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1. Femring
2. Femtrace
3. Estradiol 3-acetate
4. Estradiol-3-acetate
5. 4245-41-4
6. Estradiol Acetate [usan]
7. E3a
8. 5r97f5h93p
9. Estradiol Acetate (usan)
10. Dsstox_cid_25867
11. Dsstox_rid_81186
12. Dsstox_gsid_45867
13. [(8r,9s,13s,14s,17s)-17-hydroxy-13-methyl-6,7,8,9,11,12,14,15,16,17-decahydrocyclopenta[a]phenanthren-3-yl] Acetate
14. Menoring
15. Cas-4245-41-4
16. 3-o-acetylestradiol
17. Estradiol, 3-acetate
18. 17beta-estradiol 3-acetate
19. Unii-5r97f5h93p
20. E 3a
21. Estradiol-acetate
22. Femring (tn)
23. 3-acetoxyestra-1,3,5(10)-trien-17beta-ol
24. 17beta-hydroxy-3-acetoxyestra-1,3,5(10)-triene
25. Schembl148561
26. Estra-1,3,5(10)-triene-3,17beta-diyl 3-acetate
27. Chembl1200430
28. Dtxsid7045867
29. Estradiol Acetate [vandf]
30. Chebi:135981
31. Estradiol 3-acetate [mi]
32. Estradiol Acetate [mart.]
33. Estradiol Acetate [who-dd]
34. Tox21_111359
35. Tox21_113661
36. Db13952
37. Estradiol Acetate [orange Book]
38. Ncgc00249885-01
39. D04061
40. 3-acetoxy-oestra-1,3,5(10)-trien-17beta-ol
41. 17beta-hydroxyestra-1,3,5(10)-trien-3-yl Acetate
42. 3-(acetyloxy)estra-1,3,5(10)-trien-17.beta.-ol
43. Q27262772
44. 17.beta.-hydroxyestra-1,3,5(10)-trien-3-yl Acetate
45. Estra-1,3,5(10)-triene-3,17-diol, (17beta)-, 3-acetate
46. Estra-1,3,5(10)-triene-3,17-diol, (17 Beta)-, 3-acetate
47. Estra-1,3,5(10)-triene-3,17-diol, (17.beta.)-, 3-acetate
| Molecular Weight | 314.4 g/mol |
|---|---|
| Molecular Formula | C20H26O3 |
| XLogP3 | 2.8 |
| Hydrogen Bond Donor Count | 1 |
| Hydrogen Bond Acceptor Count | 3 |
| Rotatable Bond Count | 2 |
| Exact Mass | 314.18819469 g/mol |
| Monoisotopic Mass | 314.18819469 g/mol |
| Topological Polar Surface Area | 46.5 Ų |
| Heavy Atom Count | 23 |
| Formal Charge | 0 |
| Complexity | 476 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 5 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 1 |
Femring is indicated for the treatment of vasomotor and urogenital symptoms associated with menopause. Use of Femring (estradiol acetate) has been shown to improve symptoms caused by atrophy of the vagina (such as dryness, burning, pruritus and dyspareunia) and/or the lower urinary tract (urinary urgency and dysuria).
FDA Label
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 (ER) and Estrogen Receptor Beta (ER). 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.
Absorption
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.
Route of Elimination
Estradiol, estrone and estriol are excreted in the urine along with glucuronide and sulfate conjugates.
Volume of Distribution
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.
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.
S73 | METXBIODB | Metabolite Reaction Database from BioTransformer | DOI:10.5281/zenodo.4056560
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.
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