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Target intelligence / Profile preview
3-alpha-hydroxysteroid dehydrogenase (3α-HSD)
- Target
- 3α-HSD
- Molecular classification
- Enzyme, Aldo-keto reductase (AKR) superfamily, Oxidoreductase (specifically acting on the CH-OH group with NAD+ or NADP+ as acceptor)
01
Overview
3-alpha-hydroxysteroid dehydrogenase is an enzyme of the aldo-keto reductase superfamily that catalyzes the reversible conversion of 3-ketosteroids to 3α-hydroxysteroids, modulating the biological activity of androgens, estrogens, and progestins[1][5][9]. The enzyme exists in multiple isoforms (notably AKR1C1, AKR1C2, AKR1C3, and AKR1C4 in humans), each displaying unique tissue distribution and substrate specificity. By altering the occupancy of steroid hormone receptors, 3α-HSDs are central to hormone-dependent cellular processes, regulation of metabolism, and pathological states such as cancer and endocrine disorders. Structure-function studies highlight a conserved catalytic mechanism and a central role in steroid hormone balance, making this enzyme family a potential target for selective chemical inhibition[1][3][5][9].
- Other names
- 3α-HSDAKR1C1, AKR1C2, AKR1C3, AKR1C4 (human isoforms)3-hydroxysteroid dehydrogenase (sometimes less specific)Androsterone reductase (context-specific)Human chlordecone reductase (type 1 isoform)
02
Mechanism of action
Competitive inhibition of ketosteroid reduction/oxidation active site Alteration of receptor ligand availability (by changing steroid levels, affecting downstream hormone signaling)
03
Biological functions
Steroid hormone metabolism (conversion of 3-ketosteroids to 3α-hydroxysteroids)Regulation of androgen, estrogen, and progesterone receptor occupancyMetabolism of progestins, bile acids, prostaglandins, and xenobioticsInactivation of potent androgens (e.g., conversion of dihydrotestosterone to 3α-androstanediol)Control of intracellular steroid levels ("intracrinology")
04
Disease associations
Cancer (especially hormone-dependent cancers such as prostate and breast cancer)Neuroendocrine and psychiatric conditions (through effects on neurosteroids)Liver diseases (due to high hepatic expression of certain isoforms)Others: disorders of steroid metabolism, metabolic syndrome
05
Safety considerations
Isoform redundancy and tissue specificity: Multiple isoforms with overlapping activities can make selective targeting difficultPotential disruption of endogenous steroid pathways (risk of hormonal imbalance)Limited specificity of currently available inhibitors; off-target effects in steroid metabolism
06
Interacting drugs
Finasteride and dutasteride
1 more in the full profile.
07
Biomarkers
Intracellular ratio of 3-ketosteroids/3α-hydroxysteroidsAKR1C isoform expression profile in tissue (e.g., increased AKR1C2/3 in prostate cancer)Steroid metabolite levels in plasma, urine, or tissue
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