Antiestrogen

Last updated
Antiestrogen
Drug class
Fulvestrant.svg
Fulvestrant, a steroidal antiestrogen and a drug used in the treatment of breast cancer.
Class identifiers
Synonyms Estrogen antagonists; Estrogen blockers; Estradiol antagonists
Use Breast cancer; Infertility; Male hypogonadism; Gynecomastia; transgender men
ATC code L02BA
Biological target Estrogen receptor
Chemical class Steroidal; Nonsteroidal (triphenylethylene, others)
External links
MeSH D020847
Legal status
In Wikidata

Antiestrogens, also known as estrogen antagonists or estrogen blockers, are a class of drugs which prevent estrogens like estradiol from mediating their biological effects in the body. They act by blocking the estrogen receptor (ER) and/or inhibiting or suppressing estrogen production. [1] [2] Antiestrogens are one of three types of sex hormone antagonists, the others being antiandrogens and antiprogestogens. [3] Antiestrogens are commonly used to stop steroid hormones, estrogen, from binding to the estrogen receptors leading to the decrease of estrogen levels. [4] Decreased levels of estrogen can lead to complications in sexual development. [5]

Contents

Types and examples

Antiestrogens include selective estrogen receptor modulators (SERMs) like tamoxifen, clomifene, and raloxifene, the ER silent antagonist and selective estrogen receptor degrader (SERD) fulvestrant, [6] [7] aromatase inhibitors (AIs) like anastrozole, and antigonadotropins including androgens/anabolic steroids, progestogens, and GnRH analogues.

Estrogen receptors (ER) like ERα and ERβ include activation function 1 (AF1) domain and activation function 2 (AF2) domain in which SERMS act as antagonists for the AF2 domain, while “pure” antiestrogens like ICI 182,780 and ICI 164,384 are antagonists for the AF1 and AF2 domains. [8]

Although aromatase inhibitors and antigonadotropins can be considered antiestrogens by some definitions, they are often treated as distinct classes. [9] Aromatase inhibitors and antigonadotropins reduce the production of estrogen, while the term "antiestrogen" is often reserved for agents reducing the response to estrogen. [10]

Medical uses

Antiestrogens are used for:

Side effects

In women, the side effects of antiestrogens include hot flashes, osteoporosis, breast atrophy, vaginal dryness, and vaginal atrophy. In addition, they may cause depression and reduced libido.

Pharmacology

Antiestrogens act as antagonists of the estrogen receptors, ERα and ERβ.

