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Estrone (E1), sold under the brand names Estragyn, Kestrin, and Theelin among many others, is an estrogen medication and naturally occurring steroid hormone which has been used in menopausal hormone therapy and for other indications.[5][8][9][10][1][2] It has been available as an aqueous suspension or oil solution that is given by injection into muscle and as a vaginal cream that is applied inside of the vagina.[1][2][3][4] It can also be taken by mouth as estradiol/estrone/estriol (brand name Hormonin) or in the form of prodrugs like estrone sulfate, as in estropipate (piperazine estrone sulfate; Ogen) and conjugated estrogens (mostly sodium estrone sulfate; Premarin).[11][2][5]

Estrone (medication)
Estrone molecule ball.png
Clinical data
Trade namesEstragyn, Kestrin, Theelin, many others
SynonymsOestrone; E1; Follicular hormone; Folliculin; Folliculine; Follikulin; Theelin; Ketohydroxyestrin; Oxohydroxyestrin; 3-Hydroxyestra-1,3,5(10)-trien-17-one
Routes of
Intramuscular injection, vaginal, by mouth (as E2/E1/E3 or as estrone sulfate)[1][2][3][4][5]
Drug classEstrogen
ATC code
Legal status
Legal status
Pharmacokinetic data
BioavailabilityOral: very low[6]
Protein binding96%:[5][7]
Albumin: 80%
SHBG: 16%
• Free: 2–4%
MetabolismLiver (via hydroxylation, sulfation, glucuronidation)[5]
Estrone sulfate[5]
Estrone glucuronide[5]
• Others[5]
Elimination half-lifeIV: 20–30 minutes[5]
CAS Number
PubChem CID
Chemical and physical data
Molar mass270.366 g/mol g·mol−1
3D model (JSmol)
Melting point254.5 °C (490.1 °F)

Side effects of estrogens like estrone include breast tenderness, breast enlargement, headache, nausea, fluid retention, and edema, among others.[5] Estrone is a naturally occurring and bioidentical estrogen, or an agonist of the estrogen receptor, the biological target of estrogens like endogenous estradiol.[5] It is a relatively weak estrogen, with much lower activity than estradiol.[5] However, estrone is converted in the body into estradiol, which provides most of its estrogenic potency.[5] As such, estrone is a prodrug of estradiol.[5]

Estrone was first discovered in 1929, and was introduced for medical use shortly thereafter.[12][13][14] Although it has been used clinically in the past, estrone has largely been discontinued and is mostly no longer marketed.[9][15]


Medical usesEdit

Estrone has been marketed in intramuscular and vaginal formulations and was used as an estrogen in the treatment of symptoms of low estrogen levels such as hot flashes and vaginal atrophy in postmenopausal or ovariectomized women.[13] Estrone has also been used as an antigonadotropin and form of high-dose estrogen to treat prostate cancer in men as well as a form of high-dose estrogen to treat breast cancer in women.[16][17] It has since largely been discontinued and is mostly no longer available, having been superseded by other estrogens with better potency and pharmacokinetics (namely oral bioavailability and duration).[18][15]

Regardless of route of administration, if estrone is taken by a woman with an intact uterus, it should be combined with a progestogen such as progesterone to offset the risk of endometrial hyperplasia and cancer.[1][5]

Estrone has been used by intramuscular injection at a dosage of 0.1 to 0.5 mg given 2 or 3 times per week for the treatment of menopausal symptoms such as hot flashes and vaginal atrophy, and at a dosage of 0.1 to 1.0 mg weekly in single or divided doses for the treatment of female hypogonadism, surgical castration, and primary ovarian failure.[19] The range of single doses of estrone by intramuscular injection that are typically used clinically in women is 0.1 to 5 mg.[20] High doses of intramuscular estrone have been used for prostate cancer in men and for breast cancer in women.[16][17]

Estrogen dosages for breast cancer

Route/form Estrogen Dosage
Oral Estradiol 10 mg 3x/day
AI-resistant: 2 mg 1–3x/day
Estradiol valerate AI-resistant: 2 mg 1–3x/day
Conjugated estrogens 10 mg 3x/day
Ethinylestradiol 0.5–1 mg 3x/day
Diethylstilbestrol 5 mg 3x/day
Dienestrol 5 mg 3x/day
IM or SC injection Estradiol benzoate 5 mg 2–3x/week
Estradiol dipropionate 5 mg 2–3x/week
Estradiol valerate 30 mg 1x/2 weeks
Polyestradiol phosphate 40–80 mg 1x/4 weeks
Estrone 5 mg ≥3x/week
Notes: (1) Only in women who are at least 5 years postmenopausal. (2) Dosages are not necessarily equivalent. Sources: See template.

