1.1.1.213: 3alpha-hydroxysteroid 3-dehydrogenase (Re-specific)

This is an abbreviated version, for detailed information about 3alpha-hydroxysteroid 3-dehydrogenase (Re-specific), go to the full flat file.

Reaction

a 3alpha-hydroxysteroid
+
NAD(P)+
=
a 3-oxosteroid
+
NAD(P)H
+
H+

Synonyms

17beta-hydroxysteroid dehydrogenase type 5, 3-alpha hydroxysteroid oxidoreductase, 3-alpha-HSO, 3alpha-HSD, 3alpha-HSD type 3, 3alpha-HSD/CR, 3alpha-HSD3, 3alpha-HSOR, 3alpha-hydroxysteroid dehydrogenase, 3alpha-hydroxysteroid dehydrogenase (B-specific), 3alpha-hydroxysteroid dehydrogenase type 2, 3alpha-hydroxysteroid dehydrogenase/carbonyl reductase, 3alpha-hydroxysteroid oxido-reductase, 3alpha-hydroxysteroid oxidoreductase, 3alpha-hydroxysteroid:NAD(P) oxidoreductase, 3alphaHSD, A-specific 3alpha-hydroxysteroid dehydrogenase, AKR1C17, AKR1C2, AKR1C3, AKR1C4, AKR1C9, alpha-HSD/CR, B-specific 3alpha-hydroxysteroid dehydrogenase, bile acid-binding protein, DD2, dihydrodiol dehydrogenase, HSDH, More, NAD+-dependent 3alpha-HSD, NADP(H)-dependent 3alpha-HSD, type 2 3alpha-hydroxysteroid dehydrogenase/type 5 17beta-hydroxysteroid dehydrogenase, type 3 3-alpha-hydroxysteroid dehydrogenase, type 3 3alpha-HSD, type 3 3alpha-hydroxysteroid dehydrogenase, type 5 beta-hydroxysteroid dehydrogenase

ECTree

     1 Oxidoreductases
         1.1 Acting on the CH-OH group of donors
             1.1.1 With NAD+ or NADP+ as acceptor
                1.1.1.213 3alpha-hydroxysteroid 3-dehydrogenase (Re-specific)

Inhibitors

Inhibitors on EC 1.1.1.213 - 3alpha-hydroxysteroid 3-dehydrogenase (Re-specific)

