Editing Antiandrogen (section)

===Androgen synthesis inhibitors===
{{Main|Androgen synthesis inhibitor}}

Androgen synthesis inhibitors are [[enzyme inhibitor]]s that prevent the [[biosynthesis]] of androgens.<ref name="FiggChau2010" /> This process occurs mainly in the [[gonad]]s and [[adrenal gland]]s, but also occurs in other tissues like the [[prostate gland]], [[skin]], and [[hair follicle]]s. These drugs include aminoglutethimide, ketoconazole,<ref name = "pmid2652864">{{cite journal |vauthors=Witjes FJ, Debruyne FM, Fernandez del Moral P, Geboers AD | title = Ketoconazole high dose in management of hormonally pretreated patients with progressive metastatic prostate cancer. Dutch South-Eastern Urological Cooperative Group | journal = Urology | volume = 33 | issue = 5 | pages = 411–5 |date=May 1989 | pmid = 2652864 | doi = 10.1016/0090-4295(89)90037-X }}</ref> and abiraterone acetate.<ref name="IIIBarbieri2013" /><ref name="FiggChau2010" /><ref name="Held-Warmkessel2006">{{cite book| vauthors = Held-Warmkessel J |title= Contemporary Issues in Prostate Cancer: A Nursing Perspective|url=https://books.google.com/books?id=dZe4ZSVDdBsC&pg=PA275|year=2006|publisher=Jones & Bartlett Learning|isbn=978-0-7637-3075-8|pages=275–}}</ref> Aminoglutethimide inhibits cholesterol side-chain cleavage enzyme, also known as P450scc or CYP11A1, which is responsible for the conversion of [[cholesterol]] into [[pregnenolone]] and by extension the production of all steroid hormones, including the androgens.<ref name="IIIBarbieri2013" /> Ketoconazole and abiraterone acetate are inhibitors of the enzyme CYP17A1, also known as 17α-hydroxylase/17,20-lyase, which is responsible for the conversion of [[pregnane]] steroids into androgens, as well as the conversion of [[mineralocorticoid]]s into glucocorticoids.<ref name="IIIBarbieri2013" /><ref name="FiggChau2010" /> Because these drugs all prevent the formation of glucocorticoids in addition to androgens, they must be combined with a glucocorticoid like [[prednisone]] to avoid [[adrenal insufficiency]].<ref name="Held-Warmkessel2006" /> A newer drug currently under development for treatment of prostate cancer, [[seviteronel]], is selective for inhibition of the 17,20-lyase functionality of CYP17A1, and for this reason, unlike earlier drugs, does not require concomitant treatment with a glucocorticoid.<ref name="pmid27154414">{{cite journal | vauthors = Bird IM, Abbott DH | title = The hunt for a selective 17,20 lyase inhibitor; learning lessons from nature | journal = J. Steroid Biochem. Mol. Biol. | volume = 163 | pages = 136–46 | year = 2016 | pmid = 27154414 | doi = 10.1016/j.jsbmb.2016.04.021 | pmc=5046225}}</ref>

====5α-Reductase inhibitors====
5α-Reductase inhibitors such as finasteride and dutasteride are inhibitors of [[5α-reductase]], an enzyme that is responsible for the formation of DHT from testosterone.<ref name = Flores>{{Cite journal |vauthors=Flores E, Bratoeff E, Cabeza M, Ramirez E, Quiroz A, Heuze I | title = Steroid 5alpha-reductase inhibitors | journal = Mini-Reviews in Medicinal Chemistry | volume = 3 | pages = 225–37 |date=May 2003 | pmid = 12570838 | issue = 3 | doi=10.2174/1389557033488196}}</ref> DHT is between 2.5- and 10-fold more potent than testosterone as an androgen<ref name="MozayaniRaymon2011">{{cite book| vauthors = Mozayani A, Raymon L |title=Handbook of Drug Interactions: A Clinical and Forensic Guide|url=https://books.google.com/books?id=NhBJ6kg_uP0C&pg=PA656|date=18 September 2011|publisher=Springer Science & Business Media|isbn=978-1-61779-222-9|pages=656–}}</ref> and is produced in a [[tissue-selective]] manner based on [[gene expression|expression]] of 5α-reductase.<ref name="Bhagavan2002">{{cite book| vauthors = Bhagavan NV |title=Medical Biochemistry|url=https://books.google.com/books?id=b7Dc9bOs9uAC&pg=PA787 |year=2002|publisher=Academic Press|isbn=978-0-12-095440-7|pages=787–}}</ref> Tissues in which DHT forms at a high rate include the [[prostate gland]], [[skin]], and [[hair follicle]]s.<ref name="BologniaJorizzo" /><ref name="Bhagavan2002" /> In accordance, DHT is involved in the [[pathophysiology]] of benign prostatic hyperplasia, pattern hair loss, and hirsutism, and 5α-reductase inhibitors are used to treat these conditions.<ref name="BologniaJorizzo" /><ref name="Bhagavan2002" /><ref name="pmid27672412">{{cite journal | vauthors = Hirshburg JM, Kelsey PA, Therrien CA, Gavino AC, Reichenberg JS | title = Adverse Effects and Safety of 5-alpha Reductase Inhibitors (Finasteride, Dutasteride): A Systematic Review | journal = J Clin Aesthet Dermatol | volume = 9 | issue = 7 | pages = 56–62 | year = 2016 | pmid = 27672412 | pmc = 5023004 }}</ref>