3.2.1.143: poly(ADP-ribose) glycohydrolase
This is an abbreviated version!
For detailed information about poly(ADP-ribose) glycohydrolase, go to the full flat file.
Word Map on EC 3.2.1.143
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3.2.1.143
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polyadp-ribose
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polyadp-ribosylation
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parp-1
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polymerase-1
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adp-ribosylation
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genotoxic
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parylation
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gallotannins
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analysis
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drug development
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parthanatos
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automodification
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adp-ribosylhydrolase
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pharmacology
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padpr
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olaparib
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molecular biology
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aif
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medicine
- 3.2.1.143
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polyadp-ribose
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polyadp-ribosylation
- parp-1
- polymerase-1
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adp-ribosylation
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genotoxic
-
parylation
- gallotannins
- analysis
- drug development
-
parthanatos
-
automodification
-
adp-ribosylhydrolase
- pharmacology
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padpr
- olaparib
- molecular biology
- aif
- medicine
Reaction
Synonyms
ADP-ribose glycohydrolase, ADP-ribosyl-acceptor hydrolase 3, ADPRHL2, ARH3, DrPARG, FOXG_05947, Genbank AB019366-derived protein GI 6518480, Genbank U78975-derived protein GI 2062407, glycohydrolase, poly(adenosine diphosphoribose), glycohydrolase, poly(adenosine diphosphoribose) (cattle clone 4/5), glycohydrolase, poly(adenosine diphosphoribose) (Rattus norvegicus strain BUF gene Parg), PAR glycohydrolase, PAR glycohydrolase, PARG, PARG1, PARG110, PARG111, PARG59, poly (ADP-ribose) glycohydrolase, poly(adenosine diphosphoribose) glycohydrolase, poly(adenosine diphosphoribose) glycosidase, poly(ADP-ribose) glycohydrolase, poly(ADP-ribose) glycohydrolase (Arabidopsis thaliana gene At2g31860), poly(ADP-ribose) glycohydrolase (Arabidopsis thaliana gene At2g31870), poly(ADP-ribose) glycohydrolase (cattly clone 4/5), poly(ADP-ribose) glycohydrolase 1, poly(ADP-ribose)glycohydrolase, poly(ADP-ribosyl) glycohydrolase, poly-ADP-glycohydrolase
ECTree
3.2.1.143 poly(ADP-ribose) glycohydrolaseAdvanced search results
results (
results (Inhibitors
Inhibitors on EC 3.2.1.143 - poly(ADP-ribose) glycohydrolase
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INHIBITOR 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
IMAGE
(3Z)-5-bromo-1-(2,6-dichlorobenzyl)-3-[4-oxo-3-[2-(1H-tetrazol-5-yl)ethyl]-2-thioxo-1,3-thiazolidin-5-ylidene]-1,3-dihydro-2H-indol-2-one
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specific detergent-insensitive inhibition
(3Z)-5-chloro-1-(2,6-dichlorobenzyl)-3-[4-oxo-3-[2-(1H-tetrazol-5-yl)ethyl]-2-thioxo-1,3-thiazolidin-5-ylidene]-1,3-dihydro-2H-indol-2-one
-
specific detergent-insensitive inhibition
1,2,3,4,6-pentakis-O-galloyl-beta-D-glucoside
-
about 25% inhibition at 10 microM in vitro
1,3,6-tris-O-galloyl-beta-D-glucoside
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about 25% inhibition at 10 microM in vitro
1,3-diethyl-N-(1-methylcyclopropyl)-2,4-dioxo-quinazoline-6-sulfonamide
-
1,3-dimethyl-N-(1-methylcyclopropyl)-2,4-dioxo-quinazoline-6-sulfonamide
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1-(cyclopropylmethyl)-N-(1-methylcyclopropyl)-3-[(1-methylpyrazol-4-yl)methyl]-2,4-dioxo-quinazoline-6-sulfonamide
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1-(cyclopropylmethyl)-N-(1-methylcyclopropyl)-3-[(2-methylthiazol-5-yl)methyl]-2,4-dioxo-quinazoline-6-sulfonamide
-
1-(cyclopropylmethyl)-N-(1-methylcyclopropyl)-3-[(3-methylisoxazol-5-yl)methyl]-2,4-dioxo-quinazoline-6-sulfonamide