Estrogen dosages for prostate cancer

Route/form Estrogen Dosage
Oral Estradiol 1–2 mg 3x/day
Conjugated estrogens 1.25–2.5 mg 3x/day
Ethinylestradiol 0.15–2 mg/day
Ethinylestradiol sulfonate 1–2 mg 1x/week
Diethylstilbestrol 1–3 mg/day
Dienestrol 5 mg/day
Hexestrol 5 mg/day
Fosfestrol 120–480 mg 1–3x/day
Chlorotrianisene 12–24 mg/day
Quadrosilan 900 mg/day
Estramustine phosphate 140–1400 mg/day
Transdermal patch Estradiol 2–6x 100 μg/day
Scrotal: 1x 100 μg/day
IM or SC injection Estradiol benzoate 1.66 mg 3x/week
Estradiol dipropionate 5 mg 1x/week
Estradiol valerate 10–40 mg 1x/1–2 weeks
Estradiol undecylate 100 mg 1x/4 weeks
Polyestradiol phosphate Alone: 160–320 mg 1x/4 weeks
With oral EE: 40–80 mg 1x/4 weeks
Estrone 2–4 mg 2–3x/week
IV injection Fosfestrol 300–1200 mg 1–7x/week
Estramustine phosphate 240–450 mg/day
Note: Dosages are not necessarily equivalent. Sources: See template.

Available formsEdit

Estrone for intramuscular injection was provided as 1, 2, 2.5, 3, 4, and 5 mg/mL aqueous suspensions and/or oil solutions.[21][16][22][23][24] It has also been available in the form of vaginal creams (1 mg/g (0.1%)) and suppositories (0.2 mg, 0.25 mg) as well as subcutaneous pellet implants and oral tablets (1.25 mg).[20][3][1][22][23][24] A combined oral tablet formulation containing estradiol (0.3 mg, 0.6 mg), estrone (0.7 mg, 1.4 mg), and estriol (0.135 mg, 0.27 mg) has been marketed under the brand name Hormonin as well.[22][25][11][26][27] In addition, a combined injectable preparation containing estrone (1 mg) and progesterone (10 mg) is available in the form of ampoules under the brand name Synergon.[28][29][30][31][32]

Although estrone by intramuscular injection was originally formulated as an oil solution, it was soon replaced by formulations of estrone as an aqueous suspension due to a longer duration of action of these formulations.[33][34][24][17]

Side effectsEdit



Estrone is an estrogen, specifically an agonist of the estrogen receptors ERα and ERβ.[5][38] It is a far less potent estrogen than is estradiol, and as such is a relatively weak estrogen.[5][38] Given by subcutaneous injection in mice, estradiol is about 10-fold more potent than estrone and about 100-fold more potent than estriol.[39] According to one study, the relative binding affinities of estrone for the human ERα and ERβ were 4.0% and 3.5% of those estradiol, respectively, and the relative transactivational capacities of estrone at the ERα and ERβ were 2.6% and 4.3% of those of estradiol, respectively.[38] In accordance, the estrogenic activity of estrone has been reported to be approximately 4% of that of estradiol.[5] Because estrone can be transformed into estradiol, which is far more potent as an estrogen in comparison, most of the estrogenic potency of estrone in vivo is actually due to conversion into estradiol.[5] As such, similarly to the case of estrone sulfate, estrone is considered to be a prodrug of estradiol.[5][40] Some in vitro research has suggested that estrone might be able to partially antagonize the actions of estradiol,[41][42][43] but this does not appear to be of clinical significance.[5][44][45][46]

Relative activities of estradiol and related estrogens at the estrogen receptors

Estrogen ERα (%) ERβ (%) ERα (%) ERβ (%) ERα (%) ERβ (%)
Estradiol 100 100 100 100 100 100
Estrone 4.0 3.5 2.6 4.3 65.0 123
Estriol 11.3 17.6 10.6 16.6 93.8 93.8
Ethinylestradiol 233 37.8 213 27.2 91.4 78.0
Notes: At the human estrogen receptors. Sources: See template.