Affinities of estrogen receptor ligands for the ERα and ERβ
Ligand Other names Relative binding affinities (RBA, %)a Absolute binding affinities (Ki, nM)aAction
ERα ERβ ERα ERβ
Estradiol E2; 17β-Estradiol1001000.115 (0.04–0.24)0.15 (0.10–2.08)Estrogen
Estrone E1; 17-Ketoestradiol16.39 (0.7–60)6.5 (1.36–52)0.445 (0.3–1.01)1.75 (0.35–9.24)Estrogen
Estriol E3; 16α-OH-17β-E212.65 (4.03–56)26 (14.0–44.6)0.45 (0.35–1.4)0.7 (0.63–0.7)Estrogen
Estetrol E4; 15α,16α-Di-OH-17β-E24.03.04.919Estrogen
Alfatradiol 17α-Estradiol20.5 (7–80.1)8.195 (2–42)0.2–0.520.43–1.2Metabolite
16-Epiestriol 16β-Hydroxy-17β-estradiol7.795 (4.94–63)50 ? ?Metabolite
17-Epiestriol 16α-Hydroxy-17α-estradiol55.45 (29–103)79–80 ? ?Metabolite
16,17-Epiestriol 16β-Hydroxy-17α-estradiol1.013 ? ?Metabolite
2-Hydroxyestradiol 2-OH-E222 (7–81)11–352.51.3Metabolite
2-Methoxyestradiol 2-MeO-E20.0027–2.01.0 ? ?Metabolite
4-Hydroxyestradiol 4-OH-E213 (8–70)7–561.01.9Metabolite
4-Methoxyestradiol 4-MeO-E22.01.0 ? ?Metabolite
2-Hydroxyestrone 2-OH-E12.0–4.00.2–0.4 ? ?Metabolite
2-Methoxyestrone 2-MeO-E1<0.001–<1<1 ? ?Metabolite
4-Hydroxyestrone 4-OH-E11.0–2.01.0 ? ?Metabolite
4-Methoxyestrone 4-MeO-E1<1<1 ? ?Metabolite
16α-Hydroxyestrone 16α-OH-E1; 17-Ketoestriol2.0–6.535 ? ?Metabolite
2-Hydroxyestriol 2-OH-E32.01.0 ? ?Metabolite
4-Methoxyestriol 4-MeO-E31.01.0 ? ?Metabolite
Estradiol sulfate E2S; Estradiol 3-sulfate<1<1 ? ?Metabolite
Estradiol disulfate Estradiol 3,17β-disulfate0.0004 ? ? ?Metabolite
Estradiol 3-glucuronide E2-3G0.0079 ? ? ?Metabolite
Estradiol 17β-glucuronide E2-17G0.0015 ? ? ?Metabolite
Estradiol 3-gluc. 17β-sulfate E2-3G-17S0.0001 ? ? ?Metabolite
Estrone sulfate E1S; Estrone 3-sulfate<1<1>10>10Metabolite
Estradiol benzoate EB; Estradiol 3-benzoate10 ? ? ?Estrogen
Estradiol 17β-benzoate E2-17B11.332.6 ? ?Estrogen
Estrone methyl ether Estrone 3-methyl ether0.145 ? ? ?Estrogen
ent-Estradiol 1-Estradiol1.31–12.349.44–80.07 ? ?Estrogen
Equilin 7-Dehydroestrone13 (4.0–28.9)13.0–490.790.36Estrogen
Equilenin 6,8-Didehydroestrone2.0–157.0–200.640.62Estrogen
17β-Dihydroequilin 7-Dehydro-17β-estradiol7.9–1137.9–1080.090.17Estrogen
17α-Dihydroequilin 7-Dehydro-17α-estradiol18.6 (18–41)14–320.240.57Estrogen
17β-Dihydroequilenin 6,8-Didehydro-17β-estradiol35–6890–1000.150.20Estrogen
17α-Dihydroequilenin 6,8-Didehydro-17α-estradiol20490.500.37Estrogen
Δ8-Estradiol 8,9-Dehydro-17β-estradiol68720.150.25Estrogen
Δ8-Estrone 8,9-Dehydroestrone19320.520.57Estrogen
Ethinylestradiol EE; 17α-Ethynyl-17β-E2120.9 (68.8–480)44.4 (2.0–144)0.02–0.050.29–0.81Estrogen
Mestranol EE 3-methyl ether ?2.5 ? ?Estrogen
Moxestrol RU-2858; 11β-Methoxy-EE35–435–200.52.6Estrogen
Methylestradiol 17α-Methyl-17β-estradiol7044 ? ?Estrogen
Diethylstilbestrol DES; Stilbestrol129.5 (89.1–468)219.63 (61.2–295)0.040.05Estrogen
Hexestrol Dihydrodiethylstilbestrol153.6 (31–302)60–2340.060.06Estrogen
Dienestrol Dehydrostilbestrol37 (20.4–223)56–4040.050.03Estrogen
Benzestrol (B2) –114 ? ? ?Estrogen
Chlorotrianisene TACE1.74 ?15.30 ?Estrogen
Triphenylethylene TPE0.074 ? ? ?Estrogen
Triphenylbromoethylene TPBE2.69 ? ? ?Estrogen
Tamoxifen ICI-46,4743 (0.1–47)3.33 (0.28–6)3.4–9.692.5SERM
Afimoxifene 4-Hydroxytamoxifen; 4-OHT100.1 (1.7–257)10 (0.98–339)2.3 (0.1–3.61)0.04–4.8SERM
Toremifene 4-Chlorotamoxifen; 4-CT ? ?7.14–20.315.4SERM
Clomifene MRL-4125 (19.2–37.2)120.91.2SERM
Cyclofenil F-6066; Sexovid151–152243 ? ?SERM
Nafoxidine U-11,000A30.9–44160.30.8SERM
Raloxifene –41.2 (7.8–69)5.34 (0.54–16)0.188–0.5220.2SERM
Arzoxifene LY-353,381 ? ?0.179 ?SERM
Lasofoxifene CP-336,15610.2–16619.00.229 ?SERM
Ormeloxifene Centchroman ? ?0.313 ?SERM
Levormeloxifene 6720-CDRI; NNC-460,0201.551.88 ? ?SERM
Ospemifene Deaminohydroxytoremifene0.82–2.630.59–1.22 ? ?SERM
Bazedoxifene – ? ?0.053 ?SERM
Etacstil GW-56384.3011.5 ? ?SERM
ICI-164,384 –63.5 (3.70–97.7)1660.20.08Antiestrogen