-
1-ethyl-N-(1-methylcyclopropyl)-3-[(1-methylpyrazol-4-yl)-methyl]-2,4-dioxo-quinazoline-6-sulfonamide
-
1-ethyl-N-(1-methylcyclopropyl)-3-[(3-methylisoxazol-5-yl)-methyl]-2,4-dioxo-quinazoline-6-sulfonamide
-
1-ethyl-N-(1-methylcyclopropyl)-3-[(5-methyl-1,3,4-thiadiazol-2-yl)methyl]-2,4-dioxo-quinazoline-6-sulfonamide
-
1-methyl-N-(1-methylcyc lopropyl)-2,4-dioxo-3-(3-thienylmethyl)quinazoline-6-sulfonamide
-
1-methyl-N-(1-methylcyclopropyl)-2,4-dioxo-1,2,3,4-tetrahydroquinazoline-6-sulfonamide
-
-
1-methyl-N-(1-methylcyclopropyl)-2,4-dioxo-3-(1H-pyrazol-4-ylmethyl)quinazoline-6-sulfonamide
-
1-methyl-N-(1-methylcyclopropyl)-2,4-dioxo-3-(2-pyridylmethyl)quinazoline-6-sulfonamide
-
1-methyl-N-(1-methylcyclopropyl)-2,4-dioxo-3-(3-pyridylmethyl)quinazoline-6-sulfonamide
-
1-methyl-N-(1-methylcyclopropyl)-2,4-dioxo-3-(4-pyridylmethyl)quinazoline-6-sulfonamide
-
1-methyl-N-(1-methylcyclopropyl)-2,4-dioxo-3-(thiadiazol-4-ylmethyl)quinazoline-6-sulfonamide
-
1-methyl-N-(1-methylcyclopropyl)-2,4-dioxo-3-(thiazol-2-ylmethyl)quinazoline-6-sulfonamide
-
1-methyl-N-(1-methylcyclopropyl)-2,4-dioxo-3-(thiazol-5-ylmethyl)quinazoline-6-sulfonamide
-
1-methyl-N-(1-methylcyclopropyl)-2,4-dioxo-3-phenacyl-quinazoline-6-sulfonamide
-
1-methyl-N-(1-methylcyclopropyl)-2,4-dioxo-3-phenyl-quinazoline-6-sulfonamide
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1-methyl-N-(1-methylcyclopropyl)-2,4-dioxo-3-prop-2-ynyl-quinazoline-6-sulfonamide
-
1-methyl-N-(1-methylcyclopropyl)-2,4-dioxo-3-[2-oxo-2-(4-pyridyl)ethyl]quinazoline-6-sulfonamide
-
1-methyl-N-(1-methylcyclopropyl)-3-(oxazol-4-ylmethyl)-2,4-dioxo-quinazoline-6-sulfonamide
-
1-methyl-N-(1-methylcyclopropyl)-3-(oxetan-3-ylmethyl)-2,4-dioxo-quinazoline-6-sulfonamide
-
1-methyl-N-(1-methylcyclopropyl)-3-[(1-methylpyrazol-3-yl)-methyl]-2,4-dioxo-quinazoline-6-sulfonamide
-
1-methyl-N-(1-methylcyclopropyl)-3-[(1-methylpyrazol-4-yl)-methyl]-2,4-dioxo-quinazoline-6-sulfonamide
-
1-methyl-N-(1-methylcyclopropyl)-3-[(1-methyltetrazol-5-yl)-methyl]-2,4-dioxo-quinazoline-6-sulfonamide
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1-methyl-N-(1-methylcyclopropyl)-3-[(2-methyl-4-phenyl-thiazol-5-yl)methyl]-2,4-dioxo-quinazoline-6-sulfonamide
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1-methyl-N-(1-methylcyclopropyl)-3-[(2-methylpyrazol-3-yl)-methyl]-2,4-dioxo-quinazoline-6-sulfonamide
-
1-methyl-N-(1-methylcyclopropyl)-3-[(2-methylthiazol-4-yl)-methyl]-2,4-dioxo-quinazoline-6-sulfonamide
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1-methyl-N-(1-methylcyclopropyl)-3-[(2-methylthiazol-5-yl)-methyl]-2,4-dioxo-quinazoline-6-sulfonamide
-
1-methyl-N-(1-methylcyclopropyl)-3-[(3-methyl-1,2,4-oxadiazol-5-yl)methyl]-2,4-dioxo-quinazoline-6-sulfonamide
-
1-methyl-N-(1-methylcyclopropyl)-3-[(3-methyl-1H-pyrazol-5-yl)methyl]-2,4-dioxo-quinazoline-6-sulfonamide
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1-methyl-N-(1-methylcyclopropyl)-3-[(3-methylimidazol-4-yl)-methyl]-2,4-dioxo-quinazoline-6-sulfonamide
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1-methyl-N-(1-methylcyclopropyl)-3-[(3-methylisoxazol-5-yl)-methyl]-2,4-dioxo-quinazoline-6-sulfonamide
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1-methyl-N-(1-methylcyclopropyl)-3-[(4-methyl-1,2,4-triazol-3-yl)methyl]-2,4-dioxo-quinazoline-6-sulfonamide
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1-methyl-N-(1-methylcyclopropyl)-3-[(4-methyl-1,2,5-oxadiazol-3-yl)methyl]-2,4-dioxo-quinazoline-6-sulfonamide
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1-methyl-N-(1-methylcyclopropyl)-3-[(4-methylthiadiazol-5-yl)-methyl]-2,4-dioxo-quinazoline-6-sulfonamide
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1-methyl-N-(1-methylcyclopropyl)-3-[(5-methyl-1,3,4-oxadiazol-2-yl)methyl]-2,4-dioxo-quinazoline-6-sulfonamide
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1-methyl-N-(1-methylcyclopropyl)-3-[(5-methyl-1,3,4-thiadiazol-2-yl)methyl]-2,4-dioxo-quinazoline-6-sulfonamide
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1-methyl-N-(1-methylcyclopropyl)-3-[(5-methylisoxazol-3-yl)-methyl]-2,4-dioxo-quinazoline-6-sulfonamide
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1-methyl-N-(1-methylcyclopropyl)-3-[(5-methylisoxazol-4-yl)-methyl]-2,4-dioxo-quinazoline-6-sulfonamide
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1-[(1,3-dimethyl-1H-pyrazol-5-yl)methyl]-N-(1-methylcyclopropyl)-3-[(2-methyl-1,3-thiazol-5-yl)methyl]-2,4-dioxo-1,2,3,4-tetrahydroquinazoline-6-sulfonamide
