Please wait a moment until all data is loaded. This message will disappear when all data is loaded.
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
(-)-epicatechin
-
serves as prodrug for conversion into apocynin-like NAD(P)H oxidase inhibitors
(-)-epicatechin glucuronide
-
acts both as a superoxide anion scavenger,and inhibitory to NAD(P)H oxidase, with apocynin-like mode of NADPH oxidase inhibition
(-)-epigallocatechin gallate
(-)-epigallocatechin-3-O-(3-O-methyl)-gallate
-
inhibition of intracellular reactive oxygen species generation
(1R)-1-[(2R,2'R,5R,5'R)-5'-[(1R)-1-hydroxyundec-3-yn-1-yl]octahydro-2,2'-bifuran-5-yl]dodec-4-yn-1-ol
-
-
(1R)-1-[(2R,2'R,5R,5'R)-5'-[(1R)-1-hydroxyundecyl]octahydro-2,2'-bifuran-5-yl]dodecan-1-ol
-
-
(1R,1'R)-1,1'-((2R,2'R,5R,5'R)-octahydro-2,2'-bifuran-5,5'-diyl)-bis-(6-(4-n-butylphenoxy)hex-3-yn-1-ol)
-
-
(1R,1'R)-1,1'-((2R,2'R,5R,5'R)-octahydro-2,2'-bifuran-5,5'-diyl)-bis-(6-(4-n-butylphenoxy)hexan-1-ol)
-
-
(2Z)-2-(5-hydroxy-4,6-dimethyl-2-oxo-1,2-dihydro-3H-indol-3-ylidene)-N,N-di(prop-2-en-1-yl)hydrazinecarbothioamide
-
complete inhibition at 0.01 mM
(3Z)-3-(3,4-dihydroxybenzylidene)-5-nitro-1,3-dihydro-2H-indol-2-one
-
complete inhibition at 0.01 mM
(3Z)-3-[4-hydroxy-3,5-di(propan-2-yl)benzylidene]-1,3-dihydro-2H-indol-2-one
-
complete inhibition at 0.01 mM
(5'Z)-5'-[(4-heptyl-5-methyl-1H-pyrrol-2-yl)methylidene]-4'-methoxy-1H,5'H-2,2'-bipyrrole
-
i.e. PG-L-1, prodigosin analogue, a red pigment isolated from marine bacterial strain. Significant inhibition of superoxide anion production by phorbol 12-myristate 13-acetate stimulated RAW 264.7 cells. (5'Z)-5'-[(4-heptyl-5-methyl-1H-pyrrol-2-yl)methylidene]-4'-methoxy-1H,5'H-2,2'-bipyrrole strongly inhibits the association of subunits p47phox and Rac in the plasma membrane
1-(2-chlorobenzyl)-4-methyl-5-[3-(2-oxopyrrolidin-1-yl)propyl]-2-phenyl-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
1-(4-fluorobenzyl)-5-[2-(1H-indol-3-yl)ethyl]-4-methyl-2-phenyl-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
1-acetyl-2-(2-chlorophenyl)-4-methyl-5-(pyridin-3-ylmethyl)-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
1-acetyl-4-methyl-2-(2-methylphenyl)-5-(pyridin-3-ylmethyl)-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
1-acetyl-4-methyl-2-phenyl-5-(pyridin-3-ylmethyl)-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
1-[(3-methoxyphenyl)acetyl]-4-methyl-2-phenyl-5-(pyridin-3-ylmethyl)-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
15-cis-(4-propyl-cyclohexyl)-16,17,18,19,20-pentanor-9-deoxy-9alpha,6-nitrilo-prostaglandin F1 methyl ester
-
0.021 mM, 50% inhibition of the enzyme in neutrophils possible due to scavenging of O2-, inhibition of SDS-induced activation in cell free extracts, 0.22 mM, 50% inhibition
2,3,8,9-tetrahydroxy-5-(2-hydroxy-5-nitrobenzyl)phenanthridin-6(5H)-one
-
complete inhibition at 0.01 mM
2,3,8,9-tetrahydroxy-5-(3-nitrobenzyl)phenanthridin-6(5H)-one
-
complete inhibition at 0.01 mM
2,3,8,9-tetrahydroxy-5-(4-nitrobenzyl)phenanthridin-6(5H)-one
-
93% inhibition at 0.01 mM
2,3,8,9-tetrahydroxy-5-[2-(phenylsulfonyl)benzyl]phenanthridin-6(5H)-one
-
95% inhibition at 0.01 mM
2,4,5-trimethyl-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
2,4-dimethyl-3-methylidene-5-(pyridin-2-ylmethyl)-1,2,3,5-tetrahydro-6H-pyrazolo[4,3-c]pyridin-6-one
-
-
2-(1,3-benzothiazol-2-yl)-1-(2-chlorobenzyl)-4-methyl-5-(morpholin-4-yl)-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
