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(5Z)-7-[(1R,2R,3R,5S)-3,5-dihydroxy-2-[(1E,3S)-3-hydroxy-5-phenylpent-1-en-1-yl]cyclopentyl]-N-ethylhept-5-enamide
bimatoprost
(5Z)-7-[(1R,4S,5S,6R)-6-[(1E)-oct-1-en-1-yl]-2-azabicyclo[2.2.1]hept-5-yl]hept-5-enoic acid
ONO1370
(5Z)-7-[(1R,4S,5S,6R)-6-[(1E,3S)-3-hydroxyoct-1-en-1-yl]-2-azabicyclo[2.2.1]hept-5-yl]hept-5-enoic acid
ONO1349
(5Z)-7-[(1S,4S,5S,6R)-2-methyl-6-[(1E)-oct-1-en-1-yl]-2-azabicyclo[2.2.1]hept-5-yl]hept-5-enoic acid
ONO1373
(Z)-7-[(1R,4S,5S,6R)-((E)-6-oct-1-enyl)-2-aza-bicyclo[2.2.1]hept-5-yl]-hept-5-enoic acid
inhibition of PGH2 9,11-endoperoxide reductase activity, slight inhibition of prostamide D2 11-ketoreductase and PGD2 11-ketoreductase activity
(Z)-7-[(1R,4S,5S,6R)-2-methyl-6-((E)-oct-1-enyl)-2-aza-bicyclo[2.2.1]hept-5-yl]-hept-5-enoic acid
inhibition of PGH2 9,11-endoperoxide reductase activity, slight inhibition of prostamide D2 11-ketoreductase and PGD2 11-ketoreductase activity, competitive, binds to the active site
(Z)-7-[(1R,4S,5S,6R)-6-((E)-(S)-3-hydroxy-oct-1-enyl)-2-aza-bicyclo[2.2.1]hept-5-yl]-hept-5-enoic acid
inhibition of PGH2 9,11-endoperoxide reductase activity, slight inhibition of prostamide D2 11-ketoreductase and PGD2 11-ketoreductase activity
1-(4-aminobenzyl)-5-methoxy-2-methylindoleacetic acid
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15-deoxy-DELTA12,14-prostaglandin J2
15d-PGJ2, the enzyme inhibitor attenuates proliferation, inhibits collagen gel contraction and induces activation of the apoptotic marker, caspase-3, in CRL1762 keloid fibroblasts
2-(1-(4-chlorobenzoyl)-5-methoxy-1H-indol-3-yl)-N-((trifluoromethyl)sulfonyl)acetamide
257fold selectivity for isoform AKR1C3 over isoform AKR1C2
3-(1-(4-chlorobenzoyl)-3-ethyl-5-methoxy-1H-indol-2-yl)-propanoic acid
540fold selectivity for isoform AKR1C3 over isoform AKR1C2
3-(1-(4-chlorobenzoyl)-5-methoxy-2-methyl-1H-indol-3-yl)-propanoic acid
257fold selectivity for isoform AKR1C3 over isoform AKR1C2
4-carboxy-2',4'-dinitrodiphenylamine
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4-carboxy-2-aminodiphenylamine
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4-chloro-N-(4-tolyl)-anthranilic acid
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4-chloro-N-phenylanthranilic acid
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4-nitro-N-phenylanthranilic acid
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4-nitrobenzaldehyde
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competitive inhibition of PGD2 but not of PGH2 reduction
5-methyl-N-phenylanthranilic acid
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acetate
occupies the oxyanion hole of the active site, 2 complex structures
AgNO3
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at 0.05 mM 87-100% inhibition, depending on the substrate
CdSO4
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at 5 mM 91-100% inhibition, depending on the substrate
CuSO4
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at 5 mM 93-96% inhibition, depending on the substrate; the liver-type isozyme is 2fold less sensitive than the lung-type isozyme
HgCl2
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at 1 mM 94-100% inhibition, depending on the substrate; IC50 = 0.3 mM, the liver-type isozyme is 2fold less sensitive than the lung-type isozyme
indomethacin methyl ester
specific inhibition of isoform AKR1C3 versus AKR1C1 and AKR1C3
N-(4-chlorobenzoyl)-melatonin
ponalrestat
specific inhibitor developed to block AKR1B1 activity. Application reduces prostaglandin F2alpha production in response to interleukin IL-1beta in both cultured endometrial cells and endometrial explants
rutin
binding structure at the substrate binding site
tert-butyl hydroperoxide
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ZnSO4
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at 5 mM 71-100% inhibition, depending on the substrate
9,10-phenanthrenequinone
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competitive inhibition of PGD2 but not of PGH2 reduction; competitive inhibitor of the reduction of prostaglandin D2, not of prostaglandin H2
9,10-phenanthrenequinone
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9,10-phenanthrenequinone
the prostaglandin D2 11-ketoreductase activity of PGFS is competitively inhibited by 9,10-phenanthrenequinone
9,10-phenanthrenequinone
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9,10-phenanthrenequinone
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competitive inhibition of the PGD2 11-ketoreductase activity, not of PGH2 9-,11-endoperoxide reductase activity
bimatoprost
ethyl amide analogue of 17-phenyl-trinor PGF2alpha, inhibits all enzyme activities noncompetitively at low concentration, binds to a site different from the active site; potent inhibitor
bimatoprost
inhibits the prostaglandin D2 11-ketoreductase activity as well as the prostaglandin H2 9,11-endoperoxide reductase activity of PGFS
Flufenamic acid
nonsteroidal anti-inflammatory drug, binds to both the active site and the beta-hairpin loop at the opposite end of the central beta-barrel, complex structure
flurbiprofen
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Ibuprofen