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1-[(2,4-dimethyl-1,3-thiazol-5-yl)methyl]-N-(1-methylcyclopropyl)-2-oxo-3-(1,2,4-thiadiazol-5-yl)-2,3-dihydro-1H-benzimidazole-5-sulfonamide
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1-[(2,4-dimethylthiazol-5-yl)methyl]-3-methyl-N-(1-methylcyclopropyl)-2,4-dioxo-quinazoline-6-sulfonamide
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1-[(2,4-dimethylthiazol-5-yl)methyl]-N-(1-methylcyclopropyl)-3-[(1-methylpyrazol-4-yl)methyl]-2,4-dioxo-quinazoline-6-sulfonamide
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1-[(2,4-dimethylthiazol-5-yl)methyl]-N-(1-methylcyclopropyl)-3-[(2-methylthiazol-5-yl)methyl]-2,4-dioxo-quinazoline-6-sulfonamide
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1-[(2,5-dimethylpyrazol-3-yl)methyl]-3-methyl-N-(1-methylcyclopropyl)-2,4-dioxo-quinazoline-6-sulfonamide
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1-[(2,5-dimethylpyrazol-3-yl)methyl]-N-(1-methylcyclopropyl)-3-[(1-methylpyrazol-4-yl)methyl]-2,4-dioxo-quinazoline-6-sulfonamide
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1-[(2,5-dimethylpyrazol-3-yl)methyl]-N-(1-methylcyclopropyl)-3-[(2-methylthiazol-5-yl)methyl]-2,4-dioxo-quinazoline-6-sulfonamide
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1-[(2,5-dimethylpyrazol-3-yl)methyl]-N-(1-methylcyclopropyl)-3-[(3-methylisoxazol-5-yl)methyl]-2,4-dioxo-quinazoline-6-sulfonamide
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1-[(2,5-dimethylpyrazol-3-yl)methyl]-N-(1-methylcyclopropyl)-3-[(5-methyl-1,3,4-thiadiazol-2-yl)methyl]-2,4-dioxo-quinazoline-6-sulfonamide
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1-[(2-fluorophenyl)methyl]-3-methyl-N-(1-methylcyclopropyl)-2,4-dioxo-quinazoline-6-sulfonamide
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1-[(2-methoxyphenyl)methyl]-3-methyl-N-(1-methylcyclopropyl)-2,4-dioxo-quinazoline-6-sulfonamide
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1-[(3-fluorophenyl)methyl]-3-methyl-N-(1-methylcyclopropyl)-2,4-dioxo-quinazoline-6-sulfonamide
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1-[(3-methoxyphenyl)methyl]-3-methyl-N-(1-methylcyclopropyl)-2,4-dioxo-quinazoline-6-sulfonamide
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1-[(4-fluorophenyl)methyl]-3-methyl-N-(1-methylcyclopropyl)-2,4-dioxo-quinazoline-6-sulfonamide
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1-[(4-methoxyphenyl)methyl]-3-methyl-N-(1-methylcyclopropyl)-2,4-dioxo-quinazoline-6-sulfonamide
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12-O-tetradecanoyl-phorbol-13-acetate
reduction of nuclear enzyme activity to 30-40% of control, cytosolic activity remains unchanged. Reduction is suppressed by protein kinase C inhibitor H7. Enzyme expression is reduced in presence of 12-O-tetradecanoyl-phorbol-13-acetate
2-N3-adenosine diphosphate (hydroxymethyl)pyrrolidinediol
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50% inhibition at 0.290 mM, native protein and 50% inhibition at 0.148 mM, recombinant catalytic fragment
3,5-dichloro-2-hydroxy-N-(4-(naphthalen-2-yloxy)-3-(trifluoromethyl)phenyl)benzamide
-
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3,5-dichloro-2-hydroxy-N-m-tolylbenzamide
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between 10% and 30% inhibition at 0.5 mM
3,5-dichloro-2-hydroxy-N-o-tolylbenzamide
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between 10% and 30% inhibition at 0.5 mM
3,5-dichloro-2-hydroxy-N-p-tolylbenzamide
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between 10% and 30% inhibition at 0.5 mM
3,5-dichloro-N-(2-chlorophenyl)-2-hydroxybenzamide
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between 10% and 30% inhibition at 0.5 mM
3,5-dichloro-N-(3-chloro-4-(naphthalen-2-yloxy)phenyl)-2-hydroxy-N-methylbenzamide
-
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3,5-dichloro-N-[3-chloro-4-(naphthalen-2-yloxy)cyclohexa-1,5-dien-1-yl]-2-hydroxybenzamide
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3-(1H-imidazol-4-ylmethyl)-1-methyl-N-(1-methylcyclopropyl)-2,4-dioxo-quinazoline-6-sulfonamide
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3-(3-furylmethyl)-1-methyl-N-(1-methylcyclopropyl)-2,4-dioxoquinazoline-6-sulfonamide
-
3-(cyanomethyl)-1-(cyclopropylmethyl)-N-(1-methylcyclopropyl)-2,4-dioxo-quinazoline-6-sulfonamide
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3-(cyanomethyl)-1-methyl-N-(1-methylcyclopropyl)-2,4-dioxoquinazoline-6-sulfonamide
