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Antigonadotropin

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Title: Antigonadotropin  
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Subject: Cyproterone acetate, Cyanoketone, Metyrapone, 20α,22R-Dihydroxycholesterol, Steroid
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Antigonadotropin

Antigonadotropin
Drug class
Use For the treatment of androgen and estrogen-related medical conditions.
Biological target GnRH receptor, gonadotropin receptors (FSHR, LHR), sex steroid receptors (AR, ER, PR)
ATC code G03XA

An antigonadotropin is a drug which suppresses the activity and/or downstream effects of one or both of the gonadotropins follicle-stimulating hormone (FSH) and luteinizing hormone (LH). This results in an inhibition of the hypothalamic-pituitary-gonadal (HPG) axis, and thus a decrease in the levels of the androgen, estrogen, and progestogen sex steroids in the body. Antigonadotropins are used for a variety of purposes, including for the treatment hormonally-sensitive cancers, to delay precocious puberty and puberty in transgender youth, as a form of chemical castration to reduce the sex drives of individuals (namely males) with hypersexuality or pedophilia, and to treat estrogen-associated conditions in women such as menorrhagia and endometriosis.

The most well-known and widely used antigonadotropins are the gonadotropin-releasing hormone (GnRH) analogues (both agonists and antagonists).[1] However, many other drugs have antigonadotropic properties as well, including compounds acting on sex steroid hormone receptors such as progestogens, androgens, and estrogens (due to negative feedback on the HPG axis),[2][3] as well as steroid synthesis inhibitors such as danazol and gestrinone.[1][4] Some antigonadotropins have a multimodal action, such as cyproterone acetate, which exerts its effects via acting as an antiandrogen, progestin, and steroid synthesis inhibitor.[5][6] Since progestins have relatively little effect on sexual differentiation compared to the other sex steroids, potent ones such as medroxyprogesterone acetate and chlormadinone acetate are often used at high doses specifically for their antigonadotropic effects.[2][7][8]

See also

References

  1. ^ a b Jonathan S. Berek; Emil Novak (2007). Berek and Novak's Gynecology. Lippincott Williams & Wilkins. p. 212.  
  2. ^ a b de Lignières B, Silberstein S (April 2000). "Pharmacodynamics of oestrogens and progestogens". Cephalalgia : an International Journal of Headache 20 (3): 200–7.  
  3. ^ Gooren L (October 1989). "Androgens and estrogens in their negative feedback action in the hypothalamo-pituitary-testis axis: site of action and evidence of their interaction". Journal of Steroid Biochemistry 33 (4B): 757–61.  
  4. ^ Singh H, Jindal DP, Yadav MR, Kumar M (1991). "Heterosteroids and drug research". Progress in Medicinal Chemistry 28: 233–300.  
  5. ^ Moltz L, Römmler A, Post K, Schwartz U, Hammerstein J (April 1980). "Medium dose cyproterone acetate (CPA): effects on hormone secretion and on spermatogenesis in men". Contraception 21 (4): 393–413.  
  6. ^ Ayub M, Levell MJ (July 1987). "Inhibition of rat testicular 17 alpha-hydroxylase and 17,20-lyase activities by anti-androgens (flutamide, hydroxyflutamide, RU23908, cyproterone acetate) in vitro". J. Steroid Biochem. 28 (1): 43–7.  
  7. ^ Bercovici JP (September 1987). "[Progestational contraception]". La Revue Du Praticien (in French) 37 (38): 2277–8, 2281–4.  
  8. ^ Chassard D, Schatz B (2005). "[The antigonadrotropic activity of chlormadinone acetate in reproductive women]". Gynécologie, Obstétrique & Fertilité (in French) 33 (1-2): 29–34.  
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