2-(1,3-benzothiazol-2-yl)-4-ethyl-5-(2-methoxyethyl)-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
2-(1,3-benzothiazol-2-yl)-4-methyl-1-(pyridin-2-ylmethyl)-5-(tetrahydrofuran-2-ylmethyl)-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
2-(1,3-benzothiazol-2-yl)-4-methyl-5-(morpholin-4-yl)-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
2-(1,3-benzothiazol-2-yl)-5-[2-(1H-imidazol-4-yl)ethyl]-4-methyl-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
2-(1,3-benzothiazol-2-yl)-5-[2-(1H-indol-3-yl)ethyl]-4-methyl-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
2-(2,5-dichlorobenzyl)-4-methyl-3-methylidene-5-(pyridin-2-ylmethyl)-1,2,3,5-tetrahydro-6H-pyrazolo[4,3-c]pyridin-6-one
-
-
2-(2-chloro-4-fluorobenzyl)-4-methyl-3-methylidene-5-(pyridin-2-ylmethyl)-1,2,3,5-tetrahydro-6H-pyrazolo[4,3-c]pyridin-6-one
-
-
2-(2-chloro-4-fluorophenyl)-4,5-dimethyl-1H-pyrazolo[4,3-c]-pyridine-3,6(2H,5H)-dione
-
-
2-(2-chloro-4-fluorophenyl)-4-methyl-5-(pyridin-2-ylmethyl)-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
2-(2-chloro-4-fluorophenyl)-5-(2-pyridin-2-ylethyl)-4-(pyrrolidin-1-ylmethyl)-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
2-(2-chlorophenyl)-4,5-dimethyl-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
2-(2-chlorophenyl)-4-(2-fluorophenyl)-5-methyl-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
2-(2-chlorophenyl)-4-([methyl(phenyl)amino]methyl)-5-[2-(pyridin-2-yl)ethyl]-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
2-(2-chlorophenyl)-4-methyl-5-(3-phenylprop-2-yn-1-yl)-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
2-(2-chlorophenyl)-4-methyl-5-(4-[(4-methylpiperazin-1-yl)methyl]benzyl)-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
2-(2-chlorophenyl)-4-methyl-5-(pyridin-2-ylmethyl)-1H-pyrazolo-[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
2-(2-chlorophenyl)-4-methyl-5-[(6-morpholin-4-ylpyridin-2-yl)-methyl]-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
2-(2-chlorophenyl)-4-methyl-5-[4-(4-methylpiperazin-1-yl)-4-oxobutyl]-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
2-(2-chlorophenyl)-4-[(4-fluorophenoxy)methyl]-5-methyl-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
2-(2-chlorophenyl)-4-[[4-(3-methoxyphenyl)piperazin-1-yl]-methyl]-5-methyl-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
2-(2-chlorophenyl)-4-[[methyl(phenyl)amino]methyl]-5-(pyridin-4-ylmethyl)-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
2-(2-chlorophenyl)-5-(3-ethoxypropyl)-4-methyl-1-(pyridin-2-ylmethyl)-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
2-(2-chlorophenyl)-5-(3-hydroxypropyl)-4-methyl-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
2-(2-chlorophenyl)-5-(cyclohexylmethyl)-4-methyl-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
2-(2-chlorophenyl)-5-[(1-methyl-1H-pyrazol-3-yl)methyl]-4-[[methyl(pyridin-3-ylmethyl)amino]methyl]-1H-pyrazolo[4,3-c]-pyridine-3,6(2H,5H)-dione
-
-
2-(2-chlorophenyl)-5-[2-(dimethylamino)ethyl]-4-methyl-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
2-(2-fluorophenyl)-4,5-dimethyl-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
2-(2-methoxyethyl)-4-methyl-3-methylidene-5-(pyridin-2-ylmethyl)-1,2,3,5-tetrahydro-6H-pyrazolo[4,3-c]pyridin-6-one
-
-
2-(3,4-dihydroxyphenyl)-3,7-dihydroxy-6-methoxy-4H-chromen-4-one
-
complete inhibition at 0.01 mM
2-(3,4-dihydroxyphenyl)-5,7-dihydroxy-4H-chromen-4-one
-