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3-(cyanomethyl)-1-[(2,5-dimethylpyrazol-3-yl)methyl]-N-(1-methylcyclopropyl)-2,4-dioxo-quinazoline-6-sulfonamide
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3-(cyanomethyl)-N-(1-methylcyclopropyl)-2,4-dioxo-1-prop-2-ynyl-quinazoline-6-sulfonamide
-
3-(cyclohexylmethyl)-1-methyl-N-(1-methylcyclopropyl)-2,4-dioxo-quinazoline-6-sulfonamide
-
3-(cyclopropylmethyl)-1-methyl-N-(1-methylcyclopropyl)-2,4-dioxo-quinazoline-6-sulfonamide
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3-(isothiazol-5-ylmethyl)-1-methyl-N-(1-methylcyclopropyl)-2,4-dioxo-quinazoline-6-sulfonamide
-
3-(isoxazol-5-ylmethyl)-1-methyl-N-(1-methylcyclopropyl)-2,4-dioxo-quinazoline-6-sulfonamide
-
3-benzyl-1-methyl-N-(1-methylcyclopropyl)-2,4-dioxo-quinazoline-6-sulfonamide
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3-bromo-5-chloro-N-[5-chloro-2-[(1-chloronaphthalen-2-yl)oxy]phenyl]-2-hydroxybenzamide
-
-
3-bromo-N-[2-[2-bromo-6-methyl-3-(propan-2-yl)phenoxy]-5-chlorophenyl]-5-chloro-2-hydroxybenzamide
-
-
3-ethyl-1-methyl-N-(1-methylcyclopropyl)-2,4-dioxo-quinazoline-6-sulfonamide
-
3-galloyl-D-glucose
-
about 50% inhibition at 1 microM, 65% inhibition at 10 microM, about 85% at 100 microM in vitro, no inhibitory effect in HeLa cell death at 10 microM, induced by methylating agent 1-methyl-3-nitro-1-nitrosoguanidine (100 microM), because cell-permeability is probably hindered
3-methyl-N-(1-methylcyclopropyl)-1-[(2-methylpyrazol-3-yl)-methyl]-2,4-dioxo-quinazoline-6-sulfonamide
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3-methyl-N-(1-methylcyclopropyl)-2,4-dioxo-1-(2-pyridylmethyl)quinazoline-6-sulfonamide
-
3-methyl-N-(1-methylcyclopropyl)-2,4-dioxo-1-(3-pyridylmethyl)quinazoline-6-sulfonamide
-
3-methyl-N-(1-methylcyclopropyl)-2,4-dioxo-1-(4-pyridylmethyl)quinazoline-6-sulfonamide
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3-[(1-ethylpyrazol-4-yl)methyl]-1-methyl-N-(1-methylcyclopropyl)-2,4-dioxo-quinazoline-6-sulfonamide
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3-[(2,4-dimethylthiazol-5-yl)methyl]-1-methyl-N-(1-methylcyclopropyl)-2,4-dioxo-quinazoline-6-sulfonamide
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3-[(2-aminothiazol-5-yl)methyl]-1-methyl-N-(1-methylcyclopropyl)-2,4-dioxo-quinazoline-6-sulfonamide
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3-[(3,5-dimethylisoxazol-4-yl)methyl]-1-methyl-N-(1-methylcyclopropyl)-2,4-dioxo-quinazoline-6-sulfonamide
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3-[(5Z)-5-[1-(2-chlorobenzyl)-2-oxo-1,2-dihydro-3H-indol-3-ylidene]-4-oxo-2-thioxo-1,3-thiazolidin-3-yl]propanoic acid
-
specific detergent-insensitive inhibition
3-[(5Z)-5-[5-bromo-1-(2,6-dichlorobenzyl)-2-oxo-1,2-dihydro-3H-indol-3-ylidene]-4-oxo-2-thioxo-1,3-thiazolidin-3-yl]propanoic acid
-
specific detergent-insensitive inhibition
3-[(5Z)-5-[5-bromo-1-(2-chloro-6-fluorobenzyl)-2-oxo-1,2-dihydro-3H-indol-3-ylidene]-4-oxo-2-thioxo-1,3-thiazolidin-3-yl]propanoic acid
-
specific detergent-insensitive inhibition
3-[(5Z)-5-[5-chloro-1-(2,6-dichlorobenzyl)-2-oxo-1,2-dihydro-3H-indol-3-ylidene]-4-oxo-2-thioxo-1,3-thiazolidin-3-yl]propanoic acid
3-[[1-(cyanomethyl)pyrazol-4-yl]methyl]-1-methyl-N-(1-methylcyclopropyl)-2,4-dioxo-quinazoline-6-sulfonamide
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8-chlorophenylthioadenosine 5'-diphosphate (hydroxymethyl)pyrrolidinediol
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50% inhibition at 0.12 mM, recombinant catalytic fragment
8-n-octyl-amino-adenosine 5'-diphosphate (hydroxymethyl)pyrrolidinediol
binding structure with mutant enzyme K616A/Q617A/K618A/E688A/K689A/K690A
8-N3-adenosine diphosphate (hydroxymethyl)pyrrolidinediol
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50% inhibition at 390 nM, native protein and 50% inhibition at 0.0014 mM, recombinant catalytic fragment
adenosine 5'-diphosphate (hydroxymethyl)pyrrolidinediol
ADP-HPD, binding structure with mutant enzyme K616A/Q617A/K618A/E688A/K689A/K690A
adenosine 5'-diphosphate-(hydroxymethyl)-pyrrolidinediol
ADP-HPD, an analogue of ADP-ribose
adenosine diphosphate (hydroxymethyl)pyrrolidine
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50% inhibition at 0.019 mM, native protein and 50% inhibition at 0.063 mM, recombinant catalytic fragment
adenosine diphosphate (hydroxymethyl)pyrrolidine-monoalcohol
