![]() | |
Names | |
---|---|
IUPAC name | |
Systematic IUPAC name
(1R,3aS,3bR,5aS,9aS,9bS,11aS)-1-Acetyl-1-hydroxy-9a,11a-dimethylhexadecahydro-7H-cyclopenta[a]phenanthren-7-one | |
Other names | |
Identifiers | |
3D model (
JSmol)
|
|
ChEMBL | |
ChemSpider | |
PubChem
CID
|
|
CompTox Dashboard (
EPA)
|
|
| |
| |
Properties | |
C21H32O3 | |
Molar mass | 332.484 g·mol−1 |
Except where otherwise noted, data are given for materials in their
standard state (at 25 °C [77 °F], 100 kPa).
|
5α-Pregnan-17α-ol-3,20-dione, also known as 17α-hydroxy-dihydroprogesterone (17‐OH-DHP) is an endogenous steroid, a metabolite of 17α-hydroxyprogesterone.
5α-Pregnan-17α-ol-3,20-dione (17‐OH-DHP) is a progestogen, i.e., it binds to the progesterone receptors. However, 17‐OH-DHP is better studied as a metabolic intermediate than a progestogen per se.
17‐OH-DHP is the first intermediate product within the androgen backdoor pathway [7] in which 17α-hydroxyprogesterone (17‐OHP) is 5α-reduced and finally converted to 5α-dihydrotestosterone (DHT) without testosterone intermediate. The subsequent intermediate products in the pathway are 5α-pregnane-3α,17α-diol-20-one, androsterone and 5α-androstane-3α,17β-diol. [9] [10] The primary feature of the androgen backdoor pathway is that 17α-hydroxyprogesterone (17-OHP) can be 5α-reduced and finally converted to 5α-dihydrotestosterone (DHT) via an alternative route that bypasses the conventional [11] intermediates androstenedione and testosterone. [12] [13]
5α-Pregnan-17α-ol-3,20-dione is produced by 5α-reduction of 17-OHP. The reaction is catalyzed by SRD5A1 [14] and possibly, SRD5A2 enzymes. [7] While the role of the SRD5A1 enzyme in this reaction is well established, it is unclear whether SRD5A2 is also involved. [13] Some authors [2] [14] claim that the reduction of 17-OHP to 17OHDHP by SRD5A1 is not "sufficient" or "efficient", as supported by measurements of rat SRD5A2 activity in a 1971 study. [15] In a later study, conducted in 2017, however, it has been shown that recombinant human SRD5A1 and SRD5A2 can catalyze the reduction of 17-OHP at comparable rates to the reduction of progesterone. [16] Given both isozymes may be expressed in fetal tissues of both sexes, [17] [18] the action of SRD5A2 in this reaction in humans is yet to be established. [7]
![]() | |
Names | |
---|---|
IUPAC name | |
Systematic IUPAC name
(1R,3aS,3bR,5aS,9aS,9bS,11aS)-1-Acetyl-1-hydroxy-9a,11a-dimethylhexadecahydro-7H-cyclopenta[a]phenanthren-7-one | |
Other names | |
Identifiers | |
3D model (
JSmol)
|
|
ChEMBL | |
ChemSpider | |
PubChem
CID
|
|
CompTox Dashboard (
EPA)
|
|
| |
| |
Properties | |
C21H32O3 | |
Molar mass | 332.484 g·mol−1 |
Except where otherwise noted, data are given for materials in their
standard state (at 25 °C [77 °F], 100 kPa).
|
5α-Pregnan-17α-ol-3,20-dione, also known as 17α-hydroxy-dihydroprogesterone (17‐OH-DHP) is an endogenous steroid, a metabolite of 17α-hydroxyprogesterone.
5α-Pregnan-17α-ol-3,20-dione (17‐OH-DHP) is a progestogen, i.e., it binds to the progesterone receptors. However, 17‐OH-DHP is better studied as a metabolic intermediate than a progestogen per se.
17‐OH-DHP is the first intermediate product within the androgen backdoor pathway [7] in which 17α-hydroxyprogesterone (17‐OHP) is 5α-reduced and finally converted to 5α-dihydrotestosterone (DHT) without testosterone intermediate. The subsequent intermediate products in the pathway are 5α-pregnane-3α,17α-diol-20-one, androsterone and 5α-androstane-3α,17β-diol. [9] [10] The primary feature of the androgen backdoor pathway is that 17α-hydroxyprogesterone (17-OHP) can be 5α-reduced and finally converted to 5α-dihydrotestosterone (DHT) via an alternative route that bypasses the conventional [11] intermediates androstenedione and testosterone. [12] [13]
5α-Pregnan-17α-ol-3,20-dione is produced by 5α-reduction of 17-OHP. The reaction is catalyzed by SRD5A1 [14] and possibly, SRD5A2 enzymes. [7] While the role of the SRD5A1 enzyme in this reaction is well established, it is unclear whether SRD5A2 is also involved. [13] Some authors [2] [14] claim that the reduction of 17-OHP to 17OHDHP by SRD5A1 is not "sufficient" or "efficient", as supported by measurements of rat SRD5A2 activity in a 1971 study. [15] In a later study, conducted in 2017, however, it has been shown that recombinant human SRD5A1 and SRD5A2 can catalyze the reduction of 17-OHP at comparable rates to the reduction of progesterone. [16] Given both isozymes may be expressed in fetal tissues of both sexes, [17] [18] the action of SRD5A2 in this reaction in humans is yet to be established. [7]