complete inhibition at 0.01 mM
2-(3,4-dihydroxyphenyl)-5-hydroxy-3,7-dimethoxy-4H-chromen-4-one
-
88% inhibition at 0.01 mM
2-(3-chlorophenyl)-4,5-dimethyl-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
2-(4-chlorobenzyl)-4-methyl-3-methylidene-5-(pyridin-2-ylmethyl)-1,2,3,5-tetrahydro-6H-pyrazolo[4,3-c]pyridin-6-one
-
-
2-(4H-3,1-benzothiazin-2-yl)-1-benzyl-4-methyl-5-(tetrahydrofuran-2-ylmethyl)-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
2-(7-chloroquinolin-4-yl)-4-methyl-3-methylidene-5-(pyridin-2-ylmethyl)-1,2,3,5-tetrahydro-6H-pyrazolo[4,3-c]pyridin-6-one
-
-
2-benzyl-4-methyl-3-methylidene-5-(pyridin-2-ylmethyl)-1,2,3,5-tetrahydro-6H-pyrazolo[4,3-c]pyridin-6-one
-
-
2-bromohexadecanal
-
irreversible
2-hydroxy-5-[(2-hydroxybenzyl)amino]benzoic acid
-
89% inhibition at 0.01 mM
2-iodohexadecanal
-
irreversible
2-iodoicosanal
-
weak inhibition
2-iodooctanal
-
irreversible
2-[(2,3,8,9-tetrahydroxy-6-oxophenanthridin-5(6H)-yl)methyl]benzonitrile
-
97% inhibition at 0.01 mM
2-[(2E)-2-(3,4-dihydroxybenzylidene)hydrazinyl]-N-(3-nitrophenyl)-2-oxoacetamide
-
96% inhibition at 0.01 mM
2-[2-(4-chlorophenoxy)ethyl]-4-methyl-3-methylidene-5-(pyridin-2-ylmethyl)-1,2,3,5-tetrahydro-6H-pyrazolo[4,3-c]pyridin-6-one
-
-
2-[4-(benzyloxy)phenyl]-4,5-dimethyl-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
3'-(or 4'-)methylluteolin
-
-
3'-O-methyl epicatechin
-
-
3,5,7-trihydroxy-2-(4-hydroxy-3-methylphenyl)-4H-chromen-4-one
-
94% inhibition at 0.01 mM
3,5,7-trihydroxy-2-(4-hydroxyphenyl)-4H-chromen-4-one
-
complete inhibition at 0.01 mM
3-(3,4-dihydroxycyclohexa-2,4-dien-1-yl)-2,7-dihydroxy-4H-chromen-4-one
-
86% inhibition at 0.01 mM
3-(3-chlorophenyl)-N-[2-(piperazin-1-yl)phenyl]-1,4,6,7-tetrahydro-5H-pyrazolo[4,3-c]pyridine-5-carboxamide
-
Shionigi compound
3-(3-chlorophenyl)-N-[4-(piperidin-4-yl)phenyl]pyrazolo[1,5-a]pyrimidine-5-carboxamide
-
-
3-(4,5-dimethyl-3,6-dioxo-1,3,5,6-tetrahydro-2H-pyrazolo[4,3-c]pyridin-2-yl)benzonitrile
-
-
4'-O-methyl epicatechin
-
-
4,5-dimethyl-2-(4-phenyl-1,3-thiazol-2-yl)-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
4,5-dimethyl-2-(5-[(4-methylpiperazin-1-yl)sulfonyl]pyridin-2-yl)-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
4-(2-amino-ethyl)-benzolsulphonyl-fluoride
4-(2-aminoethyl)-benzenesulfonyl fluoride
-
-
4-(2-aminoethyl)benzenesulfonyl fluoride
-
significantly reduces reactive oxygen species production, NADPH oxidase activity, and all the apoptotic events, and cell death induced by both 5 mM KCl and staurosporin
4-methyl-2-(2-methylphenyl)-5-(pyridine-2-ylmethyl)-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
4-methyl-2-phenyl-5-(2-phenylethyl)-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
4-methyl-2-phenyl-5-(pyridin-3-ylmethyl)-1H-pyrazolo[4,3-c]-pyridine-3,6(2H,5H)-dione
-
-
4-methyl-3-methylidene-2-(2-phenylethyl)-5-(pyridin-2-ylmethyl)-1,2,3,5-tetrahydro-6H-pyrazolo[4,3-c]pyridin-6-one
-
-
4-methyl-3-methylidene-2-[2-(morpholin-4-yl)ethyl]-5-(pyridin-2-ylmethyl)-1,2,3,5-tetrahydro-6H-pyrazolo[4,3-c]pyridin-6-one
-
-
4-methyl-5-(3-phenoxybenzyl)-2-([1,2,4]triazolo[4,3-b]pyridazin-6-yl)-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
4-[(4-fluorophenoxy)methyl]-5-(2-methoxyethyl)-2-(2-morpholin-4-ylethyl)-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
4-[(benzyloxy)methyl]-2-(2-chlorophenyl)-5-(pyrazin-2-ylmethyl)-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
