View source for 11-Deoxycortisol

{{Use dmy dates|date=December 2023}}
{{cs1 config|name-list-style=vanc}}
{{Use American English|date=February 2024}}
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| verifiedrevid = 390185893
| ImageFile1 = {{wikidata|property|raw|P117}}
| ImageSize1 = 220px
| ImageAlt1 = Cortodoxone chemical structure
| ImageFile2 = {{wikidata|property|raw|P8224}}
| ImageSize2 = 220px
| ImageAlt2 = Cortodoxone 3D ball molecule view
| IUPACName = 17α,21-Dihydroxypregn-4-ene-3,20-dione
| SystematicName = (1''R'',3a''S'',3b''R'',9a''R'',9b''S'',11a''S'')-1-Hydroxy-1-(2-hydroxy-1-oxoethyl)-9a,11a-dimethyl-1,2,3,3a,3b,4,5,8,9,9a,9b,10,11,11a-tetradecahydro-7''H''-cyclopenta[''a'']phenanthren-7-one
| OtherNames = 11-Deoxycortisol; 11-Deoxycortisone; Cortoxelone; 17α,21-Dihydroxyprogesterone; 11-Desoxycortisol; 11-Deoxyhydrocortisone; 11-Desoxyhydrocortisone; 17α-Hydroxy-11-deoxycorticosterone; Reichstein's Substance S; Compound S; Cortodoxone; Cortexolone,
|Section1={{Chembox Identifiers
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| ChemSpiderID = 389582
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| UNII = WDT5SLP0HQ
| InChI = 1/C21H30O4/c1-19-8-5-14(23)11-13(19)3-4-15-16(19)6-9-20(2)17(15)7-10-21(20,25)18(24)12-22/h11,15-17,22,25H,3-10,12H2,1-2H3/t15-,16+,17+,19+,20+,21+/m1/s1
| InChIKey = WHBHBVVOGNECLV-OBQKJFGGBG
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| StdInChI = 1S/C21H30O4/c1-19-8-5-14(23)11-13(19)3-4-15-16(19)6-9-20(2)17(15)7-10-21(20,25)18(24)12-22/h11,15-17,22,25H,3-10,12H2,1-2H3/t15-,16+,17+,19+,20+,21+/m1/s1
| StdInChIKey_Ref = {{stdinchicite|changed|chemspider}}
| StdInChIKey = WHBHBVVOGNECLV-OBQKJFGGSA-N
| CASNo_Ref = {{cascite|correct|CAS}}
| CASNo =152-58-9
| PubChem =440707
| KEGG_Ref = {{keggcite|changed|kegg}}
| KEGG = D03595
| ChEBI_Ref = {{ebicite|changed|EBI}}
| ChEBI = 28324
| SMILES = O=C4\C=C2/[C@]([C@H]1CC[C@@]3([C@@](O)(C(=O)CO)CC[C@H]3[C@@H]1CC2)C)(C)CC4
| ChEMBL_Ref = {{ebicite|changed|EBI}}
| ChEMBL = 253144
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|Section2={{Chembox Properties
| C=21 | H=30 | O=4
| Appearance =
| Density =
| MeltingPtC = 215
| BoilingPt =
| Solubility =
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|Section3={{Chembox Hazards
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}}'''11-Deoxycortisol''', also known as '''cortodoxone''' ([[International Nonproprietary Name|INN]]), '''cortexolone'''<ref name="pmid32847976">{{cite journal | vauthors = Rosette C, Agan FJ, Rosette N, Mazzetti A, Moro L, Gerloni M | title = The dual androgen receptor and glucocorticoid receptor antagonist CB-03-10 as a potential treatment for tumors that have acquired GR-mediated resistance to AR blockade | journal = Molecular Cancer Therapeutics | pages = 2256–2266| date = August 2020 | volume = 19 | issue = 11 | pmid = 32847976 | doi = 10.1158/1535-7163.MCT-19-1137 | s2cid = 221345484 | doi-access = free | url = https://figshare.com/articles/journal_contribution/22520836 }}</ref><ref name="pmid18173113">{{cite journal | vauthors = Iaderets VV, Andriushina VA, Bartoshevich IE, Domracheva AG, Novak MI, Stytsenko TS, Voĭshvillo NE | title = [A study of steroid hydroxylation activity of Curvularia lunata mycelium] | language = ru | journal = Prikladnaia Biokhimiia I Mikrobiologiia | volume = 43 | issue = 6 | pages = 695–700 | date = 2007 | pmid = 18173113 }}</ref><ref name="pmid17066954">{{cite journal | vauthors = Manosroi J, Chisti Y, Manosroi A | title = Biotransformation of cortexolone to hydrocortisone by molds using a rapid color development assay | journal = Prikladnaia Biokhimiia I Mikrobiologiia | volume = 42 | issue = 5 | pages = 547–51 | date = 2006 | pmid = 17066954 }}</ref><ref name="pmid12798358">{{cite journal | vauthors = Lisowska K, Długoński J | title = Concurrent corticosteroid and phenanthrene transformation by filamentous fungus Cunninghamella elegans | journal = The Journal of Steroid Biochemistry and Molecular Biology | volume = 85 | issue = 1 | pages = 63–9 | date = May 2003 | pmid = 12798358 | doi = 10.1016/s0960-0760(03)00136-5 | s2cid = 384672 }}</ref> as well as '''17α,21-dihydroxyprogesterone''' or '''17α,21-dihydroxypregn-4-ene-3,20-dione''',<ref name="HillMakin1991">{{cite book|author1=R.A. Hill|author2=H.L.J. Makin|author3=D.N. Kirk|author4=G.M. Murphy|title=Dictionary of Steroids|url=https://books.google.com/books?id=qw5X0NK1A90C&pg=PA338|date=23 May 1991|publisher=CRC Press|isbn=978-0-412-27060-4|pages=338–}}</ref> is an [[endogenous]] [[glucocorticoid]] [[steroid hormone]], and a [[metabolic intermediate]] toward [[cortisol]]. It was first described by [[Tadeusz Reichstein]] in 1938 as Substance S,<ref name="doi101002">{{cite journal|url=https://onlinelibrary.wiley.com/doi/10.1002/hlca.193802101183|doi=10.1002/hlca.193802101183|title=Über Bestandteile der Nebennierenrinde. 21. Mitteilung. Die Konstitution der Substanzen R und S|year=1938|journal=Helvetica Chimica Acta|volume=21|pages=1490–1497|vauthors=Reichstein T|url-access=subscription|access-date=5 October 2020|archive-date=10 October 2020|archive-url=https://web.archive.org/web/20201010063404/https://onlinelibrary.wiley.com/doi/10.1002/hlca.193802101183|url-status=live}}</ref> thus has also been referred to as '''Reichstein's Substance S'''<ref name="HillMakin1991" /> or '''Compound S'''.<ref name="pmid12231120">{{cite journal | vauthors = Wudy SA, Hartmann M, Homoki J | title = Determination of 11-deoxycortisol (Reichstein's compound S) in human plasma by clinical isotope dilution mass spectrometry using benchtop gas chromatography-mass selective detection | journal = Steroids | volume = 67 | issue = 10 | pages = 851–7 | date = September 2002 | pmid = 12231120 | doi = 10.1016/s0039-128x(02)00052-1| s2cid = 29970823 }}</ref><ref name="pmid12466339">{{cite journal | vauthors = Berneis K, Staub JJ, Gessler A, Meier C, Girard J, Müller B | title = Combined stimulation of adrenocorticotropin and compound-S by single dose metyrapone test as an outpatient procedure to assess hypothalamic-pituitary-adrenal function | journal = The Journal of Clinical Endocrinology and Metabolism | volume = 87 | issue = 12 | pages = 5470–5 | date = December 2002 | pmid = 12466339 | doi = 10.1210/jc.2001-011959| doi-access = free }}</ref>