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50% inhibition at 330nM, native protein and 50% inhibition at 440 nM, recombinant catalytic fragment
Congo red
-
detergent-sensitive inhibition with complete loss of inhibition in the presence of detergent
ethacridine lactate
PARG inhibitor, synergized with ibrutinib in TEX and OCI-AML2 leukemia cell lines. The combination of ibrutinib and ethacridine induces a synergistic increase in reactive oxygen species that is functionally important to explain the observed cell death, synergistic cytotoxicity of ibrutinib and ethacridine. The ibrutinib-ethacridine combination is preferentially cytotoxic to a subset of primary AML cells compared to normal hematopoietic cells
GPI 16552
-
pharmacological inhibitor, treatment of wild-type mice shows a protective effect in dinitrobenzene sulfonic acid-induced colitis
GPI 18214
-
pharmacological inhibitor, treatment of wild-type mice shows a protective effect in dinitrobenzene sulfonic acid-induced colitis
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guanosine 5'-diphosphate (hydroxymethyl)pyrrolidinediol
-
50% inhibition above 1 mM, native protein and 50% inhibition at 0.970 mM,+ recombinant catalytic fragment
methyl 2-O-galloyl-beta-D-glucoside
-
about 25% inhibition at 1 microM, 65% inhibition at 10 microM, about 85% inhibition at 100 microM in vitro
methyl 3-O-galloyl-beta-D-glucoside
-
about 25% inhibition at 1 microM, 65% inhibition at 10 microM, about 85% inhibition at 100 microM in vitro
N'1,N'4-bis[(E)-(2,3,4-trihydroxyphenyl)methylidene]benzene-1,4-dicarbohydrazide
-
N'1,N'4-bis[(E)-(3,4-dihydroxyphenyl)methylidene]benzene-1,4-dicarbohydrazide
-
slight inhibition
N'1-[(E)-(2,3,4-trihydroxyphenyl)methylidene]-N'3-[(Z)-(2,3,4-trihydroxyphenyl)methylidene]benzene-1,3-dicarbohydrazide
-
-
N'1-[(E)-(2,3,4-trihydroxyphenyl)methylidene]-N'4-[(Z)-(2,3,4-trihydroxyphenyl)methylidene]benzene-1,4-dicarbohydrazide
-
-
N'1-[(E)-(2,3-dihydroxyphenyl)methylidene]-N'3-[(Z)-(2,3-dihydroxyphenyl)methylidene]benzene-1,3-dicarbohydrazide
-
-
N'1-[(E)-(2,4,6-trihydroxyphenyl)methylidene]-N'3-[(Z)-(2,4,6-trihydroxyphenyl)methylidene]benzene-1,3-dicarbohydrazide
-
-
N'1-[(E)-(2,4,6-trihydroxyphenyl)methylidene]-N'4-[(Z)-(2,4,6-trihydroxyphenyl)methylidene]benzene-1,4-dicarbohydrazide
-
-
N'1-[(E)-(2,4-dihydroxyphenyl)methylidene]-N'3-[(Z)-(2,4-dihydroxyphenyl)methylidene]benzene-1,3-dicarbohydrazide
-
-
N'1-[(E)-(3,4,5-trihydroxyphenyl)methylidene]-N'3-[(Z)-(3,4,5-trihydroxyphenyl)methylidene]benzene-1,3-dicarbohydrazide
-
-
N'1-[(E)-(3,4,5-trihydroxyphenyl)methylidene]-N'4-[(Z)-(3,4,5-trihydroxyphenyl)methylidene]benzene-1,4-dicarbohydrazide
-
-
N'1-[(E)-(3,4-dihydroxyphenyl)methylidene]-N'3-[(Z)-(3,4-dihydroxyphenyl)methylidene]benzene-1,3-dicarbohydrazide
-
-
N'1-[(E)-(4,6-dihydroxycyclohexa-1,3-dien-1-yl)methylidene]-N'4-[(E)-(2,4-dihydroxyphenyl)methylidene]benzene-1,4-dicarbohydrazide
-
slight inhibition
N'1-[(E)-(5,6-dihydroxycyclohexa-1,3-dien-1-yl)methylidene]-N'4-[(E)-(2,3-dihydroxyphenyl)methylidene]benzene-1,4-dicarbohydrazide
-
slight inhibition
N-(1-cyanocyclopropyl)-1,3-dimethyl-2,4-dioxo-quinazoline-6-sulfonamide
-
N-(1-methylcyclopropyl)-3-[(1-methylpyrazol-4-yl)methyl]-1-(oxetan-3-ylmethyl)-2,4-dioxo-quinazoline-6-sulfonamide
-
N-(1-methylcyclopropyl)-3-[(1-methylpyrazol-4-yl)methyl]-2,4-dioxo-1-prop-2-ynyl-quinazoline-6-sulfonamide
-
N-(1-methylcyclopropyl)-3-[(2-methylthiazol-5-yl)methyl]-2,4-dioxo-1-prop-2-ynyl-quinazoline-6-sulfonamide
-
N-(1-methylcyclopropyl)-3-[(3-methylisoxazol-5-yl)methyl]-1-(oxetan-3-ylmethyl)-2,4-dioxo-quinazoline-6-sulfonamide
-
N-(1-methylcyclopropyl)-3-[(3-methylisoxazol-5-yl)methyl]-2,4-dioxo-1-prop-2-ynyl-quinazoline-6-sulfonamide
-
N-bis-(3-phenyl-propyl)9-oxo-fluorene-2,7-diamide
-
i.e. GPI 16552, pharmacological inhibitor. Enzyme inhibition results in significant reduction of spinal cord inflammation and tissue injury, neutrophil infiltration, cytokine production, and apoptosis upon spinal cord injury. Additionally, inhibition significantly ameliorates the recovery of limb function
N-cyclopropyl-1,3-dimethyl-2,4-dioxo-1,2,3,4-tetrahydroquinazoline-6-sulfonamide
-
N-ethyl-1,3-dimethyl-2,4-dioxo-1,2,3,4-tetrahydroquinazoline-6-sulfonamide
-
N-[4-[(3-bromonaphthalen-2-yl)oxy]-3-chlorophenyl]-3,5-dichloro-2-hydroxybenzamide
-
-
N6-benzyladenosine 5'-diphosphate (hydroxymethyl)pyrrolidinediol
-
50% inhibition above 1 mM, recombinant catalytic fragment
N6-hexyladenosine 5'-diphosphate (hydroxymethyl)pyrrolidinediol
-
50% inhibition at 0.51 mM, recombinant catalytic fragment