Fulvestrant ICI-182,78043.5 (9.4–325)21.65 (2.05–40.5)0.421.3Antiestrogen
Propylpyrazoletriol PPT49 (10.0–89.1)0.120.4092.8ERα agonist
16α-LE2 16α-Lactone-17β-estradiol14.6–570.0890.27131ERα agonist
16α-Iodo-E2 16α-Iodo-17β-estradiol30.22.30 ? ?ERα agonist
Methylpiperidinopyrazole MPP110.05 ? ?ERα antagonist
Diarylpropionitrile DPN0.12–0.256.6–1832.41.7ERβ agonist
8β-VE2 8β-Vinyl-17β-estradiol0.3522.0–8312.90.50ERβ agonist
Prinaberel ERB-041; WAY-202,0410.2767–72 ? ?ERβ agonist
ERB-196 WAY-202,196 ?180 ? ?ERβ agonist
Erteberel SERBA-1; LY-500,307 ? ?2.680.19ERβ agonist
SERBA-2 – ? ?14.51.54ERβ agonist
Coumestrol –9.225 (0.0117–94)64.125 (0.41–185)0.14–80.00.07–27.0Xenoestrogen
Genistein –0.445 (0.0012–16)33.42 (0.86–87)2.6–1260.3–12.8Xenoestrogen
Equol –0.2–0.2870.85 (0.10–2.85) ? ?Xenoestrogen
Daidzein –0.07 (0.0018–9.3)0.7865 (0.04–17.1)2.085.3Xenoestrogen
Biochanin A –0.04 (0.022–0.15)0.6225 (0.010–1.2)1748.9Xenoestrogen
Kaempferol –0.07 (0.029–0.10)2.2 (0.002–3.00) ? ?Xenoestrogen
Naringenin –0.0054 (<0.001–0.01)0.15 (0.11–0.33) ? ?Xenoestrogen
8-Prenylnaringenin 8-PN4.4 ? ? ?Xenoestrogen
Quercetin –<0.001–0.010.002–0.040 ? ?Xenoestrogen
Ipriflavone –<0.01<0.01 ? ?Xenoestrogen
Miroestrol –0.39 ? ? ?Xenoestrogen
Deoxymiroestrol –2.0 ? ? ?Xenoestrogen
β-Sitosterol –<0.001–0.0875<0.001–0.016 ? ?Xenoestrogen
Resveratrol –<0.001–0.0032 ? ? ?Xenoestrogen
α-Zearalenol –48 (13–52.5) ? ? ?Xenoestrogen
β-Zearalenol –0.6 (0.032–13) ? ? ?Xenoestrogen
Zeranol α-Zearalanol48–111 ? ? ?Xenoestrogen
Taleranol β-Zearalanol16 (13–17.8)140.80.9Xenoestrogen
Zearalenone ZEN7.68 (2.04–28)9.45 (2.43–31.5) ? ?Xenoestrogen
Zearalanone ZAN0.51 ? ? ?Xenoestrogen
Bisphenol A BPA0.0315 (0.008–1.0)0.135 (0.002–4.23)19535Xenoestrogen
Endosulfan EDS<0.001–<0.01<0.01 ? ?Xenoestrogen
Kepone Chlordecone0.0069–0.2 ? ? ?Xenoestrogen
o,p'-DDT –0.0073–0.4 ? ? ?Xenoestrogen
p,p'-DDT –0.03 ? ? ?Xenoestrogen
Methoxychlor p,p'-Dimethoxy-DDT0.01 (<0.001–0.02)0.01–0.13 ? ?Xenoestrogen
HPTE Hydroxychlor; p,p'-OH-DDT1.2–1.7 ? ? ?Xenoestrogen
Testosterone T; 4-Androstenolone<0.0001–<0.01<0.002–0.040>5000>5000Androgen
Dihydrotestosterone DHT; 5α-Androstanolone0.01 (<0.001–0.05)0.0059–0.17221–>500073–1688Androgen
Nandrolone 19-Nortestosterone; 19-NT0.010.2376553Androgen
Dehydroepiandrosterone DHEA; Prasterone0.038 (<0.001–0.04)0.019–0.07245–1053163–515Androgen
5-Androstenediol A5; Androstenediol6173.60.9Androgen
4-Androstenediol –0.50.62319Androgen
4-Androstenedione A4; Androstenedione<0.01<0.01>10000>10000Androgen
3α-Androstanediol 3α-Adiol0.070.326048Androgen
3β-Androstanediol 3β-Adiol3762Androgen
Androstanedione 5α-Androstanedione<0.01<0.01>10000>10000Androgen
Etiocholanedione 5β-Androstanedione<0.01<0.01>10000>10000Androgen
Methyltestosterone 17α-Methyltestosterone<0.0001 ? ? ?Androgen
Ethinyl-3α-androstanediol 17α-Ethynyl-3α-adiol4.0<0.07 ? ?Estrogen
Ethinyl-3β-androstanediol 17α-Ethynyl-3β-adiol505.6 ? ?Estrogen
Progesterone P4; 4-Pregnenedione<0.001–0.6<0.001–0.010 ? ?Progestogen
Norethisterone NET; 17α-Ethynyl-19-NT0.085 (0.0015–<0.1)0.1 (0.01–0.3)1521084Progestogen
Norethynodrel 5(10)-Norethisterone0.5 (0.3–0.7)<0.1–0.221453Progestogen
Tibolone 7α-Methylnorethynodrel0.5 (0.45–2.0)0.2–0.076 ? ?Progestogen
Δ4-Tibolone 7α-Methylnorethisterone0.069–<0.10.027–<0.1 ? ?Progestogen
3α-Hydroxytibolone –2.5 (1.06–5.0)0.6–0.8 ? ?Progestogen
3β-Hydroxytibolone –1.6 (0.75–1.9)0.070–0.1 ? ?Progestogen
Footnotes:a = (1) Binding affinity values are of the format "median (range)" (# (#–#)), "range" (#–#), or "value" (#) depending on the values available. The full sets of values within the ranges can be found in the Wiki code. (2) Binding affinities were determined via displacement studies in a variety of in-vitro systems with labeled estradiol and human ERα and ERβ proteins (except the ERβ values from Kuiper et al. (1997), which are rat ERβ). Sources: See template page.