Relative affinities (%) of estradiol and related estrogens at steroid hormone proteins

Estradiol 2.6 7.9 100 0.6 0.13 8.7–12 <0.1
Estrone <1 <1 35 <1 <1 2.7 <0.1
Estriol <1 <1 15 <1 <1 <0.1 <0.1
Ethinylestradiol 15–25 1–3 112 1–3 <1 0.18 <0.1
Notes: Values are percentages (%). Reference ligands (100%) were progesterone for the PR, testosterone for the AR, E2 for the ER, DEXA for the GR, aldosterone for the MR, DHT for SHBG, and cortisol for CBG. Sources: See template.

Relative oral potencies of estrogens

Estradiol Bioidentical 1.0 1.0 1.0 1.0 1.0 1.0 1.0 1.0 1.0 1.0
Estrone Bioidentical ? ? ? 0.3 0.3 ? ? ? ? ?
Estriol Bioidentical 0.3 0.3 0.1 0.3 0.3 0.2 ? ? ? 0.67
Estrone sulfate Bioidentical ? 0.9 0.9 0.9 0.9 0.5 0.9 0.7 1.5 0.56–1.7
Conjugated estrogens Natural 1.2 1.5 2.0 1.1 1.0 1.5 3.0 1.5 5.0 1.3–4.5
Equilin sulfate Natural ? ? 1.0 ? ? 6.0 7.5 6.0 7.5 ?
Ethinylestradiol Synthetic 120 150 400 120 100 400 500 600 350 2.9–5.0
Diethylstilbestrol Synthetic ? ? ? 3.4 ? ? 25.6 24.5 19.5 5.7–7.5
Notes: Values are ratios, with estradiol as standard (i.e., 1.0). Abbreviations: HF = Clinical relief of hot flashes. VE = Increased proliferation of vaginal epithelium. UCa = Decrease in UCa. FSH = Suppression of FSH levels. LH = Suppression of LH levels. HDL-C, SHBG, CBG, and AGT = Increase in the serum levels of these liver proteins. Liver = Ratio of liver estrogenic effects to general/systemic estrogenic effects (specifically hot flashes relief and gonadotropin suppression). Type: Bioidentical = Identical to those found in humans. Natural = Naturally occurring but not identical to those found in humans (e.g., estrogens of other species). Synthetic = Man-made, does not occur naturally in animals or in the environment. Sources: See template.

Parenteral potencies and durations of steroidal estrogens

Estrogen EPD (14 days) CIC-D (month) Duration
Estradiol 40–60 mg 10 mg ≈ 2 days
Estradiol benzoate 25–35 mg 5–10 mga 5 mg ≈ 4–6 days
Estradiol dipropionate 25–30 mg 5 mg ≈ 5–8 days
Estradiol valerate 20–30 mg 5 mg 5 mg ≈ 7–8 days; 10 mg ≈ 10–14 days
Estradiol cypionate 20–30 mg 5 mg 5 mg ≈ 11–14 days
Estradiol benzoate (aq. susp.) 20 mg ? mg ≈ 21 days
Estradiol enantate ? 5–10 mg 10 mg ≈ 20–30 days
Estradiol undecylateb ? 5–10 mga 10–20 mg ≈ 40–60 days; 25–50 mg ≈ 60–120 days
Polyestradiol phosphate 40–60 mg 40–50 mg ≈ 30 days; 320 mg = >84 daysc
Estriol ? 1 mg ≈ <1 day
Polyestriol phosphate ? 50 mg ≈ 30 days; 80 mg ≈ 60 days
Estrone (aq. susp.) ? ?
Note: All are via i.m. injection of oil solution, unless noted otherwise (except for PEP and PE3P, which are used as aqueous solutions). Footnotes: a = Studied but never marketed. b = An effective OID of EU is 20–30 mg/month. c = The t1/2 of PEP after a 320-mg dose is 70 days. Sources: See template.