4-[[(2-chlorobenzyl)oxy]methyl]-2-(2-chlorophenyl)-5-methyl-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
4-[[2-(1,3-benzothiazol-2-yl)-4-methyl-3,6-dioxo-1,2,3,6-tetrahydro-5H-pyrazolo[4,3-c]pyridin-5-yl]methyl]benzoic acid
-
-
4-[[2-(2-chlorophenyl)-4-methyl-3,6-dioxo-1,2,3,6-tetrahydro-5H-pyrazolo[4,3-c]pyridin-5-yl]methyl]benzenesulfonamide
-
-
4-[[benzyl(methyl)amino]methyl]-2-(2-chloro-4-fluorophenyl)-5-(3-methoxypropyl)-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
5,7-dihydroxy-2-(4-hydroxyphenyl)-4H-chromen-4-one
-
complete inhibition at 0.01 mM
5-(1,3-benzodioxol-5-ylmethyl)-4-methyl-2-phenyl-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
5-(E)-6,9-deoxa-6,9alpha-methylene-15-cyclopentyl-16,17,18,19,20-pentanor-prostaglandin I2
-
inhibition of sodiumdodecylsulfate-induced activation in cell free extracts, 0.17 mM, 50% inhibition
5-(furan-2-ylmethyl)-4-methyl-2-phenyl-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
5-benzyl-2-(4-fluorophenyl)-4-methyl-1H-pyrazolo[4,3-c]pyridine-3,6(2H,5H)-dione
-
-
5-cyclopropyl-2-[1-(2-fluoro-benzyl)-1H-pyrazolo[3,4-b]pyridine-3-yl]pyrimidin-4-ylamine
-
i.e. BAY 41-2272, inhibits the induction of the expression of subunits p22phox and gp91phox by 11alpha,9alpha-epoxymethanoprostaglandin F 2alpha. Enhances nitric oxide-induced relaxations in a concentration-dependent manner
5-[(2,5-dihydroxybenzyl)amino]-2-hydroxybenzoic acid
-
82% inhibition at 0.01 mM
alpha-chymotrypsin
-
desensitization of activity to Ca2+
-
aminoethylbenzenesulfonylfluoride
-
treatment blocks the induction of reactive oxygen species production by the dopaminergic toxin MPP+. Co-treatment with inhibitors aminoethylbenzenesulfonylfluoride, apocynin, or diphenylene iodinium significantly suppresses MPP*-induced cell death and attenuates MPP*-induced increases in caspase-3 enzymatic activity
angiotensin
-
angiotensin-(1-7) decreases the elevated levels of renal NADPH oxidase activity and attenuates the activation of subunit NOX-4 gene expression in the diabetic hypertensive kidney. Angiotensin-(1-7) treatment increases sodium excretion but does not affect mean arterial pressure in diabetic hypertensive rats. The significant increase in urinary protein in the diabetic compared to control hypertensive rat is reduced by angiotensin-(1-7). Angiotensin-(1-7) treatment also attenuates the diabetes-induced increase in renal vascular responsiveness to endothelin-1, norepinephrine, and angiotensin II in hypertensive rats, but significantly increases the vasodilation of the renal artery of hypertensive and diabetic hypertensive rats to the vasodilator agonists
ATDITGPIILQTYRA
-
a peptide inhibitor derived from human p47phox
AYRRNSVRFL
-
inhibits NADPH oxidase activation
AYRRNSVRFVRFLN
-
a peptide inhibitor derived from human p47phox
betaPix
-
guanine nucleotide exchange factor, overexpression of the central PH domain of betaPix results in inhibition of superoxide anion generation in response to EGF
-
betulinic acid
-
attenuates the expression of NAD(P)H oxidase subunits Nox4 and p22phox, thereby reducing oxidative stress and improving endothelial nitric oxide synthase function. Treated cells show in increased production of bioactive nitric oxide
Cdc42
-
a small monomeric GTPase, competitive inhibitor of Nox2, might also be a competitive inhibitor of Nox1
-
CERLVRFWRSQQKVV
-
a peptide inhibitor derived from human gp91phox/NOX2
CoA