==Function==
[[File:Steroidogenesis.svg|thumb|left|[[Steroidogenesis]], showing 11-deoxycortisol in the pathway from [[cholesterol]] to [[cortisol]].<ref name="HäggströmRichfield2014">{{cite journal|last1=Häggström|first1=Mikael|last2=Richfield|first2=David |year=2014|title=Diagram of the pathways of human steroidogenesis|journal=WikiJournal of Medicine|volume=1|issue=1|doi=10.15347/wjm/2014.005|issn=2002-4436|doi-access=free}}</ref>]]11-Deoxycortisol acts as a [[glucocorticoid]], though is less potent than [[cortisol]].<ref name="pmid31090904">{{cite journal | vauthors = Engels M, Pijnenburg-Kleizen KJ, Utari A, Faradz SM, Oude-Alink S, van Herwaarden AE, Span PN, Sweep FC, Claahsen-van der Grinten HL | title = Glucocorticoid Activity of Adrenal Steroid Precursors in Untreated Patients With Congenital Adrenal Hyperplasia | journal = The Journal of Clinical Endocrinology and Metabolism | volume = 104 | issue = 11 | pages = 5065–5072 | date = November 2019 | pmid = 31090904 | doi = 10.1210/jc.2019-00547| doi-access = free }}</ref>

11-Deoxycortisol is synthesized from [[17α-hydroxyprogesterone]] by [[21-hydroxylase]] and is converted to [[cortisol]] by [[11β-hydroxylase]].