Clinical effectsEdit

In clinical research in the 1930s, estrone was given via intramuscular injection to ovariectomized women in order to study its effects and to elucidate the biological properties of estrogens in humans.[35][36][37] In these studies, prior to administration of estrone, amenorrhea, atrophy of the breasts (as well as flaccidity and small and non-erectile nipples), vagina, and endometrium, vaginal dryness, and subjective symptoms of ovariectomy (e.g., hot flashes, mood changes) were all present in the women.[35][36][37] Treatment with estrone was found to dose- and time-dependently produce a variety of effects, including breast changes, reproductive tract changes of the vagina, cervix, and endometrium/uterus, and relief from the subjective symptoms of ovariectomy, as well as increased libido.[35][36][37] Breast changes specifically included enlargement and a sense of fullness, increased sensitivity and pigmentation of the nipples as well as nipple erection, tingling within the breast mammary glandular tissue, and aching and soreness of the breasts.[35][36][37] Reproductive tract changes included increased growth, thickness, and differentiation of the endometrium, and reversal of vaginal and cervical atrophy, which were accompanied by increased congestion of the cervix and mucous discharge from the cervix, uterine cramps and needle-like pains, pelvic fullness, a "bearing-down" sensation, and increased vaginal lubrication, as well as uterine bleeding both during treatment and in the days following cessation of injections.[35][36][37] Endometrial hyperplasia also occurred with sufficiently high doses of estrone.[35][36][37]

Clinical research has confirmed the nature of estrone as an inactive prodrug of estradiol.[5][44][45][46] With oral administration of estradiol, the ratio of estradiol levels to estrone levels is about 5 times higher on average than under normal physiological circumstances in premenopausal women and with parenteral (non-oral) routes of estradiol.[5] Oral administration of menopausal replacement dosages of estradiol results in low, follicular phase levels of estradiol, whereas estrone levels resemble the high levels seen during the first trimester of pregnancy.[5][47][48] In spite of markedly elevated levels of estrone with oral estradiol but not with transdermal estradiol, clinical studies have shown that doses of oral and transdermal estradiol achieving similar levels of estradiol possess equivalent and non-significantly different potency in terms of measures including suppression of luteinizing hormone and follicle-stimulating hormone levels, inhibition of bone resorption, and relief of menopausal symptoms such as hot flashes.[5][44][45][46] In addition, estradiol levels were found to correlate with these effects, while estrone levels did not.[44][45] These findings confirm that estrone has very low estrogenic activity, and also indicate that estrone does not diminish the estrogenic activity of estradiol.[5][44][45][46] This contradicts some in vitro research suggesting that estrone might be able to partially antagonize the actions of estradiol.[41][42][43]



Like estradiol, estrone has poor oral bioavailability.[11][6] It has been said that, taken by mouth in non-micronized form, a dose of 25 mg estrone is approximately equivalent to 2.5 mg conjugated estrogens, 50 µg ethinylestradiol, or 1 mg diethylstilbestrol in terms of estrogenic potency.[49] Due to its weak oral activity, estrone has been used parenterally instead, for instance by intramuscular injection or vaginal administration.[2][3][4] The pharmacokinetics of vaginal estrone have been studied.[50]

Estrone in oil solution by intramuscular injection has a shorter duration than estrone in aqueous suspension by intramuscular injection.[33] Estrone in oil solution by intramuscular injection is rapidly absorbed, while estrone in aqueous suspension has a prolonged period of absorption.[51] Upon intramuscular injection of estrone in aqueous solution, the water from the preparation is absorbed and a microcrystalline depot of estrone that is slowly absorbed by the body is formed.[34] This is responsible for the prolonged duration of estrone in aqueous suspension compared to oil solution.[33][34]


Unlike estradiol and estriol, estrone is not accumulated in target tissues.[5][52] In terms of plasma protein binding, estrone is bound approximately 16% to sex hormone-binding globulin (SHBG) and 80% to albumin,[5] with the remainder (2.0 to 4.0%) circulating free or unbound.[7] Estrone has about 24% of the relative binding affinity of estradiol for SHBG, and hence is relatively poorly bound to SHBG.[5][11]