History

The first nonsteroidal antiestrogen was discovered by Lerner and coworkers in 1958. [11] Ethamoxytriphetol (MER-25) was the first antagonist of the ER to be discovered, [12] followed by clomifene and tamoxifen. [13] [14]

See also

Related Research Articles

<span class="mw-page-title-main">Clomifene</span> Infertility treatment for women

Clomifene, also known as clomiphene, is a medication used to treat infertility in women who do not ovulate, including those with polycystic ovary syndrome. It is taken by mouth.

<span class="mw-page-title-main">Selective estrogen receptor modulator</span> Drugs acting on the estrogen receptor

Selective estrogen receptor modulators (SERMs), also known as estrogen receptor agonists/antagonists (ERAAs), are a class of drugs that act on estrogen receptors (ERs). Compared to pure ER agonists–antagonists, SERMs are more tissue-specific, allowing them to selectively inhibit or stimulate estrogen-like action in various tissues.

<span class="mw-page-title-main">Tamoxifen</span> Medication

Tamoxifen, sold under the brand name Nolvadex among others, is a selective estrogen receptor modulator used to prevent breast cancer in women and men. It is also being studied for other types of cancer. It has been used for Albright syndrome. Tamoxifen is typically taken daily by mouth for five years for breast cancer.

<span class="mw-page-title-main">Estrogen receptor</span> Proteins activated by the hormone estrogen

Estrogen receptors (ERs) are proteins found in cells that function as receptors for the hormone estrogen (17β-estradiol). There are two main classes of ERs. The first includes the intracellular estrogen receptors, namely ERα and ERβ, which belong to the nuclear receptor family. The second class consists of membrane estrogen receptors (mERs), such as GPER (GPR30), ER-X, and Gq-mER, which are primarily G protein-coupled receptors. This article focuses on the nuclear estrogen receptors.

Hormonal therapy in oncology is hormone therapy for cancer and is one of the major modalities of medical oncology, others being cytotoxic chemotherapy and targeted therapy (biotherapeutics). It involves the manipulation of the endocrine system through exogenous or external administration of specific hormones, particularly steroid hormones, or drugs which inhibit the production or activity of such hormones. Because steroid hormones are powerful drivers of gene expression in certain cancer cells, changing the levels or activity of certain hormones can cause certain cancers to cease growing, or even undergo cell death. Surgical removal of endocrine organs, such as orchiectomy and oophorectomy can also be employed as a form of hormonal therapy.