11-Deoxycortisol in mammals has limited [[biological activity]] and mainly acts as [[metabolic intermediate]] within the [[glucocorticoid]] pathway, leading to [[cortisol]].<ref name="merckmanuals">{{cite news |title=Congenital Adrenal Hyperplasia Caused by 11Beta-Hydroxylase Deficiency |newspaper=Merck Manuals Professional Edition |url=https://www.merckmanuals.com/professional/pediatrics/endocrine-disorders-in-children/congenital-adrenal-hyperplasia-caused-by-11beta-hydroxylase-deficiency |access-date=3 October 2020 |archive-date=25 September 2020 |archive-url=https://web.archive.org/web/20200925031158/https://www.merckmanuals.com/professional/pediatrics/endocrine-disorders-in-children/congenital-adrenal-hyperplasia-caused-by-11beta-hydroxylase-deficiency |url-status=live }}</ref> However, in [[sea lamprey]]s, an early jawless fish species that originated over 500 million years ago, 11-deoxycortisol plays a crucial role as the primary and ultimate glucocorticoid hormone with mineralocorticoid properties; 11-deoxycortisol also takes part, by binding to specific corticosteroid receptors, in intestinal osmoregulation in sea lamprey at [[metamorphosis]], during which they develop [[seawater]] tolerance before downstream migration.<ref name="pmid33741310">{{cite journal | vauthors = Barany A, Shaughnessy CA, McCormick SD | title = Corticosteroid control of Na+/K+-ATPase in the intestine of the sea lamprey (Petromyzon marinus) | journal = General and Comparative Endocrinology | volume = 307 | issue = | pages = 113756 | date = March 2021 | pmid = 33741310 | doi = 10.1016/j.ygcen.2021.113756| s2cid = 232296805 }}</ref> Sea lampreys do not possess the [[11β-hydroxylase]] enzyme ([[CYP11B1]]) responsible for converting 11-deoxycortisol to cortisol and [[11-deoxycorticosterone]] to [[corticosterone]], as observed in mammals. The absence of this enzyme in sea lampreys indicates the existence of a complex and highly specific corticosteroid signaling pathway that emerged at least 500 million years ago with the advent of early vertebrates. The lack of cortisol and corticosterone in sea lampreys suggests that the presence of the 11β-hydroxylase enzyme may have been absent during the early stages of vertebrate evolution.<ref name="pmid32699304">{{cite journal | vauthors = Shaughnessy CA, Barany A, McCormick SD | title = 11-Deoxycortisol controls hydromineral balance in the most basal osmoregulating vertebrate, sea lamprey (Petromyzon marinus) | journal = Scientific Reports | volume = 10 | issue = 1 | pages = 12148 | date = July 2020 | pmid = 32699304 | pmc = 7376053 | doi = 10.1038/s41598-020-69061-4 | bibcode = 2020NatSR..1012148S | url = }}</ref> The absence of cortisol and corticosterone in sea lampreys suggests that the [[11β-hydroxylase]] enzyme may not have been present early in vertebrate evolution.<ref name="pmid20643930">{{cite journal | vauthors = Close DA, Yun SS, McCormick SD, Wildbill AJ, Li W | title = 11-deoxycortisol is a corticosteroid hormone in the lamprey | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 107 | issue = 31 | pages = 13942–7 | date = August 2010 | pmid = 20643930 | pmc = 2922276 | doi = 10.1073/pnas.0914026107| bibcode = 2010PNAS..10713942C | doi-access = free }}</ref>{{clear|left}}