NADH-dependent oxidase activities is strongly inhibited by addition of free CoA, whereas NADPH dependent activity is not; NADH-dependent oxidase activities is strongly inhibited by addition of free CoA, whereas NADPH dependent activity is not; NADH-dependent oxidase activities is strongly inhibited by addition of free CoA, whereas NADPH dependent activity is not; NADH-dependent oxidase activities is strongly inhibited by addition of free CoA, whereas NADPH dependent activity is not
COMT-methylated procyanidin B2
-
-
-
CSTRVRRQLDRNLTFHK
-
a peptide inhibitor derived from human gp91phox/NOX2
diphenylene iodinium chloride
EGTA
-
almost complete inhibition at 0.5 mM
endothelin-1
-
inhibits NADPH oxidase activity, superoxide generation, and cell proliferation in human abdominal aortic endothelial cells via the ETB1-Pyk2-Rac1-Nox1 pathway. Endothelin-1 significantly attenuates NADPH oxidase activity and cell proliferation, which can be abolished by silencing of the Nox1 gene. RNA interference silencing of ETB1 receptors significantly increases NADPH oxidase activity, and blocks the inhibitory effect of endothelin-1 on NADPH oxidase activity. Endothelin-1 also attenuates angiotensin II-induced activation of NADPH oxidase and cell proliferation
epigallocatechin gallate
-
-
FAVHHDEEDVITG
-
a peptide inhibitor derived from human gp91phox/NOX2
FIRHIALLGFEKRFV
-
a peptide inhibitor derived from human p47phox
GK-136901
-
inhibition of NOX1 and NOX4
gp91ds
-
fusion peptide that inhibits assembly of NADPH oxidase by mimicking the gp91phox docking site for the cytoplasmic p47phox subunit. gp91ds prevents NADPH oxidase activity, cytokine release, and neurotoxicity induced by HIV regulatory protein Tat in primary microglia
-
hemin
-
hemin treatment increases hemin oxidase-1 expression and activity in aorta and kidney of apolipoprotein Edeficient mice and significantly reduces both NADPH oxidase activity and superoxide generation in situ
IRNAHSIHQRSRKRL
-
a peptide inhibitor derived from human p47phox
ISNSESGPRGVHFIFNKENF
-
a peptide inhibitor derived from human gp91phox/NOX2
isorhamnetin glucuronide
-
-
KTIELQMKKKGFKM
-
a peptide inhibitor derived from human gp91phox/NOX2
LKLKKIYFYWLCRDTHAF
-
a peptide inhibitor derived from human gp91phox/NOX2
LKSVWYKYCN
-
a peptide inhibitor derived from human gp91phox/NOX2
LKSVWYKYCNN
-
a peptide inhibitor derived from human gp91phox/NOX2
lucensomycin
-
0.02 mM, 50% inhibition
methyl 2-hydroxy-5-[(2-hydroxybenzyl)amino]benzoate
-
91% inhibition at 0.01 mM
N'1,N'2-bis[(E)-(2,3-dihydroxyphenyl)methylidene]ethanedihydrazide
-
complete inhibition at 0.01 mM
N'1,N'2-bis[(E)-(3,4-dihydroxyphenyl)methylidene]ethanedihydrazide
-
complete inhibition at 0.01 mM
N-(1-cyclohexylethyl)-4-phenylphthalazin-1-amine
-
-
N-(3-aminophenyl)-N'-[1-(4-hydroxy-3-methoxyphenyl)ethyl]ethanediamide
-
complete inhibition at 0.01 mM
N-[(3Z)-3-(4-hydroxy-3-methoxybenzylidene)-2-oxo-2,3-dihydro-1H-indol-5-yl]acetamide
-
complete inhibition at 0.01 mM
N-[1-(3,4-dihydroxyphenyl)ethyl]-N'-(3-nitrophenyl)ethanediamide
-
complete inhibition at 0.01 mM
N-[2-(2-chlorophenyl)-4-methyl-3,6-dioxo-1,2,3,6-tetrahydro-5H-pyrazolo[4,3-c]pyridin-5-yl]-2-(4-fluorophenoxy)acetamide
-
-
N-[2-(4-hydroxy-phenyl)-ethyl]-2-(2, 5-dimethoxy-phenyl)-3-(3-methoxy-4-hydroxy-phenyl)-acrylamide
N-[3-(4,5-dimethyl-3,6-dioxo-1,3,5,6-tetrahydro-2H-pyrazolo[4,3-c]pyridin-2-yl)phenyl]acetamide
-
-
N4-(3-aminophenyl)[1]benzothieno[3,2-d]pyrimidine-4,8-diamine
-
98% inhibition at 0.01 mM