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INHIBITORS
ORGANISM
UNIPROT
COMMENTARY hide
LITERATURE
IMAGE
(2E)-3-(4-bromophenyl)-2-[4-(methylsulfonyl)phenyl]prop-2-enoic acid
-
93.3% inhibition at 0.1 mM
(2E)-3-(4-ethylphenyl)-2-[4-(methylsulfonyl)phenyl]prop-2-enoic acid
-
89.1% inhibition at 0.1 mM
(2E)-3-(4-methylphenyl)-2-[4-(methylsulfonyl)phenyl]prop-2-enoic acid
-
92.7% inhibition at 0.1 mM
(2E)-3-[4-(methylsulfanyl)phenyl]-2-[4-(methylsulfonyl)phenyl]prop-2-enoic acid
-
93.5% inhibition at 0.1 mM
(E/Z)-sulfindac
-
wild-type, W86Y and W227Y
1,10-phenanthroline
-
wild-type, W86Y and W227Y
1,7-phenanthroline
-
wild-type, W86Y and W227Y
1-(4'nitrophenyl)prop-2-en-1-ol
-
inactivation dependent on NAD+ concentration, optimal at 0.5-1.0 mM NAD+, 2-mercaptoethanol prvides a concentration-dependent protection
1-(4'nitrophenyl)prop-2-en-1-one
-
inactivation can be retarded markedly in a concentration-dependent manner by both NADH and NADPH. Competitive inhibitor of NAD+ binding, measured for androsterone oxidation
1-(4'nitrophenyl)prop-2-yn-1-one
-
competitive inhibitor of NAD+ binding, measured for androsterone oxidation
1-(4-[[(2R)-2-methylpiperidin-1-yl]sulfonyl]phenyl)-1,3-dihydro-2H-pyrrol-2-one
-
IC50 value in HCT-116 cells engineered to over-express AKR1C3 is 11 nM
1-(4-[[(2R,6S)-2,6-dimethylpiperidin-1-yl]sulfonyl]phenyl)pyrrolidin-2-one
-
IC50 value in HCT-116 cells engineered to over-express AKR1C3 is 22 nM
1-[4-(3,4-dihydroisoquinolin-2(1H)-ylsulfonyl)phenyl]pyrrolidin-2-one
-
IC50 value in HCT-116 cells engineered to over-express AKR1C3 is 24 nM
17beta-bromoacetoxy-5alpha-dihydrotestosterone
-
inactivation by modification of steroid-binding site
2'-hydroxyflavanone
-
most potent inhibitor, 0.02 mM inhibits by 98.9% and in an uncompetitive manner
2-(2,4-dioxo-1,3-thiazolidin-5-yl)-N-(2-hydroxyphenyl)acetamide
-
inhibitor is about 1000times more selective for isoform AKR1C3 over AKR1C2, and selectivity is even higher when compared with AKR1C1 and AKR1C4
2-[[(3-hydroxyphenyl)carbonyl]amino]-4,5-dimethoxybenzoic acid
-
-
2-[[(3-hydroxyphenyl)carbonyl]amino]-5-nitrobenzoic acid
-
-
21-hydroxypregn-4-ene-3,20-dione
-
-
3-((4-nitronaphthalen-1-yl)amino)benzoic acid
-
inhibitor nanomolar potency and selective inhibition of isoform AKR1C3 but also acts as an androgen receptor antagonist. It inhibits 5alpha-dihydrotestosterone stimulated androgen receptor reporter gene activity with an IC50 value of 4.7 microM and produces a concentration dependent reduction in androgen receptor levels in prostate cancer cells
3-hydroxyflavone
-
-
3-phenoxybenzoic acid
-
inhibitor carboxylic acid binds to the oxyanion site, in which the carboxylate group very closely overlays the acetate molecule found in other AKR1C3 structures and forms hydrogen bonds to the enzyme catalytic residues His117 and Tyr55, as well as to a conserved water network located in and near the SP3 subpocket. The 3-phenoxy ring extends into the SP1 subpocket and makes van der Waals contacts with the aromatic residues Phe306, Phe311 and Tyr319 that line the pocket
3-[(4-nitrophenyl)amino]benzoic acid
-
94fold selectivity for the inhibition of isoform AKR1C3 over AKR1C2
3-[[4-(methoxymethyl)phenyl]amino]benzoic acid
-
360fold selectivity for the inhibition of isoform AKR1C3 over AKR1C2
3-[[4-(trifluoromethyl)phenyl]amino]benzoic acid
3a-phenyl-2,3,3a,4-tetrahydro-1H-pyrrolo[1,2-a]benzimidazol-1-one
-