==Clinical significance==
11-Deoxycortisol in mammals has limited glucocorticoid activity, but it is the direct precursor of the major mammalian glucocorticoid, cortisol.<ref name="pmid18215163">{{cite journal | vauthors = Zöllner A, Kagawa N, Waterman MR, Nonaka Y, Takio K, Shiro Y, Hannemann F, Bernhardt R | title = Purification and functional characterization of human 11beta hydroxylase expressed in Escherichia coli | journal = The FEBS Journal | volume = 275 | issue = 4 | pages = 799–810 | date = February 2008 | pmid = 18215163 | doi = 10.1111/j.1742-4658.2008.06253.x | s2cid = 45997341 | doi-access =  }}</ref> As a result, the level of 11-deoxycortisol is measured to diagnose impaired cortisol synthesis, to find out the enzyme deficiency that causes impairment along the pathway to cortisol, and to differentiate adrenal disorders.<ref>{{cite web |url=https://www.healio.com/news/endocrinology/20190430/serum-steroid-levels-can-help-differentiate-adrenal-disorders |title=Serum steroid levels can help differentiate adrenal disorders |access-date=3 October 2020 |archive-date=7 November 2020 |archive-url=https://web.archive.org/web/20201107051241/https://www.healio.com/news/endocrinology/20190430/serum-steroid-levels-can-help-differentiate-adrenal-disorders |url-status=live }}</ref>

In [[11β-hydroxylase deficiency]], 11-deoxycortisol and [[11-deoxycorticosterone]] levels increase, and
excess of [[11-deoxycorticosterone]] leads to [[mineralocorticoid]]-based [[hypertension]]<ref name="pmid22145132">{{cite journal | vauthors = Gupta V | title = Mineralocorticoid hypertension | journal = Indian Journal of Endocrinology and Metabolism | volume =  15| issue =  Suppl 4| date = October 2011 | pages = S298-312 | pmid = 22145132 | pmc = 3230101 | doi = 10.4103/2230-8210.86972 | doi-access = free }}</ref> (as opposed to [[21-hydroxylase deficiency]], in which patients have [[hypotension|low blood pressure]] from a lack of [[mineralocorticoid]]s). Low levels of cortisol can affect blood pressure by causing a decrease in sodium retention and volume expansion. This is because cortisol plays a role in regulating the balance of water and [[electrolyte]]s in the body. When cortisol levels are low, there is less sodium reabsorption by the kidneys, leading to increased excretion of sodium through urine. This ultimately reduces blood volume and lowers blood pressure. On the other hand, high levels of cortisol can also affect blood pressure by causing an increase in sodium retention and volume expansion. Cortisol-induced hypertension is accompanied by significant sodium retention, leading to an increase in extracellular fluid volume and exchangeable sodium. This results in an increase in blood volume and subsequently increases blood pressure. The underlying mechanisms for these effects involve various factors such as suppression of the nitric oxide system, alterations in vascular responsiveness to pressor agonists like adrenaline, increased cardiac output or stroke volume due to plasma volume expansion, and potential dysregulation of glucocorticoid receptors or [[11β-hydroxylase]] enzyme activity. It's important to note that these mechanisms may be relevant not only for cortisol-induced hypertension but also for conditions such as [[Cushing's syndrome]] (excess cortisol production), apparent mineralocorticoid excess (related to defects in [[11β-hydroxylase]] enzymes), [[licorice]] abuse ([[glycyrrhetinic acid]] affecting [[glycyrrhetinic acid receptor]]),<ref name="pmid32368967">{{cite journal |vauthors=Li YL, Zhu XM, Liang H, Orvig C, Chen ZF |title=Recent Advances in Asialoglycoprotein Receptor and Glycyrrhetinic Acid Receptor-Mediated and/or pH-Responsive Hepatocellular Carcinoma- Targeted Drug Delivery |journal=Curr Med Chem |volume=28 |issue=8 |pages=1508–1534 |date=2021 |pmid=32368967 |doi=10.2174/0929867327666200505085756}}</ref> chronic renal failure (prolonged half-life of cortisol due to reduced [[11β-hydroxylase]] activity), and even essential hypertension where there may be abnormalities with [[11β-hydroxylase]] activity or glucocorticoid receptor variations.<ref name="pmid9809193">{{cite journal |vauthors=Kelly JJ, Mangos G, Williamson PM, Whitworth JA |title=Cortisol and hypertension |journal=Clin Exp Pharmacol Physiol Suppl |volume=25 |issue= |pages=S51–6 |date=November 1998 |pmid=9809193 |doi=10.1111/j.1440-1681.1998.tb02301.x |s2cid=13428727 |url=}}</ref><ref name="pmid15478032">{{cite journal |vauthors=van Uum SH, Lenders JW, Hermus AR |title=Cortisol, 11beta-hydroxysteroid dehydrogenases, and hypertension |journal=Semin Vasc Med |volume=4 |issue=2 |pages=121–8 |date=May 2004 |pmid=15478032 |doi=10.1055/s-2004-835369 |s2cid=260371999 |url=}}</ref><ref name="pmid9597634">{{cite journal |vauthors=Stewart PM |title=Cortisol, hypertension and obesity: the role of 11 beta-hydroxysteroid dehydrogenase |journal=J R Coll Physicians Lond |volume=32 |issue=2 |pages=154–9 |date=1998 |pmid=9597634 |pmc=9663025 |doi= |url=}}</ref> Low levels of cortisol lead to reduced [[vascular tone]] as cortisol helps maintain normal vascular tone by promoting vasoconstriction. Low levels of cortisol can lead to decreased vasoconstriction, resulting in relaxed blood vessels and lower overall blood pressure. Also, low cortisol levels lead to impaired fluid balance, as cortisol affects fluid balance by influencing sodium and water reabsorption in the kidneys. When cortisol levels are low, sodium absorption may be reduced, leading to increased excretion of sodium in the urine and subsequent lowering of blood volume and blood pressure. Additionally, low levels of cortisol cause a dysregulated renin-angiotensin system, as cortisol interacts with the renin-angiotensin system, which regulates blood pressure through vasoconstriction and fluid balance. Low cortisol levels can disrupt this system, leading to altered angiotensin production, reduced aldosterone secretion, and subsequently lower blood pressure. Conversely, high levels of cortisol lead to increased vascular tone, enhanced sodium retention, and increased sympathetic activity. Stress-induced release of high-level glucocorticoids such as cortisol activates the sympathetic nervous system (SNS). The SNS controls heart rate, cardiac output, and vasomotor tone, causing constriction, and thereby increasing peripheral arterial resistance, resulting in an increase in blood pressure.<ref name="pmid36807213">{{cite journal |vauthors=Lewandowski KC, Tadros-Zins M, Horzelski W, Krekora M, Lewinski A |title=Renin, Aldosterone, and Cortisol in Pregnancy-Induced Hypertension |journal=Exp Clin Endocrinol Diabetes |volume=131 |issue=4 |pages=222–227 |date=April 2023 |pmid=36807213 |pmc=10101736 |doi=10.1055/a-2025-0510 |url=}}</ref> In [[11β-hydroxylase deficiency]], 11-deoxycortisol can also be converted to [[androstenedione]] in a pathway that could explain the increase in androstenedione levels this condition.<ref name="pmid2028480">{{cite journal |vauthors=Auzéby A, Bogdan A, Touitou Y | title = Evidence for a new biologic pathway of androstenedione synthesis from 11-deoxycortisol | journal = Steroids | volume = 56 | issue = 1 | pages = 33–6 |date=January 1991 | pmid = 2028480 | doi = 10.1016/0039-128X(91)90112-9| s2cid = 6261965}}</ref>