nobotanin B
-
inhibition of enzyme activity. In presence of inhibitor, reduction of cell death after exposure to hydrogen peroxide, N-methyl-D-aspartate, or N-methyl-NÂ’-nitro-N-nitrosoguanidine
nuclear matrix proteins
-
due to non-covalent interactions of the protein with free ADP-ribose polymers
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phosphorodiamidate morpholino oligonucleotide
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antisense phosphorodiamidate morpholino oligonucleotide blocks exon 1 of the full length nuclear PARG 111 kDa isoform, slowing down the rate of nuclear poly(ADP-ribose) degradation, attenuating poly(ADP-ribose) polymerase-1 mediated cell death, reducing PARG expression as shown by immunostaining, upon incubation with 50 microM alcylating agent N-methyl-N'-nitro-N'-nitrosoguanidine to induce cell death blocking of nuclear PARG reduced cell condensation and cell death, no inhibitory influence on cytosol PARG
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poly(etheno ADP-ribose)
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inhibits hydrolysis of ribose-ribose bonds by the enzyme, highly resistant to digestion by the enzyme
Poly(G)
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inhibitory effect is eliminated when 250 mM KCl is present in the reaction mixture
RBPI-3
a rhodanine-containing mammalian PARG inhibitor, enzyme-inhibitor structure analysis, overview. RBPI-3 binds predominantly via a pi-pi stacking interaction with Tyr296 and the conserved Phe398. To accommodate the binding of RBPI-3, Phe398 moves into the adenosine binding pocket. The RBPI-3 carboxyl moiety occupies a region corresponding to the ADP-ribose alpha-phosphate group and H-bonds to main chain atoms of Lys365 and Gln254. The RBPI-3 di-chlorobenzyl moiety extends into the solvent and is disordered
siRNA
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small interfering RNA, down regulation of PARG to 50% 24 h after siRNA transfection, maximum of 84% inhibition after 72 compared to negative control with ineffective scrambled siRNA, siRNA produced in vitro from cDNA with 21-nucleotide sequence target in human coding region of the enzyme
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Tannic acid
continous decrease in activity of nuclear enzyme activity, reduction in enzyme expression
tannin
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0.01 mg/ml, 89% inhibition, competitive with respect to poly(ADP-ribose)
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3-[(5Z)-5-[5-chloro-1-(2,6-dichlorobenzyl)-2-oxo-1,2-dihydro-3H-indol-3-ylidene]-4-oxo-2-thioxo-1,3-thiazolidin-3-yl]propanoic acid
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specific detergent-insensitive inhibition
3-[(5Z)-5-[5-chloro-1-(2,6-dichlorobenzyl)-2-oxo-1,2-dihydro-3H-indol-3-ylidene]-4-oxo-2-thioxo-1,3-thiazolidin-3-yl]propanoic acid
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adenosine diphosphate (hydroxymethyl) pyrrolidinediol
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39% inhibition at 0.025 mM
adenosine diphosphate (hydroxymethyl) pyrrolidinediol
ADP-HPD, tight binding inhibitor, binding structure, overview
adenosine diphosphate (hydroxymethyl)pyrrolidinediol
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partial noncompetitive inhibition
adenosine diphosphate (hydroxymethyl)pyrrolidinediol
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i.e. APD-HPD, 50% inhibition at 0.0031 mM, native protein and 50% inhibition at 0.0042 mM, recombinant catalytic fragment
ADP-HPD
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about 40% inhibition at 1 microM, about 70% inhibition at 10 microM, about 85% inhibition at 100 microM in vitro
ADP-ribose
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inhibits poly(ADP-ribose) glycohydrolase II more strongly than poly(ADP-ribose) glycohydrolase I
ADP-ribose
binding structure with mutant enzyme K616A/Q617A/K618A/E688A/K689A/K690A
cAMP
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inhibits poly(ADP-ribose) glycohydrolase II more strongly than poly(ADP-ribose) glycohydrolase I
gallotannin
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25% inhibition at 10 micorM in vitro, reduced cell death in HeLa cells at 3 and 6 h exposure
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gallotannin
