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Medication
This article is about 17α-estradiol as a medication. For its role as a hormone, see
17α-Estradiol.
Pharmaceutical compound
Alfatradiol Trade names Avicis, Avixis, Ell-Cranell Alpha, Pantostin Other names 17α-Estradiol; 17-Epiestradiol; MX-4509; Estra-1,3,5(10)-triene-3,17α-diol; β-Estradiol (obsolete, misleading)[1] AHFS/Drugs.com International Drug Names Pregnancy(8R,9S,13S,14S,17R)-13-methyl-6,7,8,9,11,12,14,15,16,17-decahydrocyclopenta[a]phenanthrene-3,17-diol
OC1CCC3C1(C)CCC(c2cc4)C3CCc2cc4O
InChI=1S/C18H24O2/c1-18-9-8-14-13-5-3-12(19)10-11(13)2-4-15(14)16(18)6-7-17(18)20/h3,5,10,14-17,19-20H,2,4,6-9H2,1H3/t14-,15-,16+,17-,18+/m1/s1
YKey:VOXZDWNPVJITMN-SFFUCWETSA-N
YAlfatradiol, also known as 17α-estradiol and sold under the brand names Avicis, Avixis, Ell-Cranell Alpha, and Pantostin, is a weak estrogen and 5α-reductase inhibitor medication which is used topically in the treatment of pattern hair loss (androgenic alopecia or pattern baldness) in men and women.[1][2][3][4] It is a stereoisomer of the endogenous steroid hormone and estrogen 17β-estradiol (or simply estradiol).[1]
Alfatradiol is used in form of an ethanolic solution for topical application on the scalp. Similarly to other drugs against alopecia, topical or oral, it has to be applied continuously to prevent further hair loss.[5] Regrowth of hair that was already lost is only possible to a limited extent. In general, advanced alopecia does not respond well to medical treatment, which has historically been thought to be a consequence of the hair roots being lost.[6]
A university-led study (including several authors who are advisors to companies such as Pfizer) in 103 women comparing alfatradiol to minoxidil, another topical hair loss treatment, found the latter to be more effective. In contrast to minoxidil, alfatradiol did not result in an increase of hair density or thickness, but only in slowing down or stabilization of hair loss in this study.[7] In an earlier study, no systemic side effects were noted, and 17α-estradiol was found to reduce androgenic hair loss, though it was not effective at growing new hair.[8]
Other efforts of alfatradiol had been directed at neurodegenerative diseases including Parkinson's.[9]
Other hair loss medications include ketoconazole, finasteride, and dutasteride.
Nothing is known about the use of alfatradiol during pregnancy or lactation, or in patients under 18 years of age. The package leaflet recommends against using it under these circumstances.[10]
Local burning or itching is not an effect of alfatradiol, but of the ethanol in the solvent. The solution can stimulate sebum production.[10]