In [[21-hydroxylase]] deficiency, 11-deoxycortisol levels are low.<ref>{{cite book |year=2013 |publisher=Springer Science & Business Media|title=Essential Endocrinology: A Primer for Nonspecialists |isbn=978-1-4899-1692-1 |page=263}}</ref>

== History ==
In 1934, [[biochemist]] [[Tadeus Reichstein]], working in [[Switzerland]], began research on extracts from animal [[adrenal glands]] in order to isolate [[Biological activity|physiologically active]] compounds.<ref name="nobel1950">{{cite web |url=https://www.nobelprize.org/prizes/medicine/1950/reichstein/lecture/ |title=Chemistry of the Adrenal Cortex Hormones |access-date=5 October 2020 |archive-date=10 October 2020 |archive-url=https://web.archive.org/web/20201010072404/https://www.nobelprize.org/prizes/medicine/1950/reichstein/lecture/ |url-status=live }}</ref> He was publishing results of his findings along the way. By 1944, he already isolated and elucidated the chemical structure of 29 pure substances.<ref name="pmid22435119">{{cite journal | vauthors = Grzybowski A, Pietrzak K | title = Tadeusz Reichstein (1897-1996): a cofounder of modern steroid treatment in dermatology | journal = Clinics in Dermatology | volume = 30 | issue = 2 | pages = 243–7 | date = 2012 | pmid = 22435119 | doi = 10.1016/j.clindermatol.2011.09.003 | doi-access =  }}</ref> He was assigning names that consisted of the word "Substance" and a letter from the Latin alphabet to the newly found substances. In 1938, he published an article about "Substance R" and "Substance S" describing their chemical structures and properties.<ref name="doi101002"/> The Substance S since about 1955 became known as 11-Deoxycortisol.<ref name="pmid13242571">{{cite journal|url = https://www.jbc.org/content/215/2/713.long|pmid = 13242571|title = Metabolism of 11-deoxycortisol in vitro|journal = The Journal of Biological Chemistry|volume = 215|issue = 2|pages = 713–22|date = 1 August 1955|doi = 10.1016/S0021-9258(18)65996-4|doi-access = free|vauthors = Forchielli E, Rosenkrantz H, Dorfman RI|access-date = 9 November 2020|archive-date = 17 November 2020|archive-url = https://web.archive.org/web/20201117045154/https://www.jbc.org/content/215/2/713.long|url-status = live}}</ref>

