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Steroidogenesis, with progestogens inside yellow box.

Progestogens[1] (also sometimes spelled progestagens[2] or gestagens) are a group of hormones including progesterone.

The progestogens are one of the five major classes of steroid hormones, in addition to the estrogens, androgens, mineralocorticoids, and glucocorticoids. All progestogens are characterized by their basic 21-carbon skeleton, called a pregnane skeleton (C21). In similar manner, the estrogens possess an estrane skeleton (C18) and androgens, an andrane skeleton (C19).

Progestogens are named for their function in maintaining pregnancy (pro-gestational), although they are also present at other phases of the estrous and menstrual cycles. The progestogen class of hormones includes all steroids with a pregnane skeleton, that is, both naturally occurring and synthetic ones. Exogenous or synthetic hormones are usually referred to as progestins.


Progestogens as precursors to other steroids In the first step in the steroidogenic pathway, the cholesterol molecules are converted into pregnenolone ("P5") which serves as a precursor to three other progestogens (progesterone/"P4", 17α-hydroxypregnenolone, and 17α-hydroxyprogesterone). These progestogens in turn are precursors to all other steroids, including the estrogens, androgens, mineralocorticoids, and glucocorticoids. Thus, all tissues producing steroids, such as the adrenals, ovaries, and testes, must be capable of producing progestogens.

In some tissues, the enzymes required for the final product are not all located in a single cell; for example, in ovarian follicles, cholesterol is converted to androstenedione, an androgen, in the theca cells, which is further converted into estrogen in the granulosa cells. Fetal adrenal glands also produce P5 in some species, which is converted into P4 and estrogens by the placenta (see below). In the human, the fetal adrenals produce dihydroepiandrosterone via the P5 pathway.

Progestogen production by the ovary[edit]

Progesterone (P4) is the major progestogen produced by the corpus luteum in all mammalian species. Luteal cells possess the necessary enzymes to convert cholesterol to pregnenolone (P5), which is subsequently converted into P4. P4 is highest in the diestrus phase of the estrous cycle.

Progestogen production by the placenta[edit]

The role of the placenta in progestogen production varies by species. In the sheep, horse, and human, the placenta takes over the majority of progestogen production, whereas in other species the corpus luteum remains the primary source of progestogen. In the sheep and human, P4 is the major placental progestogen.

The equine placenta produces a variety of progestogens, primarily 5αDHP and 20α5P, beginning on day 60. A complete luteo-placental shift occurs by day 120-150.


Birth control[edit]

Progestins, synthetic substances with progestogenic activity are used in birth control pills, implants and the intrauterine system IUS (Mirena).


Some progestins also have potent antiandrogen properties via acting as antagonists of the androgen receptor. Examples include chlormadinone acetate, cyproterone acetate, dienogest, and drospirenone.[3] Care must be taken as to which progestin is used however, as various others conversely may have androgenic properties.

Progesterone withdrawal bleeding[edit]

In a normal menstrual cycle, declining levels of progesterone triggers menstruation. Norethindrone acetate (brand name Aygestin) and medroxyprogesterone acetate (brand name Provera) may be used to artificially induce progestogen withdrawal bleeding.[citation needed]

Cachexia Syndrome[edit]

In many people suffering from solid malignancy, especially gastric and pancreatic cancer, progestins can be employed to improve appetite and reduce wasting. In general, they are used in combination with other steroids such as dexamethasone. Their effects take several weeks to become apparent, but are relatively long-lived when compared to those of corticosteroids. Furthermore, they are recognized as being the only drugs to increase lean body mass. Megestrol acetate is the lead drug of this class for the management of cachexia.


