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2 See also  





3 References  














Template:Oral potencies of progestogens







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  • t
  • e
  • Oral potencies of progestogens[data 1]
    Compound Doses for specific uses (mg/day)[a]
    OID TFD MDT BCPD ECD
    Cycle Daily
    Allylestrenol 25 150–300 - 30 -
    Bromoketoprogesterone[b] - - 100–160 - -
    Chlormadinone acetate 1.5–4.0 20–30 3–10 1.0–4.0 2.0 5–10
    Cyproterone acetate 1.0 20–30 1.0–3.0 1.0–4.0 2.0 1.0
    Desogestrel 0.06 0.4–2.5 0.15 0.25 0.15 0.15
    Dienogest 1.0 6.0–6.3 - - 2.0–3.0 2.0
    Drospirenone 2.0 40–80 - - 3.0 2.0
    Dydrogesterone >30 140–200 10–20 20 10
    Ethisterone - 200–700 50–250 - -
    Etynodiol diacetate 2.0 10–15 - 1.0 1.0–20 -
    Gestodene 0.03 2.0–3.0 - - 0.06–0.075 0.20
    Hydroxyprogest. acetate - - 70–125 - 100 -
    Hydroxyprogest. caproate - 700–1400 70 - -
    Levonorgestrel 0.05 2.5–6.0 0.15–0.25 0.5 0.1–0.15 0.075
    Lynestrenol 2.0 35–150 5.0 10 - -
    Medrogestone 10 50–100 10 15 10
    Medroxyprogest. acetate 10 40–120 2.5–10 20–30 5–10 5.0
    Megestrol acetate >5[c] 30–70 - 5–10 1.0–5.0 5.0
    Nomegestrol acetate 1.25–5.0 100 5.0 - 2.5 3.75–5.0
    Norethandrolone[b] - - 10 - -
    Norethisterone 0.4–0.5 100–150 5–10 10–15 0.5 0.7–1.0
    Norethisterone acetate 0.5 30–60 2.5–5.0 7.5 0.6 1.0
    Norethist. acetate (micron.) - 12–14 - - -
    Noretynodrel 4.0 150–200 - 14 2.5–10 -
    Norgestimate 0.2 2.0–10 - - 0.25 0.09
    Norgestrel 0.1 12 - 0.5–2.0 - -
    Normethandrone - 150 10 - -
    Progesterone (non-micron.) >300[d] - - - - -
    Progesterone (micronized) - 4200 200–300 1000 200
    Promegestone 0.5 10 0.5 - 0.5
    Tibolone 2.5 - - - -
    Trengestone - 50–70 - - -
    Trimegestone 0.5 - 0.25–0.5 - 0.0625–0.5
    Notes and sources
    1. ^ Dosages are expressed in mg/day unless otherwise noted
  • ^ a b Never marketed as a progestogen.
  • ^ The exact OIDofMGA is unknown, but it is known to be greater than 5 mg/day.[21][22][23]
  • ^ Ovulation inhibition rate with 300 to 1,000 mg/day oral non-micronized P4 was incomplete.[24][15][25][26][27][28]
  • This template can be used to easily insert a table detailing the oral potencies of progestogens into an article. It comes with twenty-eight pre-provided references.

    This template does not have any parameters.

