1. Ethinodiol
1. Ethinodiol
2. Aethynodiolum
3. 1231-93-2
4. Etynodiolum
5. Etinodiol
6. Chebi:50785
7. 9e01c36a9s
8. Etynodiol (inn)
9. (3beta,17beta)-17-ethynylestr-4-ene-3,17-diol
10. (3beta,17alpha)-19-norpregn-4-en-20-yne-3,17-diol
11. 17alpha-ethynyl-19-norandrost-4-ene-3beta,17beta-diol
12. Etynodiol [inn]
13. 17alpha-ethynylestr-4-ene-3beta,17beta-diol
14. (3s,8r,9s,10r,13s,14s,17r)-17-ethynyl-13-methyl-2,3,6,7,8,9,10,11,12,14,15,16-dodecahydro-1h-cyclopenta[a]phenanthrene-3,17-diol
15. Etinodiolo [dcit]
16. Etinodiolo
17. Etynodiol [inn:ban]
18. Etinodiol [inn-spanish]
19. Etynodiolum [inn-latin]
20. Einecs 214-971-5
21. Unii-9e01c36a9s
22. Hsdb 7897
23. (3-beta,17-alpha)-19-norpregn-4-en-20-yne-3,17-diol
24. 17-alpha-ethynyl-19-norandrost-4-ene-3-beta,17-beta-diol
25. Ethynodiol [mi]
26. 3beta-hydroxynorethisterone
27. Etynodiol [who-dd]
28. 17alpha-ethynyl-estra-4-ene-3beta,17beta-diol
29. Schembl140933
30. 19-nor-17-alpha-pregn-4-en-20-yne-3-beta,17-diol
31. Chembl1201406
32. Dtxsid1023025
33. 19-norpregn-4-en-20-yne-3,17-diol, (3-beta,17-alpha)-
34. 3.beta.-hydroxylynestrenol
35. 19-norpregn-4-en-20-yne-3,17-diol, (3.beta.,17.alpha.)-
36. Zinc30691629
37. Db13866
38. D07939
39. Q5405158
40. (3.beta.,17.beta.)-17-ethynylestr-4-ene-3,17-diol
41. 17.alpha.-ethynyl-4-oestrene-3.beta.,17.beta.-diol
42. Estr-4-ene-3,17-diol, 17-ethynyl-, (3.beta.,17.beta.)-
| Molecular Weight | 300.4 g/mol |
|---|---|
| Molecular Formula | C20H28O2 |
| XLogP3 | 3.1 |
| Hydrogen Bond Donor Count | 2 |
| Hydrogen Bond Acceptor Count | 2 |
| Rotatable Bond Count | 1 |
| Exact Mass | 300.208930132 g/mol |
| Monoisotopic Mass | 300.208930132 g/mol |
| Topological Polar Surface Area | 40.5 Ų |
| Heavy Atom Count | 22 |
| Formal Charge | 0 |
| Complexity | 555 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 7 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 1 |
Contraceptives, Oral, Synthetic
National Library of Medicine's Medical Subject Headings online file (MeSH, 2009)
Ethynodiol diacetate and ethinyl estradiol tablets, USP are indicated for the prevention of pregnancy in women who elect to use oral contraceptives as a method of contraception. /Included in US product label/
US Natl Inst Health; DailyMed. Current Medication Information for KELNOR 1/35 (ethynodiol diacetate and ethinyl estradiol) kit (January 2011). Available from, as of March 29, 2011: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?id=37748
Cigarette smoking increases the risk of serious cardiovascular side effects from oral contraceptive use. This risk increases with age and with heavy smoking (15 or more cigarettes per day) and is quite marked in women over 35 years of age. Women who use oral contraceptives should be strongly advised not to smoke.
US Natl Inst Health; DailyMed. Current Medication Information for KELNOR 1/35 (ethynodiol diacetate and ethinyl estradiol) kit (January 2011). Available from, as of March 29, 2011: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?id=37748
Both the relative and attributable risks of cerebrovascular events (thrombotic and hemorrhagic strokes) have been reported to be increased with oral contraceptive use, although, in general, the risk was greatest among older (over 35 years), hypertensive women who also smoked. Hypertension was reported to be a risk factor for both users and nonusers, for both types of strokes, while smoking increased the risk for hemorrhagic strokes.
