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13,14-dihydro-15-prostaglandin E2
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competitive product inhibition
15-keto prostaglandin F2alpha
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43.06% residual activity at 0.1 mM
5-(2-chloro-3-((4-methylcyclohexyl)methoxy)benzylidene)-1,3-thiazolidine-2,4-dione
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5-(2-chloro-3-((5-oxo-5,6,7,8-tetrahydronaphthalen-1-yl)oxy)benzylidene)-1,3-thiazolidine-2,4-dione
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5-(2-chloro-3-(1-cyclopropylethoxy)benzylidene)-1,3- thiazolidine-2,4-dione
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5-(2-chloro-3-(2-(4-methyl-1,3-thiazolidin-5-yl)ethoxy)benzylidene)-1,3-thiazolidine-2,4-dione
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5-(2-chloro-3-(2-(cyclohexyloxy)ethoxy)benzylidene)-1,3-thiazolidine-2,4-dione
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5-(2-chloro-3-(2-(propan-2-yloxy)ethoxy)benzylidene)-1,3-thiazolidine-2,4-dione
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5-(2-chloro-3-(2-(pyridin-2-yl)ethoxy)benzylidene)-1,3-thiazolidine-2,4-dione
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5-(2-chloro-3-(2-cyclohexylethoxy)benzylidene)thiazolidine-2,4-dione
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5-(2-chloro-3-(2-cyclopentylethoxy)benzylidene)-1,3-thiazolidine-2,4-dione
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5-(2-chloro-3-(3-cyclohexylpropoxy)benzylidene)thiazolidine-2,4-dione
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5-(2-chloro-3-(3-nitrophenoxy)benzylidene)-1,3-thiazolidine-2,4-dione
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5-(2-chloro-3-(3-phenylpropoxy)benzylidene)thiazolidine-2,4-dione
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the compound significantly increases the level of PGE2 in skin defects
5-(2-chloro-3-(4-cyclohexylbutoxy)benzylidene)thiazolidine-2,4-dione
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5-(2-chloro-3-(4-nitrobenzyloxy)benzylidene)thiazolidine-2,4-dione
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5-(2-chloro-3-(4-phenylbutoxy)benzylidene)thiazolidine-2,4-dione
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5-(2-chloro-3-(cyclobutylmethoxy)benzylidene)-1,3-thiazolidine-2,4-dione
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5-(2-chloro-3-(cyclohexylmethoxy)benzylidene)thiazolidine-2,4-dione
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5-(2-chloro-3-(cyclohexyloxy)benzylidene)thiazolidine-2,4-dione
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5-(2-chloro-3-(cyclopentylmethoxy)benzylidene)-1,3-thiazolidine-2,4-dione
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5-(2-chloro-3-(cyclopentyloxy)benzylidene)-1,3-thiazolidine-2,4-dione
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5-(2-chloro-3-phenethoxybenzylidene)thiazolidine-2,4-dione
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5-(3-(benzyloxy)-2-chlorobenzylidene)thiazolidine-2,4-dione
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5-(3-(bicyclo[2.2.1]hept-2-ylmethoxy)-2-chlorobenzylidene)-1,3-thiazolidine-2,4-dione
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benzylidene acetophenone
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21.09% residual activity at 0.5 mM
Disulfiram
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0.1 mM, 61% inhibition, cofactor NADPH, substrate 15-ketoprostaglandin E2
NADH
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uncompetitive inhibition at high concentrations
Cibacron blue 3 G-A
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competitive inhibition vs. NADH, noncompetitive vs. 15-keto-prostaglandin E2
dicoumarol
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0.1 mM, 86% inhibition, cofactor NADPH, substrate 15-ketoprostaglandin E2
dicoumarol
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0.1 mM, complete inhibition
dicoumarol
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11.45% residual activity at 0.1 mM
indomethacin
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0.1 mM, 97% inhibition, cofactor NADPH, substrate 15-ketoprostaglandin E2
indomethacin
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0.1 mM, 95% inhibition
indomethacin
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14.22% residual activity at 0.1 mM
NADPH
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competitive inhibition vs. NADH, noncompetitive vs. 15-keto-prostaglandin E2
p-chloromercuribenzoate
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p-chloromercuribenzoate
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0.1 mM, complete inhibition
p-chloromercuribenzoate
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p-chloromercuribenzoate
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0.0001 mM, 85% inhibition
p-chloromercuribenzoate
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0.1 mM, 97% inhibition
quercitrin
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0.1 mM, 76% inhibition, cofactor NADPH, substrate 15-ketoprostaglandin E2
quercitrin
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95% inhibition
quercitrin
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13.14% residual activity at 0.1 mM
additional information
evaluation of non-steroidal anti-inflammatory drugs (NSAIDs) as enzyme potential inhibitors
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additional information
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evaluation of non-steroidal anti-inflammatory drugs (NSAIDs) as enzyme potential inhibitors
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additional information
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thiazolidinediones as enzyme inhibitors. No inhibition by 5-(2-chloro-3-(1-cyclopropylethoxy)benzylidene)-1,3-thiazolidine-2,4-dione
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additional information
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finasteride has no inhibitory effect
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