<span class="mw-page-title-main">Afimoxifene</span> Chemical compound

Afimoxifene, also known as 4-hydroxytamoxifen (4-OHT) and by its tentative brand name TamoGel, is a selective estrogen receptor modulator (SERM) of the triphenylethylene group and an active metabolite of tamoxifen. The drug is under development under the tentative brand name TamoGel as a topical gel for the treatment of hyperplasia of the breast. It has completed a phase II clinical trial for cyclical mastalgia, but further studies are required before afimoxifene can be approved for this indication and marketed.

<span class="mw-page-title-main">Trioxifene</span> Chemical compound

Trioxifene, or as the salt trioxifene mesylate (USAN), is a selective estrogen receptor modulator (SERM) with competitive binding activity against estradiol for the ERα and antagonistic activity against ERα-mediated gene expression, that was under preclinical and clinical development by Eli Lilly and Company for breast cancer and prostate cancer, but was abandoned. Its affinity for the rat estrogen receptor was reported to be 20% relative to estradiol.

<span class="mw-page-title-main">Triphenylethylene</span> Chemical compound

Triphenylethylene (TPE) is a simple aromatic hydrocarbon that possesses weak estrogenic activity. Its estrogenic effects were discovered in 1937. TPE was derived from structural modification of the more potent estrogen diethylstilbestrol, which is a member of the stilbestrol group of nonsteroidal estrogens.

<span class="mw-page-title-main">Ethamoxytriphetol</span> Chemical compound

Ethamoxytriphetol is a synthetic nonsteroidal antiestrogen that was studied clinically in the late 1950s and early 1960s but was never marketed. MER-25 was first reported in 1958, and was the first antiestrogen to be discovered. It has been described as "essentially devoid of estrogenic activity" and as having "very low estrogenic activity in all species tested". However, some estrogenic effects in the uterus have been observed, so it is not a pure antiestrogen but is, instead, technically a selective estrogen receptor modulator (SERM). For all intents and purposes, it is a nearly pure antiestrogen, however.

<span class="mw-page-title-main">Progonadotropin</span> Drug class

A progonadotropin, or hypergonadotropin, also known as a gonad stimulant, is a type of drug which increases the secretion of one or both of the major gonadotropins, luteinizing hormone (LH) and follicle-stimulating hormone (FSH). This, in turn, results in increased function and maintenance of the gonads and increased gonadal steroidogenesis of sex hormones such as androgens, estrogens, and progestogens. Progonadotropins are the functional opposites of antigonadotropins. They have clinical applications in the treatment of hypogonadism and infertility. Conversely, hypergonadotropic effects can occur as a side effect of some drugs. Examples of progonadotropic drugs include gonadotropin-releasing hormone (GnRH) agonists when administered in a pulsatile manner, antiestrogens such as tamoxifen, clomifene, fulvestrant, and aromatase inhibitors like anastrozole, and, only in men, pure antiandrogens such as flutamide, bicalutamide, enzalutamide, and apalutamide.

<span class="mw-page-title-main">Brilanestrant</span> Discontinued oral cancer remedy

Brilanestrant (INN) is a nonsteroidal combined selective estrogen receptor modulator (SERM) and selective estrogen receptor degrader (SERD) that was discovered by Aragon Pharmaceuticals and was under development by Genentech for the treatment of locally advanced or metastatic estrogen receptor (ER)-positive breast cancer.

<span class="mw-page-title-main">Elacestrant</span> Chemical compound

Elacestrant, sold under the brand name Orserdu, is a selective estrogen receptor degrader (SERD) used in the treatment of breast cancer. It is taken by mouth.

Estrogen deprivation therapy, also known as endocrine therapy, is a form of hormone therapy that is used in the treatment of breast cancer. Modalities include antiestrogens or estrogen blockers such as selective estrogen receptor modulators (SERMs) like tamoxifen, selective estrogen receptor degraders like fulvestrant, and aromatase inhibitors like anastrozole and ovariectomy.

<span class="mw-page-title-main">Etacstil</span> Chemical compound

Etacstil is an orally active, nonsteroidal, combined selective estrogen receptor modulator (SERM) and selective estrogen receptor degrader (SERD) that was developed for the treatment of estrogen receptor-positive breast cancer. It was shown to overcome antiestrogen resistance in breast cancer by altering the shape of the estrogen receptor, thus exhibiting SERD properties. Etacstil is a tamoxifen derivative and one of the first drugs to overcome tamoxifen-resistance. It is the predecessor of GW-7604, of which etacstil is a prodrug. This is analogous to the case of tamoxifen being a prodrug of afimoxifene (4-hydroxytamoxifen).