Estrone is conjugated into estrogen conjugates such as estrone sulfate and estrone glucuronide by sulfotransferases and glucuronidases, and can also be hydroxylated by cytochrome P450 enzymes into catechol estrogens such as 2-hydroxyestrone and 4-hydroxyestrone or into estriol.[5] Both of these transformations take place predominantly in the liver.[5] Estrone can also be reversibly converted into estradiol by 17β-HSD, and this accounts for most of its estrogenic activity.[5]

The biological half-lives of estrone and estradiol in the circulation are both about 20 to 30 minutes, whereas the biological half-life of estrone sulfate in the circulation is about 10 to 12 hours.[5] The metabolic clearance rate of estrone is 1,050 L/day/m2 and of estradiol is 580 L/day/m2, while that of estrone sulfate is 80 L/day/m2.[5] For comparison, the metabolic clearance rate of estriol is 1,110 L/day/m2.[5]

The ratio of circulating estrone to circulating estradiol is the same at about 5:1 with both oral estradiol and oral estrone sulfate.[5]

Metabolism of estrone in humans[53][54][55]
This diagram illustrates the metabolic pathways involved in the metabolism of estrogens (i.e., estradiol, estrone, and estriol) in humans.


Estrone is excreted in urine in the form of estrogen conjugates such as estrone sulfate.[5]


Structures of major endogenous estrogens
Estrone (E1)
Estriol (E3)
Note the hydroxyl (–OH) groups: estrone (E1) has one, estradiol (E2) has two, estriol (E3) has three, and estetrol (E4) has four.

Estrone, also known as estra-1,3,5(10)-trien-3-ol-17-one, is a naturally occurring estrane steroid with double bonds at the C1, C3, and C5 positions, a hydroxyl group at the C3 position, and a ketone group at the C17 position.[8][9] The name estrone was derived from the chemical terms estrin (estra-1,3,5(10)-triene) and ketone.[8][9]

A number of estrone esters exist, including the marketed esters estrone acetate, estrone sulfate, estrone tetraacetylglucoside, and estropipate (piperazine estrone sulfate) and the never-marketed esters estrone benzoate, estrone cyanate, estrone glucuronide, and estrone sulfamate.[8][9]


Estrone was discovered in 1929.[12][56] By 1931, estrone, purified from pregnancy urine, placentae, and/or amniotic fluid and for administration via intramuscular injection, was being sold commercially, for instance by Parke-Davis under the brand name Theelin in the United States and by Schering under the brand name Progynon in Germany.[12][13][57][14] Other products and brand names of purified estrone marketed by 1935 included Oestroform (British Drug Houses), Folliculin (Organon), and Menformon (Organon), as well as Amniotin (Squibb).[13][57] A partial synthesis of estrone from ergosterol was accomplished by Russell Earl Marker in 1936, and was the first chemical synthesis of estrone.[14][58] An alternative partial synthesis of estrone from cholesterol by way of dehydroepiandrosterone (DHEA) was developed by Hans Herloff Inhoffen and Walter Hohlweg in 1939 or 1940,[14] and a total synthesis of estrone was achieved by Anner and Miescher in 1948.[59]

Estrone in aqueous suspension for use by intramuscular injection was first described in 1941 and was introduced for medical use by 1946.[33][60]

Society and cultureEdit

Generic namesEdit

Estrone is the generic name of estrone in American English and its INN, USP, BAN, DCF, DCIT, and JAN.[8][9][10][15] Oestrone, in which the "O" is silent, was the former BAN of estrone and its name in British English,[8][10][9] but the spelling was eventually changed to estrone.[15]

Brand namesEdit

Estrone has been marketed under a variety of brand names, including Amniotin, Andrestraq, Aquacrine, A.T.V., Bestrone, Centrogen, Cicatral, Cormone, Crinovaryl, Cristallovar, Crystogen, Destrone, Disynformon, Endofolliculina, Estragyn, Estroject, Estrol, Estrone, Estrone-A, Estrugenone, Estrusol, Femestrone, Femidyn, Folikrin, Folipex, Folisan, Follestrine, Folliculin, Follicunodis, Follidrin, Gineburno, Glandubolin, Grietalgen, Grietalgen Hidrocort, Gynogen, Hiestrone, Hormofollin, Hormonin, Hormovarine, Kestrin, Kestrone, Ketodestrin, Kolpon, Ladies Pearl, Livifolin, Menagen, Menformon, Metharmon-F, Neo-Estrone, Oestrilin, Oestrin, Oestroform, Oestroperos, Ovex, Ovifollin, Perlatan, Progynon, Senikolp, Solliculin, Solutio Folliculinum, Synergon (in combination with progesterone), Theelin, Thelestrin, Thynestron, Tokokin, Unden, Unigen, Wehgen, and Wynestron.[8][10][9][1][15][61][62]


