|Synonyms||Dihydronandrolone; DHN; 5α-DHN; 5α-Dihydro-19-nortestosterone; 5α-Estran-17β-ol-3-one; 19-nor-5α-androstan-17β-ol-3-one|
|Chemical and physical data|
|Molar mass||276.42 g/mol|
|3D model (JSmol)|
5α-Dihydronandrolone (also known as 5α-DHN, dihydronandrolone, DHN, 5α-dihydro-19-nortestosterone, or 5α-estran-17β-ol-3-one) is a naturally occurring anabolic–androgenic steroid (AAS) and a 5α-reduced derivative of nandrolone (19-nortestosterone). It is a major metabolite of nandrolone and is formed from it by the actions of the enzyme 5α-reductase analogously to the formation of dihydrotestosterone (DHT) from testosterone.
When testosterone is 5α-reduced into DHT, which is a much more potent AAS in comparison, its effects are potentiated on a local level. The tissues in which this occurs (i.e., the tissues that express 5α-reductase) are referred to as "androgenic" tissues and include the skin, hair follicles, and prostate gland, among others. The conversion of testosterone into DHT is an important factor in the etiology of a variety of androgen-dependent conditions, including acne, excessive facial/body hair growth, scalp hair loss, prostate enlargement, and prostate cancer. Unlike the case of testosterone and DHT, 5α-DHN is a much weaker agonist of the androgen receptor (AR) than is nandrolone. For this reason, instead of local potentiation in androgenic tissues, there is a local inactivation when nandrolone is converted into 5α-DHN by 5α-reductase in these tissues. This is thought to be largely or completely responsible for the exceptionally high ratio of anabolic to androgenic effects seen with nandrolone.
The combination of nandrolone with a 5α-reductase inhibitor like finasteride or dutasteride will block the conversion of nandrolone into 5α-DHN and, unlike with testosterone and various other AAS, thereby considerably increase the propensity of nandrolone for producing androgenic side effects.
|rAR = Rat prostate androgen receptor at 4°C. hAR = Intact human MCF-7-cell androgen receptor at 37°C.|
- Kicman AT (June 2008). "Pharmacology of anabolic steroids". British Journal of Pharmacology. 154 (3): 502–21. doi:10.1038/bjp.2008.165. PMC . PMID 18500378.
- John A. Thomas (6 December 2012). Drugs, Athletes, and Physical Performance. Springer Science & Business Media. pp. 29–. ISBN 978-1-4684-5499-4.
- William Llewellyn (2011). Anabolics. Molecular Nutrition Llc. pp. 464–. ISBN 978-0-9828280-1-4.
- Bergink EW, Janssen PS, Turpijn EW, van der Vies J (June 1985). "Comparison of the receptor binding properties of nandrolone and testosterone under in vitro and in vivo conditions". J. Steroid Biochem. 22 (6): 831–6. doi:10.1016/0022-4731(85)90293-6. PMID 4021486.
- Bergink EW, Geelen JA, Turpijn EW (1985). "Metabolism and receptor binding of nandrolone and testosterone under in vitro and in vivo conditions". Acta Endocrinol Suppl (Copenh). 271: 31–7. doi:10.1530/acta.0.109S0031. PMID 3865479.