<span class="mw-page-title-main">Endoxifen</span> Chemical compound

Endoxifen, also known as 4-hydroxy-N-desmethyltamoxifen, is a nonsteroidal selective estrogen receptor modulator (SERM) of the triphenylethylene group as well as a protein kinase C (PKC) inhibitor. It is under development for the treatment of estrogen receptor-positive breast cancer and for the treatment of mania in bipolar disorder. It is taken by mouth.

<span class="mw-page-title-main">Triphenylchloroethylene</span> Synthetic form of estrogen

Triphenylchloroethylene, or triphenylchlorethylene, also known as chlorotriphenylethylene or as phenylstilbene chloride, is a synthetic nonsteroidal estrogen of the triphenylethylene group that was marketed in the 1940s for the treatment of menopausal symptoms, vaginal atrophy, lactation suppression, and all other estrogen-indicated conditions.

<span class="mw-page-title-main">ICI-164384</span> Chemical compound

ICI-164384, also known as N-n-butyl-N-methyl-11-(3,17β-dihydroxyestra-1,3,5 -trien-7α-yl)undecanamide, is a steroidal antiestrogen and a synthetic derivative of estradiol which is closely related to fulvestrant and was never marketed. It is a silent antagonist of the estrogen receptor (ER) with no intrinsic estrogenic activity and hence is a pure antiestrogen, unlike selective estrogen receptor modulators (SERMs) like tamoxifen. The drug was under development by AstraZeneca for the treatment of breast cancer but was discontinued in favor of fulvestrant, which is very similar to ICI-164384 but is more potent in comparison.

A sex-hormonal agent, also known as a sex-hormone receptor modulator, is a type of hormonal agent which specifically modulates the effects of sex hormones and of their biological targets, the sex hormone receptors. The sex hormones include androgens such as testosterone, estrogens such as estradiol, and progestogens such as progesterone. Sex-hormonal agents may be either steroidal or nonsteroidal in chemical structure and may serve to either enhance, inhibit, or have mixed effects on the function of the sex hormone systems.

<span class="mw-page-title-main">ERX-11</span> Chemical compound

ERX-11, also known as ERα coregulator-binding modulator-11, is a novel antiestrogen and experimental hormonal antineoplastic agent which is being researched for the potential treatment of estrogen receptor-positive breast cancer. It is not a competitive antagonist of the estrogen receptor (ER) like conventional antiestrogens such as tamoxifen or fulvestrant; instead of binding to the ligand-binding site of the ER, ERX-11 interacts with a different part of the ERα and blocks protein–protein interactions of the ERα with coregulators that are necessary for the receptor to act and regulate gene expression. It was designed to bind to the coregulator binding region of the ERα and inhibit the ERα/coactivator interaction, although its precise binding site and mode of action have yet to be fully elucidated and understood. Nonetheless, it is clear that ERX-11 binds within the AF-2 domain of the ERα.

Endocrine therapy is a common treatment for estrogen receptor positive breast cancer. However, resistance to this therapy can develop, leading to relapse and progression of disease. This highlights the need for new strategies to combat this resistance.

References

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  2. ↑ "antiestrogen" at Dorland's Medical Dictionary
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  5. ↑ Amenyogbe E, Chen G, Wang Z, Lu X, Lin M, Lin AY (2020-02-07). "A Review on Sex Steroid Hormone Estrogen Receptors in Mammals and Fish". International Journal of Endocrinology. 2020: 5386193. doi: 10.1155/2020/5386193 . PMC   7029290 . PMID   32089683.
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  12. ↑ Maximov PY, McDaniel RE, Jordan VC (23 July 2013). Tamoxifen: Pioneering Medicine in Breast Cancer. Springer Science & Business Media. pp. 7–. ISBN   978-3-0348-0664-0.
  13. ↑ Jordan VC (27 May 2013). Estrogen Action, Selective Estrogen Receptor Modulators and Women's Health: Progress and Promise. World Scientific. pp. 7, 112. ISBN   978-1-84816-959-3.
  14. ↑ Sneader W (23 June 2005). Drug Discovery: A History. John Wiley & Sons. pp. 198–199. ISBN   978-0-471-89979-2.

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