N4-(4-aminophenyl)[1]benzothieno[3,2-d]pyrimidine-4,8-diamine
-
complete inhibition at 0.01 mM
nitroglycerin
-
in rats treated with nitroglycerin for three days, superoxide production is increased in all aortic layers, while expression of isoforms nox1, nox2 and nox4 is significantly decreased. In vascular smooth muscle cells exposed to nitroglycerin for 6-24 h, NAD(P)H oxidase activity is increased, in spite of nox1 downregulation
Nox2ds-tat
-
inhibition of NAOX1 and NOX2
-
O-methyl-epicatechin
-
inhibits endothelial NAD(P)H oxidase activity and prevents superoxide anion formation
p-chloromercuribenzoate
-
-
p-hydroxymercuribenzoate
-
-
phallacidin
-
pretreatment of human pulmonary artery endothelial cells before induction of hyperoxia attenuates hyperoxia-induced cortical actin thickening and reactive oxygen species production
Plumbagin
-
inhibition of NOX4
procyanidin B2
-
acts both as a superoxide anion scavenger, and inhibitory to NAD(P)H oxidase, with apocynin-like mode of NADPH oxidase inhibition
propylthiouracil
-
partial
prostaglandin E1
-
inhibition of sodiumdodecylsulfate-induced activation in cell free extracts, 0.044 mM, 50% inhibition
PTKISRCPPHLLDFFK
-
a peptide inhibitor derived from human p47phox
QRRRQARPGPQSPG
-
a peptide inhibitor derived from human p47phox
quercetin 3-O-alpha-D-glucopyranoside
-
complete inhibition at 0.01 mM
quercetin glucuronide
-
-
RFVPSQHYVYMFLVK
-
a peptide inhibitor derived from human p47phox
rosuvastatin
-
rosuvastatin reduces systolic blood pressure in spontaneously hypertensive rats but does not change plasma lipid levels. Rosuvastatin treatment in spontaneously hypertensive rats significantly decreases reactive oxygen species levels, NAD(P)H activity in retinal ganglion cells, and increases retinal plasmalogen content in spontaneously hypertensive rats, but does not modify the electroretinogram response
RRNSVRFLQQRRRQA
-
a peptide inhibitor derived from human p47phox
RRSSIRNAHSIHQRSRKRLS
-
a peptide inhibitor derived from human p47phox
RSRKRLSQDAYRRNSVRFLQQR
-
a peptide inhibitor derived from human p47phox
sepiapterin
-
induction of oxidative stress, p22phox mRNA, endothelial nitric oxide synthase mRNA, and protein by glucose are lowered by concurrent incubation with sepiapterin
sinomenine
-
morphinan analog, inhibits NAD(P)H oxidase cytosolic subunit p47phox translocation to the cell membrane and thus reduces lipopolysaccharide-induced extracellular reactive oxygen species production. Protects neuron-glial cell cultures at both micro- and sub-picomolar concentrations against dopaminergic neuron death, but not protection is seen at nanomolar concentrations
sodium deoxycholate
-
no activity at 5 mg/ml
SRKRLSQDAYRRNS
-
a peptide inhibitor derived from human p47phox
STRVRRQLDRNLTF
-
a peptide inhibitor derived from human gp91phox/NOX2
sulfosuccinimidyl-3-(4-hydroxyphenyl) propionate
-
-
taxol
-
induces concentration-dependent neuronal death with apoptotoic features. Neuronal death is significantly attenuated by anti-apoptotic rugs and by antioxidants such as trolox, ascorbic acid, and tempol. Exposure to taxol increases the expression of NAD(P)H oxidase subunits p45phox and gp91phox and induces translocation of p47phox protein to the membrane in cortical cultures
telmisartan
-
0.01 mM telmisartan decreases NAD(P)H oxidase activity by 32% in MIN-6 cells
tetramethylpyrazine
-