    See also

    References

    1. ^ Schindler AE, Campagnoli C, Druckmann R, Huber J, Pasqualini JR, Schweppe KW, Thijssen JH (December 2003). "Classification and pharmacology of progestins". Maturitas. 46 Suppl 1: S7–S16. doi:10.1016/j.maturitas.2003.09.014. PMID 14670641.
  • ^ Kuhl H (2011). "Pharmacology of Progestogens" (PDF). J Reproduktionsmed Endokrinol. 8 (1): 157–177.
  • ^ 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.
  • ^ Lauritzen C (September 1990). "Clinical use of oestrogens and progestogens". Maturitas. 12 (3): 199–214. doi:10.1016/0378-5122(90)90004-P. PMID 2215269.
  • ^ Kuhl H (September 1990). "Pharmacokinetics of oestrogens and progestogens". Maturitas. 12 (3): 171–97. doi:10.1016/0378-5122(90)90003-o. PMID 2170822.
  • ^ Knörr, Karl; Knörr-Gärtner, Henriette; Beller, Fritz K.; Lauritzen, Christian (8 March 2013). Geburtshilfe und Gynäkologie: Physiologie und Pathologie der Reproduktion. Springer-Verlag. pp. 583–. ISBN 978-3-642-95583-9.
  • ^ Knörr, Karl; Beller, Fritz K.; Lauritzen, Christian (17 April 2013). Lehrbuch der Gynäkologie. Springer-Verlag. pp. 214–. ISBN 978-3-662-00942-0.
  • ^ Horský, Jan; Presl, Jiří (1981). "Hormonal Treatment of Disorders of the Menstrual Cycle". In J. Horsky; J. Presl (eds.). Ovarian Function and its Disorders: Diagnosis and Therapy. Springer Science & Business Media. pp. 309–332. doi:10.1007/978-94-009-8195-9_11. ISBN 978-94-009-8195-9.
  • ^ Ferin J (September 1972). "Orally Active Progestational Compounds. Human Studies: Effects on the Utero-Vaginal Tract". In M. Tausk (ed.). Pharmacology of the Endocrine System and Related Drugs: Progesterone, Progestational Drugs and Antifertility Agents. Vol. II. Pergamon Press. pp. 245–273. ISBN 978-0080168128. OCLC 278011135.
  • ^ Freimut A. Leidenberger; Thomas Strowitzki; Olaf Ortmann (29 August 2009). Klinische Endokrinologie für Frauenärzte. Springer-Verlag. pp. 225, 227. ISBN 978-3-540-89760-6.
  • ^ Neumann F, Düsterberg B (1998). "Entwicklung auf dem Gebiet der Gestagene" [Development in the field of progestogens]. Reproduktionsmedizin. 14 (4): 257–264. doi:10.1007/s004440050042. ISSN 1434-6931.
  • ^ Hammerstein, J. (1990). "Antiandrogens: Clinical Aspects". Hair and Hair Diseases. pp. 827–886. doi:10.1007/978-3-642-74612-3_35.
  • ^ Willibald Pschyrembel (1968). Praktische Gynäkologie: für Studierende und Ärzte. Walter de Gruyter. p. 599. ISBN 978-3-11-150424-7.
  • ^ Ufer, Joachim (1968). "Die therapeutische Anwendung der Gestagene beim Menschen" [Therapeutic Use of Progestagens in Humans]. Die Gestagene [Progestogens]. Springer-Verlag. pp. 1026–1124. doi:10.1007/978-3-642-99941-3_7. ISBN 978-3-642-99941-3. Zur Transformation des Endometriums benotigten sie 200-400 mg [ethisterone] pro Cyclus und postulierten eine etwa sechsfach schwachere Wirkung gegenuber dem Progesteron i.m. appliziert.
  • ^ a b Endrikat J, Gerlinger C, Richard S, Rosenbaum P, Düsterberg B (December 2011). "Ovulation inhibition doses of progestins: a systematic review of the available literature and of marketed preparations worldwide". Contraception. 84 (6): 549–57. doi:10.1016/j.contraception.2011.04.009. PMID 22078182. Table 1 Publications on ovulation inhibition doses of progestins: Progestin: Progesterone. Reference: Pincus (1956). Method: Urinary Pdiol. Daily dose (mg): 300.000. Total number of cycles in all subjects: 61. Total number of ovulation in all subjects: 30. % of ovulation in all subjects: 49.
  • ^ Milan Rastislav Henzl; John A. Edwards (10 November 1999). "Pharmacology of Progestins: 17α-Hydroxyprogesterone Derivatives and Progestins of the First and Second Generation". In Régine Sitruk-Ware; Daniel R. Mishell (eds.). Progestins and Antiprogestins in Clinical Practice. Taylor & Francis. pp. 101–132. ISBN 978-0-8247-8291-7.
  • ^ Kopera, Hans (1991). "Hormone der Gonaden". Hormonelle Therapie für die Frau. pp. 59–124. doi:10.1007/978-3-642-95670-6_6. ISBN 978-3-642-95670-6. ISSN 0172-777X.
  • ^ IARC Working Group on the Evaluation of Carcinogenic Risks to Humans; World Health Organization; International Agency for Research on Cancer (2007). "Annex 2: Composition of Oral and Injectable Estrogen–Progestogen Contraceptives". Combined Estrogen-progestogen Contraceptives and Combined Estrogen-progestogen Menopausal Therapy. World Health Organization. pp. 431–464. ISBN 978-92-832-1291-1.
  • ^ Lobo, Rogerio A.; Stanczyk, Frank Z. (1994). "New knowledge in the physiology of hormonal contraceptives". American Journal of Obstetrics and Gynecology. 170 (5): 1499–1507. doi:10.1016/S0002-9378(12)91807-4. ISSN 0002-9378.