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inhibition of enzyme activity. In presence of inhibitor, reduction of cell death after exposure to hydrogen peroxide, N-methyl-D-aspartate, or N-methyl-NÂ’-nitro-N-nitrosoguanidine
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histone
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due to noncovalent interactions of the protein with free ADP-ribose polymers
N-tert-butyl-9,10-dioxo-9,10-dihydroanthracene-2-sulfonamide
PDD00013907, inhibition of enzyme PARG with the small molecule leads to poly(ADP-ribose) (PAR) chain persistence in intact cells, overview. It shows cellular activity and cytotoxicity in HeLa cells
Poly(A)
-
inhibitory effect is eliminated when 250 mM KCl is present in the reaction mixture, inhibition is markedly diminished after hybridization with polyT
poly(I)
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inhibitory effect is eliminated when 250 mM KCl is present in the reaction mixture, inhibition is markedly diminished after hybridization with polyC
additional information
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gallotannin is a complex mixture of hydrolysable tannins, gallic acid and various galloyl glucose derivatives with up to 12 galloyl residues, from oak gall, that inhibits PARG; no inhibitory effect of 100 microM gallic acid, of 10 microM methyl gallate, of 10 microM 2,3-digalloyl-D-glucose, of 10 microM 2,3-digalloyl-O-methyl-D-glucose, of 10 microM 2,3-hexahydroxydiphenoyl-D-glucose, of 10 microM 2,3-di(3-galloyl,4,5-dihydroxy-benzoyl)-D-glucose, of 10 microM epigallocatechin gallate, and of 10 and 100 microM 3-galloyl-1,2-O-isopropylidene-alpha-D-glucose in vitro, the latter can act in vivo as cell-permeable precursor of 3-D-galloyl-D-glucose preventing poly(ADP-ribose) degradation, reduced cell death in HeLa cells at 3 and 6 h exposure (10 or 100 microM), cell death induction by methylating agent 1-methyl-3-nitro-1-nitrosoguanidine (100 microM), increased intracellular NAD content without 1-methyl-3-nitro-1-nitrosoguanidine, no effect in the presence of this agent
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additional information
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inhibition of PARG in HeLa cells treated with 50 microM cell death inducing alkylating agent N-methyl-N'-nitro-N'-nitrosoguanidine leads (MNNG) increases poly(ADP-ribose) levels beyond control, untreated and MNNG-treated PARG-silenced cells show a tendency to larger amounts of long (more than 20 ADP-ribose units) polymers, and a slight increase in short and medium long polymers, however PARG-silencing has no effect on cell death, no effect on translocation of apoptosis-inducing factor (AIF) into nucleus
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additional information
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not inhibited by benzamide, 3,5-dichloro-N-(3-chloro-4-(naphthalen-2-yloxy)phenyl)benzamide, 3,5-dichloro-N-(3-chloro-4-(naphthalen-2-yloxy)phenyl)-2-methoxybenzamide, 2,4-dichloro-6-((3-chloro-4-(naphthalen-2-yloxy)phenylimino)methyl)phenol, 2,4-dichloro-6-((3-chloro-4-(naphthalen-2-yloxy)phenylamino)methyl)phenol, 3,5-dichloro-2-hydroxybenzamide, 3,5-dichloro-N-(3-chloro-4-hydroxyphenyl)-2-hydroxybenzamide, and 3,5-dichloro-2-hydroxy-N-benzamide
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additional information
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small molecule inhibitor screening, detection of rhodamine-based enzyme inhibitors (RBPIs), 3-[(5Z)-5-[1-(2-fluorobenzyl)-2-oxo-1,2-dihydro-3H-indol-3-ylidene]-4-oxo-2-thioxo-1,3-thiazolidin-3-yl]propanoic acid and (3Z)-1-(2-fluorobenzyl)-3-[4-oxo-3-[2-(1H-tetrazol-5-yl)ethyl]-2-thioxo-1,3-thiazolidin-5-ylidene]-1,3-dihydro-2H-indol-2-one are inactive, RBPIs do not inhibit beta-lactamase, ADP-ribosylhydrolase 3, or poly(ADP-ribose) polymerase 1. No inhibiiton by DMO
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additional information
structure-activity relationship analysis of the enzyme inhibitors by isothermal titration calorimetry and surface plasmon resonance, molecular modelling, overview
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additional information
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structure-activity relationship analysis of the enzyme inhibitors by isothermal titration calorimetry and surface plasmon resonance, molecular modelling, overview
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additional information