inhibits the induction of NAD(P)H oxidase activity by angiotensin II and the concomitant increase of intracellular reactive oxygen species levels and ERK phosphorylation
Triton X-100
-
no activity at 2 mg/ml
VWYYRVYDIPPKFFYTRKLL
-
a peptide inhibitor derived from human gp91phox/NOX2
WWFCQMKAKRGWIPA
-
a peptide inhibitor derived from human p47phox
(-)-epigallocatechin gallate
-
inhibition of intracellular reactive oxygen species generation, inhibition of translocation of cytosolic subunits into membrane
(-)-epigallocatechin gallate
-
inhibition of intracellular reactive oxygen species generation
4-(2-amino-ethyl)-benzolsulphonyl-fluoride
-
-
4-(2-amino-ethyl)-benzolsulphonyl-fluoride
-
-
apocynin
-
in cells continuously treated with nitric oxide donors, including nitroglycerin, over 2-3 days, basal production of nitrite and nitrate is diminished. The diminished basal nitric oxide levels are mitigated by intermittent treatment allowing an 8-h daily nitrate-free interval during the 2- to 3-day treatment period. Addition of the NAD(P)H oxidase inhibitor apocynin restores the basal levels of nitric oxides that are decreased by continuous nitroglycerin treatment. Apocynin causes significant improvement of increased mRNA and protein levels of endothelial nitric oxide synthase in cells given nitroglycerin continuously over the treatment period. Apocynin also reduces endothelial production of reactive oxygen species after continuous nitroglycerin treatment
apocynin
-
blocks production of superoxide anion in sarcoplasmic reticulum of coronary arterial myocytes
apocynin
-
almost complete inhibition at 0.1 mM
apocynin
-
in sarcoplasmic reticulum vesicles isolated after exercise and tachycardia, apocynin prevents the increase in ryanodine receptor-2 S-glutathionylation, reduced calcium release activity, and completely prevents the protective effects of exercise and tachycardia on infarct size
apocynin
-
enzyme inhibitor, pretreatment of cells completely blocks insulin-stimulated activation of hypoxia-inducible factor 1
apocynin
-
significantly blunts both the generation of reactive oxygen species and induction of apoptosis induced by apigenin
apocynin
-
poor inhibitor of NADPH oxidase
apocynin
-
selective NAD(P)H oxidase inhibitor
apocynin
-
i.e. 4-hydroxy-3-methoxy-acetophenone, complete inhibition at 1 mM
apocynin
-
broad class Nox inhibitor
apocynin
-
4-hydroxy-3-methoxyacetophenonesubstituted, a natural molecule structurally related to vanillin, acts on p47phox, requires a peroxidase such as MPO
apocynin
-
inhibition of NOX1 and NOX2
apocynin
-
paraquat-induced reactive oxygen species production is inhibited by NADPH oxidase inhibitors, apocynin and diphenylene iodonium. Apocynin and diphenylene iodonium also rescue cells from paraquat-induced toxicity. The inhibitors for protein kinase C delta or extracellular signal-regulated kinases ERK1/2 can partially attenuate paraquat-induced reactive oxygen species production and cell death
apocynin
-
treatment significantly decreases angiotensin II-induced endothelin-1 RNA and peptide expression, superoxide production as well as collagen expression
apocynin
-
aortic rings from mice deificient in subunit p47phox are more sensitive to apocynin-induced dilation than wild-type aortic rings. Rho kinase inhibition reduces or prevents the inhibitory effect of apocynin on agonist-induced vasoconstriction and apocynin inhibits the phosphorylation of Rho kinase substrates
apocynin
-