Alfatradiol (top) and 17β-estradiol (bottom).Alfatradiol (17α-estradiol) is distinguished from estradiol (17β-estradiol), the predominant sex hormone in females, only by the stereochemistry of the carbon atom 17. In contrast to 17β-estradiol, 17α-estradiol, while it still binds to the estrogen receptor, has less or no feminizing estrogenic activity depending on its dosage and the tissue it is affecting.[11] Alfatradiol acts as an inhibitor of the enzyme 5α-reductase, which is responsible for the activation of testosterone to dihydrotestosterone, and which plays a role in regulating hair growth.[5] 17α-Estradiol has been studied as a therapeutic with potential to treat Alzheimer's and Parkinson's disease and other patients with neurodegenerative diseases.[12] 17α-Estradiol (as the sodium salt of its sulfated form) is a minor component (<10%) of hormone replacement products (such as conjugated estrogens, brand name Premarin), which have been studied and/or marketed in women and men since the 1930s. A survey of the effects of various forms of 17α-estradiol in humans on biochemical parameters, efficacy, estrogenicity, metabolism, safety, and tolerability has been published.[13]
Alfatradiol binds to the ERα and ERβ with 58% and 11% of the relative binding affinity of 17β-estradiol.[14] However, it has 100-fold lower estrogenic activity relative to estradiol.[15] On the other hand, alfatradiol has been found to bind to and activate the brain-expressed ER-X with a greater potency than estradiol, indicating that it may be the predominant endogenous ligand for the receptor.[16] In contrast to estradiol, alfatradiol is not a ligand of the G protein-coupled estrogen receptor (affinity >10 μM).[17]
Affinities of estrogen receptor ligands for the ERα and ERβ Ligand Other names Relative binding affinities (RBA, %)a Absolute binding affinities (Ki, nM)a Action ERα ERβ ERα ERβ Estradiol E2; 17β-Estradiol 100 100 0.115 (0.04–0.24) 0.15 (0.10–2.08) Estrogen Estrone E1; 17-Ketoestradiol 16.39 (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-E2 12.65 (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-E2 4.0 3.0 4.9 19 Estrogen Alfatradiol 17α-Estradiol 20.5 (7–80.1) 8.195 (2–42) 0.2–0.52 0.43–1.2 Metabolite 16-Epiestriol 16β-Hydroxy-17β-estradiol 7.795 (4.94–63) 50 ? ? Metabolite 17-Epiestriol 16α-Hydroxy-17α-estradiol 55.45 (29–103) 79–80 ? ? Metabolite 16,17-Epiestriol 16β-Hydroxy-17α-estradiol 1.0 13 ? ? Metabolite 2-Hydroxyestradiol 2-OH-E2 22 (7–81) 11–35 2.5 1.3 Metabolite 2-Methoxyestradiol 2-MeO-E2 0.0027–2.0 1.0 ? ? Metabolite 4-Hydroxyestradiol 4-OH-E2 13 (8–70) 7–56 1.0 1.9 Metabolite 4-Methoxyestradiol 4-MeO-E2 2.0 1.0 ? ? Metabolite 2-Hydroxyestrone 2-OH-E1 2.0–4.0 0.2–0.4 ? ? Metabolite 2-Methoxyestrone 2-MeO-E1 <0.001–<1 <1 ? ? Metabolite 4-Hydroxyestrone 4-OH-E1 1.0–2.0 1.0 ? ? Metabolite 4-Methoxyestrone 4-MeO-E1 <1 <1 ? ? Metabolite 16α-Hydroxyestrone 16α-OH-E1; 17-Ketoestriol 2.0–6.5 35 ? ? Metabolite 2-Hydroxyestriol 2-OH-E3 2.0 1.0 ? ? Metabolite 4-Methoxyestriol 4-MeO-E3 1.0 1.0 ? ? Metabolite Estradiol sulfate E2S; Estradiol 3-sulfate <1 <1 ? ? Metabolite Estradiol disulfate Estradiol 3,17β-disulfate 0.0004 ? ? ? Metabolite Estradiol 3-glucuronide E2-3G 0.0079 ? ? ? Metabolite Estradiol 17β-glucuronide E2-17G 0.0015 ? ? ? Metabolite Estradiol 3-gluc. 17β-sulfate E2-3G-17S 0.0001 ? ? ? Metabolite Estrone sulfate E1S; Estrone 3-sulfate <1 <1 >10 >10 Metabolite