In 1949, American research chemist [[Percy Lavon Julian]], in looking for ways to produce [[cortisone]], announced the synthesis of the Compound S, from the cheap and readily available [[pregnenolone]] (synthesized from the soybean oil sterol [[stigmasterol]]).<ref name="Gibbons 1949">{{cite news|date=30 September 1949|title=Science gets synthetic key to rare drug; discovery is made in Chicago|newspaper=[[Chicago Tribune]]|page=1|url=https://pqasb.pqarchiver.com/chicagotribune/access/494372192.html?dids=494372192:494372192&FMT=ABS&FMTS=ABS:AI|archive-url=https://archive.today/20130131211933/http://pqasb.pqarchiver.com/chicagotribune/access/494372192.html?dids=494372192:494372192&FMT=ABS&FMTS=ABS:AI|url-status=dead|archive-date=31 January 2013|quote=Dr. Julian's new method for synthesizing the anti-arthritis compound, cortisone, is less costly than present methods, because it eliminates the need for utilizing osmium tetroxide, a rare and expensive chemical, the Glidden company declared....But whether has Dr. Julian has also synthesized cortisone from soybeans neither he nor the Glidden company would reveal.}}</ref><ref name="CEN 1949">{{cite journal|date=10 October 1949|title=News of the week: New cortisone synthesis|journal=[[Chemical & Engineering News]]|volume=27|issue=41|pages=2936–2942|quote=Quote: A new synthesis of cortisone, eliminating the need for expensive osmium tetroxide, and the synthesis of three other compounds related to cortisone, which may possible be useful in the treatment of arthritis, have been announced by Percy L. Julian, director of research of the soya products division of the Glidden Co., Chicago. No statement was made as to further details of the new synthesis, but it was revealed that soybean products were not involved...all three [other compounds] were made from soybean sterols.|doi=10.1021/cen-v027n041.p2936}}</ref>

On 5 April 1952, [[biochemist]] Durey Peterson and [[microbiologist]] Herbert Murray at [[Upjohn]], published the first report of a breakthrough [[industrial fermentation|fermentation]] process for the microbial 11α-oxygenation of steroids (e.g. [[progesterone]]) in a single step by common [[Mold (fungus)|mold]]s of the order [[Mucorales]].<ref>{{cite journal |author1=Peterson DH|author2=Murray, HC|year=1952 |title=Microbiological oxygenation of steroids at carbon 11 |journal=[[Journal of the American Chemical Society|J Am Chem Soc]] |volume=74 |issue=7 |pages=1871–2 |doi=10.1021/ja01127a531|bibcode=1952JAChS..74.1871P }}</ref>
11α-oxygenation of Compound S produces 11α-hydrocortisone, which can be chemically oxidized to [[cortisone]], or converted by further chemical steps to 11β-hydrocortisone ([[cortisol]]).

==See also==
{{Commons category}}
* [[11-Deoxycorticosterone]]
* [[Cortexolone 17α-propionate]]

==References==
{{Reflist}}
{{Hormones}}
{{Endogenous steroids}}
{{Glucocorticoid receptor modulators}}
{{Mineralocorticoid receptor modulators}}
{{Authority control}}
{{DEFAULTSORT:Deoxycortisol, 11-}}
[[Category:Corticosteroids]]
[[Category:Glucocorticoids]]
[[Category:Metabolic intermediates]]
[[Category:Mineralocorticoids]]
[[Category:Pregnanes]]
[[Category:Steroid hormones]]
[[Category:Steroids]]