4245-41-4CC(=O)Oc1ccc2c(c1)CC[C@@H]1[C@@H]2CC[C@]2(C)[C@@H](O)CC[C@@H]12FHXBMXJMKMWVRG-SLHNCBLASA-NEstradiol acetate is a steroid ester.
4245-41-4DTXSID7045867FDA approved drugs -> Active ingredient
FDA approved drugs -> Active ingredient
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Danger
H351 (96.2%): Suspected of causing cancer [Warning Carcinogenicity]
P203, P260, P263, P264, P270, P280, P318, P405, and P501 (click each P-code to see the statement)
Aggregated GHS information provided per 26 reports by companies from 3 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.
Estrogen mediates its effects across the body through potent agonism of the Estrogen Receptor (ER), which is located in various tissues including in the breasts, uterus, ovaries, skin, prostate, bone, fat, and brain. Estradiol binds to both subtypes of the Estrogen Receptor: Estrogen Receptor Alpha (ERα) and Estrogen Receptor Beta (ERβ). Estradiol also acts as a potent agonist of G Protein-coupled Estrogen Receptor (GPER), which has recently been recognized as a major mediator of estradiol's rapid cellular effects.
Estradiol enters target cells freely (e.g., female organs, breasts, hypothalamus, pituitary) and 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. Increases in the down-stream effects of ER binding reverses some of the symptoms of menopause, which are primarily caused by a loss of estrogenic activity.
Exogenous estrogens are metabolized using the same mechanism as endogenous estrogens. Estradiol is converted reversibly to estrone, and both can be converted to estriol, which is the major urinary metabolite. Estrogens also undergo enterohepatic recirculation via sulfate and glucuronide conjugation in the liver, biliary secretion of conjugates into the intestine, and hydrolysis in the gut followed by reabsorption. In postmenopausal women, a significant proportion of the circulating estrogens exist as sulfate conjugates, especially estrone sulfate, which serves as a circulating reservoir for the formation of more active estrogens.
Estradiol acetate has known human metabolites that include 6-[(3-acetyloxy-13-methyl-6,7,8,9,11,12,14,15,16,17-decahydrocyclopenta[a]phenanthren-17-yl)oxy]-3,4,5-trihydroxyoxane-2-carboxylic acid.
Wird geladen…
CHEMBL1200430CHEBI:135981ESTRADIOL ACETATE
Estrogen Receptor Agonists [MoA]; Estrogen [EPC]; Estradiol Congeners [CS]
Drug delivery from Femring is rapid for the first hour and then declines to a relatively constant rate for the remainder of the 3-month dosing interval. Estradiol acetate is rapidly hydrolyzed to estradiol which is absorbed through the vaginal mucosa as evidenced by the mean time to maximum concentration (tmax) for estradiol of about 1 hour (range 0.25 to 1.5 hrs). Following the maximum concentration (Cmax=1129pg/mL), serum estradiol decreases rapidly such that by 24 to 48 hours postdose, serum estradiol concentrations are relatively constant through the end of the 3-month dosing interval.
Estradiol, estrone and estriol are excreted in the urine along with glucuronide and sulfate conjugates.
The distribution of exogenous estrogens is similar to that of endogenous estrogens. Estrogens are widely distributed in the body and are generally found in higher concentrations in the sex hormone target organs.
VerwendenEstrogen replacement therapy.