first-in-class chemical probes against poly(ADP-ribose) glycohydrolase (PARG) inhibit DNA repair with differential pharmacology to poly(ADP-ribose) polymerase (PARP) inhibitor olaparib. No inhibition of PARG by 1-[(1,3-dimethyl-1H-pyrazol-5-yl)methyl]-N-methyl-N-(1-methylcyclopropyl)-3-[(2-methyl-1,3-thiazol-5-yl)methyl]-2,4-dioxo-1,2,3,4-tetrahydroquinazoline-6-sulfonamide and 1-[(2,4-dimethyl-1,3-thiazol-5-yl)methyl]-N-methyl-N-(1-methylcyclopropyl)-2-oxo-3-(1,2,4-thiadiazol-5-yl)-2,3-dihydro-1H-benzimidazole-5-sulfonamide. Cytotoxicity measurements of inhibitors with different cell lines
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additional information
development of a high-throughput homogeneous time-resolved fluorescence (HTRF) assay method allows high-throughput screening for the identification and advancement of multiple validated series of tool compounds for PARG inhibition
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additional information
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development of a high-throughput homogeneous time-resolved fluorescence (HTRF) assay method allows high-throughput screening for the identification and advancement of multiple validated series of tool compounds for PARG inhibition
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additional information
specific killing of DNA damage-response deficient cells with inhibitors of poly(ADP-ribose) glycohydrolase. Single treatment therapy with PARG inhibitors can be used for treatment of certain homologous recombination-deficient tumours and provide insight into the relationship between poly(ADP-ribose) polymerase (PARP), PARG and the processes of DNA repair
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additional information
discovery and optimization of orally bioavailable quinazolinedione sulfonamides as cell-active small molecule inhibitors of DNA-damage repair enzyme poly(ADP-ribose) glycohydrolase (PARG), structure-based virtual screening and library design, overview. Physicochemical properties of 8a and 12b. Structure-activity relationships, cytotoxicity in HeLa cells, selectivity, and EC50 values, overview
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additional information
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discovery and optimization of orally bioavailable quinazolinedione sulfonamides as cell-active small molecule inhibitors of DNA-damage repair enzyme poly(ADP-ribose) glycohydrolase (PARG), structure-based virtual screening and library design, overview. Physicochemical properties of 8a and 12b. Structure-activity relationships, cytotoxicity in HeLa cells, selectivity, and EC50 values, overview
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additional information
ibrutinib synergizes with poly(ADP-ribose) glycohydrolase inhibitors to induce cell death in AML cells via a Bruton's tyrosine kinase (BTK)-independent mechanism, synergistic cytotoxicity of ibrutinib and ethacridine. The ibrutinib-ethacridine combination is preferentially cytotoxic to a subset of primary AML cells compared to normal hematopoietic cells. The inhibitory effect of ibrutinib against BTK, as knockdown of BTK does not sensitize TEX and OCI-AML2 cells to ethacridine treatment
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additional information
the N-terminal regulatory fragment can activate in trans the inactive enzyme fragment depleted with this segment. This suggests that, whereas the enzyme activity can be inhibited by disrupting the docking of this segment to its enzyme binding groove (via posttranslational modification or protein-proteins interactions), the enzyme can be reversibly activated once the disruptive factor is removed
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additional information
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the N-terminal regulatory fragment can activate in trans the inactive enzyme fragment depleted with this segment. This suggests that, whereas the enzyme activity can be inhibited by disrupting the docking of this segment to its enzyme binding groove (via posttranslational modification or protein-proteins interactions), the enzyme can be reversibly activated once the disruptive factor is removed
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additional information
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design and synthesis of phenolic hydrazide hydrazones as potent poly(ADP-ribose) glycohydrolase inhibitors, molecular docking analyses, overview
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