  • ^ Henzl, Milan R. (1986). "Contraceptive Hormones and their Clinical Use". In Samuel S. C. Yen; Robert B. Jaffe (eds.). Reproductive Endocrinology: Physiology, Pathophysiology, and Clinical Management. Saunders. pp. 643–682. ISBN 978-0-7216-9630-0.
  • ^ Ostergaard E (February 1965). "The oral progestational and anti-ovulatory properties of megestrol acetate and its therapeutic use in gynaecological disorders". J Obstet Gynaecol Br Emp. 72 (1): 45–48. doi:10.1111/j.1471-0528.1965.tb01372.x. PMID 12332461. The anti-ovulatory properties of megestrol acetate 5 mg. plus Mestranol 0.1 mg. were demonstrated in thirty-five women by direct inspection of the ovaries. When given alone, megestrol acetate 5 mg. or Mestranol 0.1 mg. did not prevent ovulation in all cases.
  • ^ Schacter L, Rozencweig M, Canetta R, Kelley S, Nicaise C, Smaldone L (March 1989). "Megestrol acetate: clinical experience". Cancer Treat. Rev. 16 (1): 49–63. doi:10.1016/0305-7372(89)90004-2. PMID 2471590. At 0.25 mg/day MA has no apparent effect on the histology of the endometrium and is not effective as a contraceptive (53). However, at doses of 0.35 and 0.5 mg/day the drug is an effective contraceptive (10). At the 0.5 mg/day dose MA does not inhibit ovulation but does reduce sperm motility in post-coital tests (68).
  • ^ Vessey, M.P.; Mears, Eleanor; Andolšek, Lidija; Ogrinc-Oven, Majda (1972). "Randomised double-blind trial of four oral progestagen-only contraceptives". The Lancet. 299 (7757): 915–922. doi:10.1016/S0140-6736(72)91492-4. ISSN 0140-6736.
  • ^ Aufrère MB, Benson H (June 1976). "Progesterone: an overview and recent advances". J Pharm Sci. 65 (6): 783–800. doi:10.1002/jps.2600650602. PMID 945344. Early studies on its use as an oral contraceptive showed that, at 300 mg/day (5th to 25th day of the menstrual cycle), progesterone was effective in preventing ovulation through four cycles (263). The related effect of larger doses of progesterone on gonadotropin excretion also has been investigated. Rothchild (264) found that continuous or intermittent intravenously administered progesterone (100-400 mg/day) for 10 days depressed the total amount of gonadotropin excreted into the urine. However, Paulsen et al. (265) found that oral progesterone at 1000 mg/day for 87 days did not have a significant effect on urinary gonadotropin excretion. The efficacy of progesterone as an oral contraceptive was never fully tested, because synthetic progestational agents, which were orally effective, were available.
  • ^ Pincus G (December 1958). "The hormonal control of ovulation and early development". Postgrad Med. 24 (6): 654–60. doi:10.1080/00325481.1958.11692305. PMID 13614060. Table 1: Effects of oral progesterone on three indexes of ovulation: Medication: Progesterone. Number: 69. Mean cycle length: 25.5 ± 0.59. Per cent positive for ovulation by: Basal temperature: 27. Endometrial biopsy: 18. Vaginal smear: 6. [...] we settled on 300 mg. per day [oral progersterone] as a significantly effective [ovulation inhibition] dosage, and this was administered from the fifth day through the twenty-fourth day of the menstrual cycle. [...] We observed each of 33 volunteer subjects during a control, nontreatment cycle and for one to three successive cycles of medication immediately following the control cycle. As indexes of the occurrence of ovulation, daily basal temperatures and vaginal smears were taken, and at the nineteenth to twenty-second day of the cycle an endometrial biopsy. [...] Although we thus demonstrated the ovulation-inhibiting activity of progesterone in normally ovulating women, oral progesterone medication had two disadvantages: (l) the large daily dosage ( 300 mg.) which presumably would have to be even larger if one sought 100 per cent inhibition1 [...]
  • ^ Pincus G (1956). "Some effects of progesterone and related compounds upon reproduction and early development in mammals". Acta Endocrinol Suppl (Copenh). 23 (Suppl 28): 18–36. doi:10.1530/acta.0.023S018. PMID 13394044.
  • ^ Stone, Abraham; Kupperman, Herbert S. (1955). "The Effects of Progesterone on Ovulation: A Preliminary Report". The Fifth International Conference on Planned Parenthood: Theme, Overpopulation and Family Planning: Report of the Proceedings, 24-29 October, 1955, Tokyo, Japan. International Planned Parenthood Federation. p. 185.
  • ^ S. Beier; B. Düsterberg; M. F. El Etreby; W. Elger; F. Neumann; Y. Nishino (1983). "Toxicology of Hormonal Fertility Regulating Agents". In Giuseppe Benagiano; Egon Diczfalusy (eds.). Endocrine Mechanisms in Fertility Regulation. Raven Press. pp. 261–346. ISBN 978-0-89004-464-3.

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