Estradiol benzoate EB; Estradiol 3-benzoate 10 ? ? ? Estrogen Estradiol 17β-benzoate E2-17B 11.3 32.6 ? ? Estrogen Estrone methyl ether Estrone 3-methyl ether 0.145 ? ? ? Estrogen ent-Estradiol 1-Estradiol 1.31–12.34 9.44–80.07 ? ? Estrogen Equilin 7-Dehydroestrone 13 (4.0–28.9) 13.0–49 0.79 0.36 Estrogen Equilenin 6,8-Didehydroestrone 2.0–15 7.0–20 0.64 0.62 Estrogen 17β-Dihydroequilin 7-Dehydro-17β-estradiol 7.9–113 7.9–108 0.09 0.17 Estrogen 17α-Dihydroequilin 7-Dehydro-17α-estradiol 18.6 (18–41) 14–32 0.24 0.57 Estrogen 17β-Dihydroequilenin 6,8-Didehydro-17β-estradiol 35–68 90–100 0.15 0.20 Estrogen 17α-Dihydroequilenin 6,8-Didehydro-17α-estradiol 20 49 0.50 0.37 Estrogen Δ8-Estradiol 8,9-Dehydro-17β-estradiol 68 72 0.15 0.25 Estrogen Δ8-Estrone 8,9-Dehydroestrone 19 32 0.52 0.57 Estrogen Ethinylestradiol EE; 17α-Ethynyl-17β-E2 120.9 (68.8–480) 44.4 (2.0–144) 0.02–0.05 0.29–0.81 Estrogen Mestranol EE 3-methyl ether ? 2.5 ? ? Estrogen Moxestrol RU-2858; 11β-Methoxy-EE 35–43 5–20 0.5 2.6 Estrogen Methylestradiol 17α-Methyl-17β-estradiol 70 44 ? ? Estrogen Diethylstilbestrol DES; Stilbestrol 129.5 (89.1–468) 219.63 (61.2–295) 0.04 0.05 Estrogen Hexestrol Dihydrodiethylstilbestrol 153.6 (31–302) 60–234 0.06 0.06 Estrogen Dienestrol Dehydrostilbestrol 37 (20.4–223) 56–404 0.05 0.03 Estrogen Benzestrol (B2) – 114 ? ? ? Estrogen Chlorotrianisene TACE 1.74 ? 15.30 ? Estrogen Triphenylethylene TPE 0.074 ? ? ? Estrogen Triphenylbromoethylene TPBE 2.69 ? ? ? Estrogen Tamoxifen ICI-46,474 3 (0.1–47) 3.33 (0.28–6) 3.4–9.69 2.5 SERM Afimoxifene 4-Hydroxytamoxifen; 4-OHT 100.1 (1.7–257) 10 (0.98–339) 2.3 (0.1–3.61) 0.04–4.8 SERM Toremifene 4-Chlorotamoxifen; 4-CT ? ? 7.14–20.3 15.4 SERM Clomifene MRL-41 25 (19.2–37.2) 12 0.9 1.2 SERM Cyclofenil F-6066; Sexovid 151–152 243 ? ? SERM Nafoxidine U-11,000A 30.9–44 16 0.3 0.8 SERM Raloxifene – 41.2 (7.8–69) 5.34 (0.54–16) 0.188–0.52 20.2 SERM Arzoxifene LY-353,381 ? ? 0.179 ? SERM Lasofoxifene CP-336,156 10.2–166 19.0 0.229 ? SERM Ormeloxifene Centchroman ? ? 0.313 ? SERM Levormeloxifene 6720-CDRI; NNC-460,020 1.55 1.88 ? ? SERM Ospemifene Deaminohydroxytoremifene 0.82–2.63 0.59–1.22 ? ? SERM Bazedoxifene – ? ? 0.053 ? SERM Etacstil GW-5638 4.30 11.5 ? ? SERM ICI-164,384 – 63.5 (3.70–97.7) 166 0.2 0.08 Antiestrogen Fulvestrant ICI-182,780 43.5 (9.4–325) 21.65 (2.05–40.5) 0.42 1.3 Antiestrogen Propylpyrazoletriol PPT 49 (10.0–89.1) 0.12 0.40 92.8 ERα agonist 16α-LE2 16α-Lactone-17β-estradiol 14.6–57 0.089 0.27 131 ERα agonist 16α-Iodo-E2 16α-Iodo-17β-estradiol 30.2 2.30 ? ? ERα agonist Methylpiperidinopyrazole MPP 11 0.05 ? ? ERα antagonist Diarylpropionitrile DPN 0.12–0.25 6.6–18 32.4 1.7 ERβ agonist 8β-VE2 8β-Vinyl-17β-estradiol 0.35 22.0–83 12.9 0.50 ERβ agonist Prinaberel ERB-041; WAY-202,041 0.27 67–72 ? ? ERβ agonist ERB-196 WAY-202,196 ? 180 ? ? ERβ agonist Erteberel SERBA-1; LY-500,307 ? ? 2.68 0.19 ERβ agonist SERBA-2 – ? ? 