Although estrone has been widely marketed in the past, it has mostly been discontinued and remains available in only a few countries.[9][15] These countries reportedly include Canada, Georgia, Monaco, and Taiwan.[15] However, estrone remains widely available throughout the world in the form of estrone sulfate, which can be found in estropipate (piperazine estrone sulfate), conjugated estrogens (Premarin), and esterified estrogens (Estratab, Menest).[9][63]


An estrone vaginal ring was developed and studied for use in menopausal hormone therapy.[64] It increased circulating estrone and estradiol levels (ratios of about 4–5 initially and then 0.8–1.5 with continuous therapy), suppressed gonadotropin levels, and relieved menopausal symptoms.[64]

Subcutaneous pellet implantation of estrone has been studied.[65][66]

See alsoEdit


  1. ^ a b c d e f Sweetman, Sean C., ed. (2009). "Sex hormones and their modulators". Martindale: The Complete Drug Reference (36th ed.). London: Pharmaceutical Press. p. 2101. ISBN 978-0-85369-840-1.
  2. ^ a b c d e Guo, J. Z.; Hahn, D. W.; Wachter, M. P. (2000). "Hormones, Estrogens and Antiestrogens". doi:10.1002/0471238961.05192018072115.a01.
  3. ^ a b c d Speroff, Leon (2015). "Women's Hormonal Health Issues": 341–354. doi:10.1007/978-3-319-13832-9_28.
  4. ^ a b c Richard A. Helms; David J. Quan (2006). Textbook of Therapeutics: Drug and Disease Management. Lippincott Williams & Wilkins. pp. 397–. ISBN 978-0-7817-5734-8.
  5. ^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad ae af ag ah ai aj ak al am an Kuhl H (2005). "Pharmacology of estrogens and progestogens: influence of different routes of administration" (PDF). Climacteric. 8 Suppl 1: 3–63. doi:10.1080/13697130500148875. PMID 16112947.
  6. ^ a b Kenneth L. Melmon; S. George Carruthers; Howard F. Morrelli; Brian B. Hoffman, David W. Nierenberg (2000). Melmon and Morrelli's Clinical Pharmacology: Basic Principles in Therapeutics. McGraw Hill Professional. pp. 614–615. ISBN 978-0-07-105406-5.
  7. ^ a b J. Larry Jameson; Leslie J. De Groot (18 May 2010). Endocrinology – E-Book: Adult and Pediatric. Elsevier Health Sciences. pp. 2813–. ISBN 1-4557-1126-8.
  8. ^ a b c d e f g J. Elks (14 November 2014). The Dictionary of Drugs: Chemical Data: Chemical Data, Structures and Bibliographies. Springer. pp. 899–. ISBN 978-1-4757-2085-3.
  9. ^ a b c d e f g h i j Index Nominum 2000: International Drug Directory. Taylor & Francis. 2000. pp. 407–. ISBN 978-3-88763-075-1.
  10. ^ a b c d I.K. Morton; Judith M. Hall (6 December 2012). Concise Dictionary of Pharmacological Agents: Properties and Synonyms. Springer Science & Business Media. pp. 207–. ISBN 978-94-011-4439-1.
  11. ^ a b c d H.J. Buchsbaum (6 December 2012). The Menopause. Springer Science & Business Media. pp. 60, 62, 64. ISBN 978-1-4612-5525-3.
  12. ^ a b c Vern L. Bullough (19 May 1995). Science In The Bedroom: A History Of Sex Research. Basic Books. pp. 128–. ISBN 978-0-465-07259-0. When Allen and Doisy heard about the [Ascheim-Zondek test for the diagnosis of pregnancy], they realized there was a rich and easily handled source of hormones in urine from which they could develop a potent extract. [...] Allen and Doisy's research was sponsored by the committee, while that of their main rival, Adolt Butenandt (b. 1903) of the University of Gottingen was sponsored by a German pharmaceutical firm. In 1929, both terms announced the isolation of a pure crystal female sex hormone, estrone, in 1929, although Doisy and Allen did so two months earlier than Butenandt.27 By 1931, estrone was being commercially produced by Parke Davis in this country, and Schering-Kahlbaum in Germany. Interestingly, when Butenandt (who shared the Nobel Prize for chemistry in 1939) isolated estrone and analyzed its structure, he found that it was a steroid, the first hormone to be classed in this molecular family.