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indomethacin
nonsteroidal anti-inflammatory drug, 1 molecule binds to the active site, complex structure
indomethacin
specific inhibition of isoform AKR1C3 versus AKR1C1 and AKR1C3
indomethacin
inhibits AKR1C3, but does not inhibit highly related AKR1C1 or AKR1C2
indomethacin
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at 0.005 mg/ml in vivo inhibition of prostaglandin formation
interferon tau
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recombinant ovine interferon tau down-regulates mRNA gene expression of the prostaglandin F synthase at a concentration of 0.000001 mg/ml
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interferon tau
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recombinant bovine interferon tau down-regulates mRNA gene expression of the prostaglandin F synthase after stimulation with oxytocin
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Meclofenamic acid
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methylglyoxal
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N-(4-chlorobenzoyl)-melatonin
specific inhibition of isoform AKR1C3 versus AKR1C1 and AKR1C3, not inhibitory to cyclooxygenases. Uncompetitive versus 9,10-phenynthrenequinone, competitive versus DELTA4-andostene-3,17-dione
N-(4-chlorobenzoyl)-melatonin
exhibits uncompetitive inhibition patterns for the reduction of 9,10-phenanthrenequinone but competitive inhibition patterns for the reduction of androstenedione by AKR1C3
naproxen
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sorbinil
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sorbinil
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significantly inhibits the prostaglandin F2alpha synthase activity of AKR1B3 in a non-competitive fashion, whereas AKR1B7 is not sensitive to the inhibitor
sulindac
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Tolrestat
inhibition of all 3 enzyme activities, most effective inhibiting the PGD2 11-ketoreductase activity
Tolrestat
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significantly inhibits the prostaglandin F2alpha synthase activity of AKR1B3 in a non-competitive fashion, whereas AKR1B7 is not sensitive to the inhibitor
Zomepirac
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additional information
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AKR1C3 is potently inhibited by non-steroidal anti-inflammatory drugs, which are protective against breast cancer
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additional information
AKR1C3 is potently inhibited by non-steroidal anti-inflammatory drugs, which are protective against breast cancer
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additional information
heat treatment of AKR1B1 at 100°C for 5 min completely inactivates the prostaglandin F2alpha synthase activity, which is strictly dependent on the presence of NADPH
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additional information
heat treatment of AKR1B1 at 100°C for 5 min completely inactivates the prostaglandin F2alpha synthase activity, which is strictly dependent on the presence of NADPH
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additional information
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heat treatment of AKR1B1 at 100°C for 5 min completely inactivates the prostaglandin F2alpha synthase activity, which is strictly dependent on the presence of NADPH
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additional information
inhibitors such as alrestatin, ponalrestat, and EBPC exhibit distinct and characteristic inhibition of prostaglandin F2alpha production in different cell models
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additional information
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inhibitors such as alrestatin, ponalrestat, and EBPC exhibit distinct and characteristic inhibition of prostaglandin F2alpha production in different cell models
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additional information
combination of indomethacin with tert-butyl hydroperoxide significantly inhibits the growth of radiation-resistant AKR1C3-over cells
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additional information
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heat treatment of AKR1B3 and AKR1B7 at 100°C for 5 min completely inactivates the prostaglandin F2alpha synthase activities, which is strictly dependent on the presence of NADPH
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additional information
less than 10% inhibition at 0.05 mM: phenolphthalein, hexestrol, medroxyprogesterone acetate, progesterone, testosterone, cortisol, dehydroepiandrosterone
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additional information
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less than 10% inhibition at 0.05 mM: phenolphthalein, hexestrol, medroxyprogesterone acetate, progesterone, testosterone, cortisol, dehydroepiandrosterone
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additional information
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no inhibition by 9,10-phenanthrenequinone
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