Pharmacokinetics of estradiol

Pharmacokinetics of estradiol
Clinical data
Routes of
administration		• By mouth (tablet)
• Sublingual (tablet)
• Intranasal (nasal spray)
• Transdermal (patch, gel, cream, emulsion, spray)
• Vaginal (tablet, cream, suppository, insert, ring)
• IM injection (oil solution)
• SC injection (aq. soln.Tooltip aqueous solution)
• Subcutaneous implant
Drug classEstrogen; Antigonadotropin
Pharmacokinetic data
BioavailabilityOral: 5% (0.1–12%)[1][2]
SL: 10% (in marmosets)[3]
IM: 100%[4]
Protein binding~98%:[1][5]
• Albumin: 60%
• SHBG: 38%
• Free: 2%
MetabolismLiver (via hydroxylation, sulfation, glucuronidation)
MetabolitesMajor (90%):[1]
• Estrone
• Estrone sulfate
• Estrone glucuronide
• Estradiol glucuronide
Elimination half-lifeOral: 13–20 hours[1]
Sublingual: 8–18 hours[6]
Transdermal (gel): 37 hours[7]
IM (as EVTooltip estradiol valerate): 4–5 days[4]
IM (as ECTooltip estradiol cypionate): 8–10 days[8]
IVTooltip Intravenous injection (as E2): 0.5–2 hours[4][9]
ExcretionUrine: 54%[1]
Feces: 6%[1]

The pharmacology of estradiol, an estrogen medication and naturally occurring steroid hormone, concerns its pharmacodynamics, pharmacokinetics, and various routes of administration.[10][11][12]

Estradiol is a naturally occurring and bioidentical estrogen, or an agonist of the estrogen receptor, the biological target of estrogens like endogenous estradiol.[10] Due to its estrogenic activity, estradiol has antigonadotropic effects and can inhibit fertility and suppress sex hormone production in both women and men.[13][14] Estradiol differs from non-bioidentical estrogens like conjugated estrogens and ethinylestradiol in various ways, with implications for tolerability and safety.[10]

Estradiol can be taken by mouth, held under the tongue, as a gel or patch that is applied to the skin, in through the vagina, by injection into muscle or fat, or through the use of an implant that is placed into fat, among other routes.[10]

  1. ^ a b c d e f Stanczyk FZ, Archer DF, Bhavnani BR (June 2013). "Ethinyl estradiol and 17β-estradiol in combined oral contraceptives: pharmacokinetics, pharmacodynamics and risk assessment". Contraception. 87 (6): 706–727. doi:10.1016/j.contraception.2012.12.011. PMID 23375353.
  2. ^ Cite error: The named reference pmid8530713 was invoked but never defined (see the help page).
  3. ^ Cite error: The named reference KuhnzBlode1993 was invoked but never defined (see the help page).
  4. ^ a b c Cite error: The named reference pmid7169965 was invoked but never defined (see the help page).
  5. ^ Falcone T, Hurd WW (2007). Clinical Reproductive Medicine and Surgery. Elsevier Health Sciences. pp. 22, 362, 388. ISBN 978-0-323-03309-1.
  6. ^ Price TM, Blauer KL, Hansen M, Stanczyk F, Lobo R, Bates GW (March 1997). "Single-dose pharmacokinetics of sublingual versus oral administration of micronized 17 beta-estradiol". Obstetrics and Gynecology. 89 (3): 340–345. doi:10.1016/S0029-7844(96)00513-3. PMID 9052581. S2CID 71641652.
  7. ^ Naunton M, Al Hadithy AF, Brouwers JR, Archer DF (2006). "Estradiol gel: review of the pharmacology, pharmacokinetics, efficacy, and safety in menopausal women". Menopause. 13 (3): 517–527. doi:10.1097/01.gme.0000191881.52175.8c. PMID 16735950. S2CID 42748448.
  8. ^ Sierra-Ramírez JA, Lara-Ricalde R, Lujan M, Velázquez-Ramírez N, Godínez-Victoria M, Hernádez-Munguía IA, et al. (December 2011). "Comparative pharmacokinetics and pharmacodynamics after subcutaneous and intramuscular administration of medroxyprogesterone acetate (25 mg) and estradiol cypionate (5 mg)". Contraception. 84 (6): 565–570. doi:10.1016/j.contraception.2011.03.014. PMID 22078184.
  9. ^ White CM, Ferraro-Borgida MJ, Fossati AT, McGill CC, Ahlberg AW, Feng YJ, et al. (1998). "The pharmacokinetics of intravenous estradiol--a preliminary study". Pharmacotherapy. 18 (6): 1343–1346. doi:10.1002/j.1875-9114.1998.tb03157.x. PMID 9855336. S2CID 9970669.
  10. ^ a b c d 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. S2CID 24616324.
  11. ^ Oettel M, Schillinger E (6 December 2012). Estrogens and Antiestrogens I: Physiology and Mechanisms of Action of Estrogens and Antiestrogens. Springer Science & Business Media. pp. 121, 226, 235–237. ISBN 978-3-642-58616-3.
  12. ^ Oettel M, Schillinger E (6 December 2012). Estrogens and Antiestrogens II: Pharmacology and Clinical Application of Estrogens and Antiestrogen. Springer Science & Business Media. pp. 163–178, 235–237, 252–253, 261–276, 538–543. ISBN 978-3-642-60107-1.
  13. ^ Stege R, Carlström K, Collste L, Eriksson A, Henriksson P, Pousette A (1988). "Single drug polyestradiol phosphate therapy in prostatic cancer". Am. J. Clin. Oncol. 11 (Suppl 2): S101–3. doi:10.1097/00000421-198801102-00024. PMID 3242384. S2CID 32650111.
  14. ^ Ockrim JL, Lalani EN, Laniado ME, Carter SS, Abel PD (May 2003). "Transdermal estradiol therapy for advanced prostate cancer--forward to the past?". J. Urol. 169 (5): 1735–7. doi:10.1097/01.ju.0000061024.75334.40. PMID 12686820.