Lipids [ST] -> Steroids [ST02] -> C18 steroids (estrogens) and derivatives [ST0201]