14.5 1.54 ERβ agonist Coumestrol – 9.225 (0.0117–94) 64.125 (0.41–185) 0.14–80.0 0.07–27.0 Xenoestrogen Genistein – 0.445 (0.0012–16) 33.42 (0.86–87) 2.6–126 0.3–12.8 Xenoestrogen Equol – 0.2–0.287 0.85 (0.10–2.85) ? ? Xenoestrogen Daidzein – 0.07 (0.0018–9.3) 0.7865 (0.04–17.1) 2.0 85.3 Xenoestrogen Biochanin A – 0.04 (0.022–0.15) 0.6225 (0.010–1.2) 174 8.9 Xenoestrogen 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-PN 4.4 ? ? ? Xenoestrogen Quercetin – <0.001–0.01 0.002–0.040 ? ? 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-Zearalanol 48–111 ? ? ? Xenoestrogen Taleranol β-Zearalanol 16 (13–17.8) 14 0.8 0.9 Xenoestrogen Zearalenone ZEN 7.68 (2.04–28) 9.45 (2.43–31.5) ? ? Xenoestrogen Zearalanone ZAN 0.51 ? ? ? Xenoestrogen Bisphenol A BPA 0.0315 (0.008–1.0) 0.135 (0.002–4.23) 195 35 Xenoestrogen Endosulfan EDS <0.001–<0.01 <0.01 ? ? Xenoestrogen Kepone Chlordecone 0.0069–0.2 ? ? ? Xenoestrogen o,p'-DDT – 0.0073–0.4 ? ? ? Xenoestrogen p,p'-DDT – 0.03 ? ? ? Xenoestrogen Methoxychlor p,p'-Dimethoxy-DDT 0.01 (<0.001–0.02) 0.01–0.13 ? ? Xenoestrogen HPTE Hydroxychlor; p,p'-OH-DDT 1.2–1.7 ? ? ? Xenoestrogen Testosterone T; 4-Androstenolone <0.0001–<0.01 <0.002–0.040 >5000 >5000 Androgen Dihydrotestosterone DHT; 5α-Androstanolone 0.01 (<0.001–0.05) 0.0059–0.17 221–>5000 73–1688 Androgen Nandrolone 19-Nortestosterone; 19-NT 0.01 0.23 765 53 Androgen Dehydroepiandrosterone DHEA; Prasterone 0.038 (<0.001–0.04) 0.019–0.07 245–1053 163–515 Androgen 5-Androstenediol A5; Androstenediol 6 17 3.6 0.9 Androgen 4-Androstenediol – 0.5 0.6 23 19 Androgen 4-Androstenedione A4; Androstenedione <0.01 <0.01 >10000 >10000 Androgen 3α-Androstanediol 3α-Adiol 0.07 0.3 260 48 Androgen 3β-Androstanediol 3β-Adiol 3 7 6 2 Androgen Androstanedione 5α-Androstanedione <0.01 <0.01 >10000 >10000 Androgen Etiocholanedione 5β-Androstanedione <0.01 <0.01 >10000 >10000 Androgen Methyltestosterone 17α-Methyltestosterone <0.0001 ? ? ? Androgen Ethinyl-3α-androstanediol 17α-Ethynyl-3α-adiol 4.0 <0.07 ? ? Estrogen Ethinyl-3β-androstanediol 17α-Ethynyl-3β-adiol 50 5.6 ? ? Estrogen Progesterone P4; 4-Pregnenedione <0.001–0.6 <0.001–0.010 ? ? Progestogen Norethisterone NET; 17α-Ethynyl-19-NT 0.085 (0.0015–<0.1) 0.1 (0.01–0.3) 152 1084 Progestogen Norethynodrel 5(10)-Norethisterone 0.5 (0.3–0.7) <0.1–0.22 14 53 Progestogen Tibolone 7α-Methylnorethynodrel 0.5 (0.45–2.0) 0.2–0.076 ? ? Progestogen Δ4-Tibolone 7α-Methylnorethisterone 0.069–<0.1 0.027–<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. Society and culture[edit]Alfatradiol is the generic name of the drug and its INNTooltip International Nonproprietary Name.[2] It is also known as 17α-estradiol.[1]
Alfatradiol is marketed under the brand names Avicis, Avixis, Ell-Cranell Alpha, and Pantostin.[2]
Alfatradiol is available in Germany and several Latin American countries, including Argentina, Brazil, and Mexico.
Alfatradiol administered systemically improved metabolic function, reduced insulin resistance, decreased intra-abdominal fat, and decreased inflammation in old male mice without inducing feminization, suggesting potential usefulness in the treatment of type 2 diabetes.[18]
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