inhibitor shows 17fold and 30fold selectivity against isoforms AKR1C2 and AKR1C1, respectively, and much higher selectivity against AKR1C4
4'-hydroxyflavanone
-
-
4-androstene-3,17-dione
-
versus substrate, the products, 4-androstene-3,17-dione and NADH, inhibit the activity uncompetitively and competitively, respectively, with respect to NAD+ in the presence of a saturated concentration of 0.004 mM of the substrate
5-bromo-2-[[(3-hydroxyphenyl)carbonyl]amino]benzoic acid
-
-
5-chloro-2-[[(3-hydroxyphenyl)carbonyl]amino]benzoic acid
-
-
5-hydroxyflavone
-
-
5beta-Pregnan-3beta-ol-20-one
-
-
6alpha-Methylprednisolone
-
-
7-hydroxyflavone
-
very potent inhibitor, 0.02 mM inhibits by 82.5%
9-(phenylcarbonyl)-2,3,6,7-tetrahydro-1H,5H,11H-pyrano[2,3-f]pyrido[3,2,1-ij]quinolin-11-one
-
competitive
acetaminophen
-
non-competitive, only androsterone oxidation, pH 7.0
acetylenic ketones
-
inactivation by forming Michael adducts with enzyme nucleophiles
-
apigenin
-
0.02 mM inhibits by ca. 50%
arachidonic acid
-
-
aspirin
-
salicylate, non-competitive, only androsterone oxidation, pH 7.0
Betamethasone
-
non-competitive
cacodylate
-
-
celecoxib
-
synthetic, nonsteroidal anti-inflammatory inhibitor, in vivo IC50: 0.050 mM in fluorometric assay, in vitro IC50: 0.050 mM in fluorometric assay
chlorogenic acid
-
-
Cibacron blue
-
nucleotide analog, competitive with respect to NADP+, noncompetitive to androsterone
cortisol
-
competitive
cortisone
-
competitive
Cu2+
-
100% inhibition at 0.1 mM
D-glucose 6-phosphate
-
-
dexamethasone
DMSO
-
33% inhibition
epigallocatechin gallate
-
-
Flufenamic acid
Hexestrol
Ibuprofen
indomethacin
iodoacetate
-
50% inhibition at 0.1 mM
isovitexin
-
-
Ketamine
-
specific inhibitor for AKR1C17, but no inhibition of AKR1C9
luteolin
-
0.02 mM inhibits by ca. 50%
Meclofenamic acid
Medroxyprogesterone acetate
-
-
Mefenamic acid
-
wild-type, W86Y and W227Y
NADH
-
the products, 4-androstene-3,17-dione and NADH, inhibit the activity uncompetitively and competitively, respectively, with respect to NAD+ in the presence of a saturated concentration of 0.004 mM of the substrate
naphthalene-1,2-dione
-
naphthalene-1,2-dione leads to the time and concentration dependent irreversible inactivation of AKR1C9 via alkylation
naproxen
-
synthetic, nonsteroidal anti-inflammatory inhibitor, in vivo IC50: 0.0094 mM in fluorometric assay, 0.016 mM in radiometric assay, in vitro IC50: 0.0027 mM in fluorometric assay
naringenin
-
very potent inhibitor, 0.02 mM inhibits by 71.9%
non-steroidal anti-inflamatory drug
-
Oxyphenybutazone
-
competitive
p-chloromercuribenzenesulfonate
-
-
p-chloromercuribenzoate
Phenolphthalein
-
AKR1C4-selective inhibitor, in vitro and in vivo inhibition, IC50: 0.0004 mM
ponalrestat
-
wild-type, W86Y and W227Y, weak inhibitor
Prednisolone
-
competitive
Prednisone
-
competitive
progesterone
-
competitive to testosterone
Prostaglandin
prostaglandin A1
-
-
prostaglandin A2alpha
-
-
Prostaglandin B1
-
-
prostaglandin E1
-
-
prostaglandin F1alpha
-
-
pyrazole
-
10% at 0.4 mM
quercetin
-
0.02 mM inhibits by ca. 50%
salicylate
-
non-competitive
silibinin
-
0.02 mM inhibits by ca. 50%
stilboestrol
-
-
testosterone
Tolmetin
-
competitive, only androsterone oxidation, pH 7.0
ursodeoxycholate
-
natural inhibitor, in vivo IC50: 0.00024 mM in fluorometric assay, 0.00014 mM in radiometric assay, in vitro IC50: 0.000049 mM in fluorometric assay
vitexin
-
-
Zomepirac
-
competitive, only androsterone oxidation, pH 7.0
zopolrestat
additional information
-