US Natl Inst Health; DailyMed. Current Medication Information for KELNOR 1/35 (ethynodiol diacetate and ethinyl estradiol) kit (January 2011). Available from, as of March 29, 2011: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?id=37748
Because of changes in practice and, also, because of some limited new data that suggest that the risk of cardiovascular disease with the use of oral contraceptives may now be less than previously observed, the Fertility and Maternal Health Drugs Advisory Committee was asked to review the topic in 1989. The Committee concluded that, although cardiovascular disease risks may be increased with oral contraceptive use after age 40 in healthy nonsmoking women (even with the newer low-dose formulations), there are greater potential health risks associated with pregnancy in older women and with the alternative surgical and medical procedures that may be necessary if such women do not have access to effective and acceptable means of contraception.
US Natl Inst Health; DailyMed. Current Medication Information for KELNOR 1/35 (ethynodiol diacetate and ethinyl estradiol) kit (January 2011). Available from, as of March 29, 2011: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?id=37748
Benign hepatic adenomas and other hepatic lesions have been associated with oral contraceptive use, although the incidence of such benign tumors is rare in the United States. Indirect calculations have estimated the attributable risk to be in the range of 3.3 cases per 100,000 for users, a risk that increases after 4 or more years of use. Rupture of benign, hepatic adenomas or other lesions may cause death through intra-abdominal hemorrhage. Therefore, such lesions should be considered in women presenting with abdominal pain and tenderness, abdominal mass, or shock. About one quarter of the cases presented because of abdominal masses; up to one half had signs and symptoms of acute intraperitoneal hemorrhage. Diagnosis may prove difficult. Studies from the U.S., Great Britain, and Italy have shown an increased risk of hepatocellular carcinoma in long-term (>8 years; relative risk of 7-20) oral contraceptive users. However, these cancers are rare in the United States, and the attributable risk (the excess incidence) of liver cancers in oral contraceptive users approaches less than 1 per 1,000,000 users.
US Natl Inst Health; DailyMed. Current Medication Information for KELNOR 1/35 (ethynodiol diacetate and ethinyl estradiol) kit (January 2011). Available from, as of March 29, 2011: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?id=37748
For more Drug Warnings (Complete) data for Ethynodiol (41 total), please visit the HSDB record page.
Absorption, distribution, excretion and metabolism of SC-11800EE, a combined steroid preparation consisting of SC-11800(ethynodiol diacetate)as gestagen and ethinyl estradiol (EE)as estrogen in 20:1 (w:w), were studied with the use of 14C-SC-11800 and 3H-EE by radiometry in female rats and by the whole body autoradiography in female normal and pregnant mice. The gestagen orally given with EE was rapidly absorbed from digestive tracts and distributed in tissues in various levels. Gestagen levels in liver and kidney exceeded that in plasma. About 75% of dosed radioactivity was excreted in feces largely via bile and more than 20% in urine within 72 hr after administration. The gestagen was metabolized extensively to more polar products and their conjugates. The pharmacokinetic behavior of the gestagen given with EE did not alter after repeated administrations for 7 days, but was slightly different from that without EE, possibly due to the estrogen effect. The pharmacokinetic behavior of the estrogen was independent from the gestagen given simultaneously. The distribution of the gestagen given with EE revealed by the whole body autoradiography in normal mice were essentially consistent with the radiometric results in rats and that in the pregnant mice showed that the gestagen in fetus was virtually nil under the present conditions.
PMID:578931 Suzuki H et al; Radioisotopes 26 (3): 152-7 (1977)
Bioavailability and pharmacokinetics of norethisterone (NE) were studied in 12 women, aged 21-37 years, after oral doses of ethynodiol diacetate (EDA). Plasma NE levels, measured by radioimmunoassay, were used to compare the bioavailability of EDA tablets (Ovulen 50; 1 mg EDA plus .05 mg ethinyl estradiol) with that of a standard oral solution of EDA. The 3 different batches of tablets studied showed different in vitro dissolution rates, 82.6%, 94.6%, and 99% at 3 hours. No marked differences were seen in the bioavailability of the tablet formulations, which were essentially bioequivalent to the solution. Peak plasma NE levels were reached within 4 hours of EDA administration in solution or tablets. Following the peak, NE plasma levels declined in 2 phases, with mean terminal elimination 1/2-lives of 4-6.9 hours. These results have shown that small variations in in vitro dissolution rates do not affect the bioavailability of NE from tablets containing EDA.
PMID:428229 Vose CW et al; Contraception 19 (2): 119-27 (1979)
Small amounts of oral contraceptive steroids have been identified in the milk of nursing mothers ...
US Natl Inst Health; DailyMed. Current Medication Information for KELNOR 1/35 (ethynodiol diacetate and ethinyl estradiol) kit (January 2011). Available from, as of March 29, 2011: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?id=37748
After oral administration, norethisterone acetate and ethynodiol diacetate are rapidly converted to norethisterone by esterases during hepatic first-pass metabolism.
