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Epipregnanolone

Names
IUPAC name 3β-Hydoxy-5β-pregnan-20-one
Systematic IUPAC name 1-phenanthren-1-yl]ethan-1-one
Other names 3β,5β-Tetrahydroprogesterone
Identifiers
CAS Number	128-21-2
3D model (JSmol)	Interactive image
ChemSpider	198867
PubChem CID	228491
UNII	3KQ00893OL
CompTox Dashboard (EPA)	DTXSID00155766
InChI InChI=1S/C21H34O2/c1-13(22)17-6-7-18-16-5-4-14-12-15(23)8-10-20(14,2)19(16)9-11-21(17,18)3/h14-19,23H,4-12H2,1-3H3/t14-,15+,16+,17-,18+,19+,20+,21-/m1/s1Key: AURFZBICLPNKBZ-GRWISUQFSA-N
SMILES CC(=O)1CC21(CC32CC43(CC(C4)O)C)C
Properties
Chemical formula	C21H34O2
Molar mass	318.501 g·mol
Except where otherwise noted, data are given for materials in their standard state (at 25 °C , 100 kPa). Infobox references

Epipregnanolone, also known as 3β-hydroxy-5β-pregnan-20-one, 3β,5β-tetrahydroprogesterone, or 3β,5β-THP, is an endogenous neurosteroid. It acts as a negative allosteric modulator of the GABA_A receptor and reverses the effects of potentiators like allopregnanolone. Epipregnanolone is biosynthesized from progesterone by the actions of 5β-reductase and 3β-hydroxysteroid dehydrogenase, with 5β-dihydroprogesterone as the intermediate in this two-step transformation.

Epipregnanolone is not a progestogen itself, but via metabolization into other steroids, behaves indirectly as one.

The sulfate of epipreganolone, epipregnanolone sulfate, is a negative allosteric modulator of the NMDA and GABA_A receptors and also acts as a TRPM3 channel activator.

Chemistry

See also

• Isopregnanolone
• 3β-Dihydroprogesterone
• Pregnanolone
• 5α-Dihydroprogesterone
• 3β-Androstanediol

References

1. Neurosteroids and Brain Function. Academic Press. 12 December 2001. pp. 18–. ISBN 978-0-08-054423-6.
2. ^ Abraham Weizman (1 February 2008). Neuroactive Steroids in Brain Function, Behavior and Neuropsychiatric Disorders: Novel Strategies for Research and Treatment. Springer Science & Business Media. pp. 6–. ISBN 978-1-4020-6854-6.
3. Jan Egebjerg; Arne Schousboe; Povl Krogsgaard-Larsen (4 October 2001). Glutamate and GABA Receptors and Transporters: Structure, Function and Pharmacology. CRC Press. pp. 248–. ISBN 978-0-7484-0881-8.
4. Beyer, C.; González-Flores, O.; Ramı́rez-Orduña, J.M.; González-Mariscal, G. (1999). "Indomethacin Inhibits Lordosis Induced by Ring A-Reduced Progestins: Possible Role of 3α-Oxoreduction in Progestin-Facilitated Lordosis". Hormones and Behavior. 35 (1): 1–8. doi:10.1006/hbeh.1998.1457. ISSN 0018-506X. PMID 10049597. S2CID 11520064.
5. Norman G. Bowery (19 June 2006). Allosteric Receptor Modulation in Drug Targeting. CRC Press. pp. 112–. ISBN 978-1-4200-1618-5.
6. Park-Chung M, Malayev A, Purdy RH, Gibbs TT, Farb DH (1999). "Sulfated and unsulfated steroids modulate gamma-aminobutyric acidA receptor function through distinct sites". Brain Res. 830 (1): 72–87. doi:10.1016/s0006-8993(99)01381-5. PMID 10350561. S2CID 44664830.
7. Issues in Pharmacology, Pharmacy, Drug Research, and Drug Innovation: 2011 Edition. ScholarlyEditions. 9 January 2012. pp. 3260–. ISBN 978-1-4649-6342-1.
8. Advances in Glutamic Acid Research and Application: 2013 Edition: ScholarlyBrief. ScholarlyEditions. 21 June 2013. pp. 104–. ISBN 978-1-4816-7049-4.

• 5β-Pregnanes
• GABAA receptor negative allosteric modulators
• Neurosteroids
• Pregnanes