  13. ^ a b c d Fluhmann CF (1938). "Estrogenic Hormones: Their Clinical Usage". Cal West Med. 49 (5): 362–6. PMC 1659459. PMID 18744783.
  14. ^ a b c d Elizabeth Siegel Watkins (6 March 2007). The Estrogen Elixir: A History of Hormone Replacement Therapy in America. JHU Press. pp. 21–. ISBN 978-0-8018-8602-7.
  15. ^ a b c d e f g
  16. ^ a b c Thomas, John A.; Keenan, Edward J. (6 December 1986). "Estrogens and Antiestrogenic Drugs". Principles of Endocrine Pharmacology. Springer Science & Business Media. pp. 135–165. doi:10.1007/978-1-4684-5036-1_7. ISBN 978-1-4684-5036-1.
  17. ^ a b c
  18. ^
  19. ^ Michel E. Rivlin (1990). Handbook of drug therapy in reproductive endocrinology and infertility. Little, Brown. p. 23. ISBN 978-0-316-74772-1. The following are dosages for parenteral [estrogens]: [...] Estrone. For vasomotor symptoms or atrophic vaginitis, 0.1 to 0.5 mg is given 2 or 3 times weekly. For female hypogonadism, castration, or primary ovarian failure, 0.1 to 1.0 mg is given weekly in single or divided doses. Further dosage adjusted according to response.
  20. ^ a b Fluhmann, C. F. (1944). "Clinical use of extracts from the ovaries". Journal of the American Medical Association. 125 (1): 1. doi:10.1001/jama.1944.02850190003001. ISSN 0002-9955.
  21. ^ Kenneth L. Becker (2001). Principles and Practice of Endocrinology and Metabolism. Lippincott Williams & Wilkins. pp. 2153–. ISBN 978-0-7817-1750-2.
  22. ^ a b c
  23. ^ a b Walter Modell (21 November 2013). Drugs in Current Use 1958. Springer. pp. 52–. ISBN 978-3-662-40303-7.
  24. ^ a b c Rodolfo Paoletti; N. Pasetto; J.L. Ambrus (6 December 2012). The Menopause and Postmenopause: The Proceedings of an International Symposium held in Rome, June 1979. Springer Science & Business Media. pp. 3–. ISBN 978-94-011-7230-1.
  25. ^ Krishna; Usha R. And Shah (1996). Menopause. Orient Blackswan. pp. 70–. ISBN 978-81-250-0910-8.
  26. ^ Gordon Campbell; Juliet Compston; Adrian Crisp (25 November 1993). The Management of Common Metabolic Bone Disorders. Cambridge University Press. pp. 48–. ISBN 978-0-521-43623-6.
  27. ^ Risto Erkkola (1 January 2006). The Menopause. Elsevier. pp. 264–. ISBN 978-0-444-51830-9.
  28. ^
  29. ^ Sweetman, Sean C., ed. (2009). "Sex hormones and their modulators". Martindale: The Complete Drug Reference (36th ed.). London: Pharmaceutical Press. pp. 2101, 2127. ISBN 978-0-85369-840-1. Estrone [...] Progesterone [...] Multi-ingredient: [...] Fr.: Synergon [...] Turk.: Synergon
  30. ^ Addo VN, Tagoe-Darko ED (June 2009). "Knowledge, practices, and attitudes regarding emergency contraception among students at a university in Ghana". Int J Gynaecol Obstet. 105 (3): 206–9. doi:10.1016/j.ijgo.2009.01.008. PMID 19232600. Synergon, a combination of progesterone and oestrone in an injectable form, is marketed to induce withdrawal bleeding in women with nongravid amenorrhea; however, it can be used as an arbortifacient [11].
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