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V91 146 (2007)
On administration of a single oral dose of [4-(14)C]ethynodiol diacetate (0.15 mg/kg) to rhesus monkey, plasma concentration of total 14C peaked after about 4 hr. About 60% of the plasma radioactivity was present as glucuronide conjugates and no unchanged drug was detected. Some 67 +/- 6% (mean +/- S.D.) of the dose of 14C was excreted in 4 days, 50 +/- 6% in urine and 18 +/- 2% in feces. Most of the urinary excretion occurred within 24 hr of dosage. Glucuronide conjugates accounted for 60% of the urinary 14C, and 46% of the fecal 14C was free steroids. Norethisterone and its tetrahydro metabolites were identified in the free, glucuronide and sulphate fractions of plasma and urine. Keto-4,5-dihydronorethisterones and trihydroxy metabolites were identified in the conjugated fractions of urine, and a complex mixture of polar metabolites was detected in feces.
PMID:7445531 Lewis CJ et al; Xenobiotica 10 (9): 705-13 (1980)
All of the 17beta-ethynyl progestins reviewed follow similar metabolic paths. For three of these, norethynodrel, ethynodiol diacetate and lynestrenol, a principal metabolite is norethindrone. Biotransformation to more polar metabolites and conjugation proceed rapidly for these three precursor drugs and norethindrone. ... The compounds appear to be readily absorbed, and they and their metabolites are excreted to a greater extent in the urine than in the feces.
PMID:411940 Ranney RE; J Toxicol Environ Health 3 (1-2): 139-66 (1977)
... The ethynodiol diacetate was metabolized extensively to more polar products and their conjugates. ...
PMID:578931 Suzuki H et al; Radioisotopes 26 (3): 152-7 (1977)
There is limited information on the metabolism of levonorgestrel, norethindrone and structurally related contraceptive steroids. Both levonorgestrel and norethindrone undergo extensive reduction of the alpha, beta-unsaturated ketone in ring A. Levonorgestrel also undergoes hydroxylation at carbons 2 and 16. The metabolites of both compounds circulate predominantly as sulfates. In urine, levonorgestrel metabolites are found primarily in the glucuronide form, whereas norethindrone metabolites are present in approximately equal amounts as sulfates and glucuronides. Of the progestogens structurally related to norethindrone, norethindrone acetate, ethynodiol diacetate, norethindrone enanthate, and perhaps lynestrenol, undergo rapid hydrolysis and are converted to the parent compound and its metabolites. There is no convincing evidence that norethynodrel is converted to norethindrone. Of the progestogens structurally related to levonorgestrel, it appears that neither desogestrel nor gestodene are transformed to the parent compound. However, there is evidence that norgestimate can be, at least partly, converted to levonorgestrel. ...
PMID:2143719 Stanczyk FZ, Roy S; Contraception 42 (1): 67-96 (1990)
Combination oral contraceptives act primarily by suppression of gonadotropins. Although the primary mechanism of this action is inhibition of ovulation, other alterations in the genital tract, including changes in the cervical mucus (which increase the difficulty of sperm entry into the uterus) and the endometrium (which may reduce the likelihood of implantation) may also contribute to contraceptive effectiveness.
US Natl Inst Health; DailyMed. Current Medication Information for KELNOR 1/35 (ethynodiol diacetate and ethinyl estradiol) kit (January 2011). Available from, as of March 29, 2011: https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?id=37748
Progesterone increases urinary sodium excretion at least in part by competition for renal mineralocorticoid receptors. In contrast, synthetic progestagens do not increase sodium excretion or even cause a slight sodium retention. /Investigators/ therefore compared the ability of progesterone and 12 progesterone like compounds to displace [3H]aldosterone from binding at cytoplasmic mineralocorticoid receptors in rat kidney. All synthetic progesteronelike steroids were less active than progesterone in competing with [3H]aldosterone for the receptor binding: progesterone 100%, 11 beta-OH progesterone 50%, 17 alpha OH-progesterone 24% and 16 alpha-methyl-progesterone 3%. Derivates of 17 alpha OH-progesterone (medrogestone 5%, dydrogestone 4%, medroxy progesterone-acetate 2% and chlormadinone-acetate 0.5%) were more potent than 19-nor-testosterone derivates: ethisterone 1%, norethisterone less than 1%, norethindrone less than 1%, norethyl-nodrel less than 1%, and ethynodiol-diacetate less than 1%. The decreased affinity of synthetic progestins for mineralocorticoid receptors explains in part the lack of natriuretic activity of these compounds.
PMID:574701 Wambach G et al; Acta Endocrinol (Copenh) 92 (3): 560-7 (1979)
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