Progesterone, similarly to androgens and estrogens through their own respective receptors, inhibits the secretion of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) via activation of the progesterone receptor as a form of negative feedback on the hypothalamic-pituitary-gonadal (HPG) axis in order to help prevent sex hormone levels from getting too high.[4][5][6] Accordingly, progesterone and other progestogens have antigonadotropic effects,[7] and at sufficient doses can markedly suppress the production of progesterone and other sex steroids such as the androgens and the estrogens.[6] As such, some of the more potent progestins including chlormadinone acetate,[5] medroxyprogesterone acetate,[8] megestrol acetate,[7] nomegestrol acetate,[9] and norethisterone acetate[10] are sometimes used as antiandrogens and/or antiestrogens in a variety of sex hormone-associated medical conditions. Progesterone itself is not generally used for this purpose as it can serve as a prohormone to the other sex steroids (as it is their endogenous precursor),[11] and hence, conversely, has the potential to produce androgenic and/or estrogenic effects as well,[11][12][13] especially at the relatively high doses at which are required for sufficient antigonadotropic activity to occur.

See also[edit]


  1. ^ "progestogen". Oxford Dictionaries. Retrieved 21 December 2012. 
  2. ^ "progestagen". Merriam-Webster. Retrieved 21 December 2012. 
  3. ^ Raudrant D, Rabe T (2003). "Progestogens with antiandrogenic properties". Drugs 63 (5): 463–92. doi:10.2165/00003495-200363050-00003. PMID 12600226. 
  4. ^ de Lignières B, Silberstein S (April 2000). "Pharmacodynamics of oestrogens and progestogens". Cephalalgia : an International Journal of Headache 20 (3): 200–7. doi:10.1046/j.1468-2982.2000.00042.x. PMID 10997774. 
  5. ^ a b Chassard D, Schatz B (2005). "[The antigonadrotropic activity of chlormadinone acetate in reproductive women]". Gynécologie, Obstétrique & Fertilité (in French) 33 (1-2): 29–34. doi:10.1016/j.gyobfe.2004.12.002. PMID 15752663. 
  6. ^ a b Brady BM, Anderson RA, Kinniburgh D, Baird DT (April 2003). "Demonstration of progesterone receptor-mediated gonadotrophin suppression in the human male". Clinical Endocrinology 58 (4): 506–12. doi:10.1046/j.1365-2265.2003.01751.x. PMID 12641635. 
  7. ^ a b Neumann F (1978). "The physiological action of progesterone and the pharmacological effects of progestogens--a short review". Postgraduate Medical Journal. 54 Suppl 2: 11–24. PMID 368741. 
  8. ^ Andrea R. Genazzani (15 January 1993). Frontiers in Gynecologic and Obstetric Investigation. Taylor & Francis. p. 320. ISBN 978-1-85070-486-7. Retrieved 29 May 2012. 
  9. ^ Lello S (March 2010). "Nomegestrol acetate: pharmacology, safety profile and therapeutic efficacy". Drugs 70 (5): 541–59. doi:10.2165/11532130-000000000-00000. PMID 20329803. 
  10. ^ Garza-Flores J, Menjívar M, Cardenas M, Reynoso M, García GA, Pérez Palacios G (January 1991). "Further studies on the antigonadotropic mechanism of action of norethisterone". The Journal of Steroid Biochemistry and Molecular Biology 38 (1): 89–93. doi:10.1016/0960-0760(91)90406-U. PMID 1825472. 
  11. ^ a b Christiane Northrup (1 June 2010). Women's Bodies, Women's Wisdom: Creating Physical and Emotional Health and Healing. Hay House, Inc. p. 552. ISBN 978-0-553-38673-8. Retrieved 29 May 2012. 
  12. ^ Ifeoma Ikenze (24 November 1998). Menopause & Homeopathy: A Guide for Women in Midlife. North Atlantic Books. p. 18. ISBN 978-1-55643-291-0. Retrieved 29 May 2012. 
  13. ^ Brandith Irwin; Mark McPherson (1 September 2002). Your Best Face Without Surgery. Hay House, Inc. p. 129. ISBN 978-1-56170-953-3. Retrieved 29 May 2012. 

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