inhibition of NAD(P)H oxidase by apocynin in ischemia-induced mice prevents blood-brain barrier damage in the ischemic hemisphere I after reperfusion
apocynin
-
inhibits NADPH oxidase and induces increased nitric oxide synthesis by eliciting a generation of reactive oxygen species, which in turn causes transcription factor NF-kappaB activation and increased expression of inducible nitric oxides
apocynin
-
selective NADPH oxidase inhibitor, inhibition of NADPH oxidase protects photoreceptors from light-induced degeneration
apocynin
-
inhibitor of NAD(P)H oxidase activation
apocynin
-
selective NAD(P)H oxidase inhibitor
apocynin
-
when luminal NaCl in kidney is switched from 10 to 80 mM, a situation of initiating maximum tubuloglomerular feedback response, superoxide anion production significantly increases. In the presence of apocynin, superoxide anion production is inhibited by 80%
apocynin
-
after 14 days, local treatment with apocynin via the adventitia, reduces superoxide generation. Apocynin significantly reduces neointima formation and proliferation of cells in both the neointima and adventitia. Nitric oxide-dependent vasorelaxation to acetylcholine, which is normally impaired in collared arteries, is improved, and apocynin suppresses the endothelial expression of intracellular adhesion molecule- and vascular cell adhesion molecule-
apocynin
-
in rabbits with heart failure induced by myocardial infarction, apocynin reduces NADPH oxidase activity, subunit p47phox protein, oxidative stress, myocyte apoptosis, and Bax protein, increases Bcl-2 protein, and ameliorates left ventricular dilatation and dysfunction
apocynin
-
also named acetovanillone, 4'-hydroxy-3'-methoxyacetophenone
apocynin
-
smoking impaires acetylcholine-induced relaxations of carotid arteries, which can be improved by the NAD(P)H oxidase inhibitor apocynin. Vascular mRNA expression of the proinflammatory cytokines IL-1, IL-6, and TNF-alpha and that of inducible nitric oxide synthase is significantly increased by both smoking and cigarette smoke extract exposure, which can be prevented by apocynin, diphenyleneiodinium, or scavenging of H2O2
apocynin
-
blocks up-regulation of epidermal growth factor receptor ligands and Akt activation by transforming growth factor-beta
apocynin
-
prevents inflammation-mediated toxicity to motor neurons induced by lipopolysaccharide
apocynin
-
apocynin does not reduce arterial pressure acutely in spontaneously hpertensive rats when given orally over 1-week intervals or when given i.v. Apocynin potently inhibits granulocyte NADPH oxidase but not vascular NADPH-oxidase dependent oxygen radical formation unless exogenous peroxidase is added to vascular preparations. Apocynin dilates rat intrarenal and coronary arteries independently of pharmacological interventions that reduce vascular superoxide radical abundance and actions
apocynin
-
inhibition of NAD(P)H oxidase in alveolar macrophage by apocynin results in down-regulation of arginase activity and decrease in arginase I mRNA
apocynin
-
apocynin reduces avascularity and apoptosis in the oxygen-induced retinopathy model
apocynin
-
treatment blocks the induction of reactive oxygen species production by the dopaminergic toxin MPP+. Co-treatment with inhibitors aminoethylbenzenesulfonylfluoride, apocynin, or diphenylene iodinium significantly suppresses MPP*-induced cell death and attenuates MPP*-induced increases in caspase-3 enzymatic activity
apocynin
-
also named acetovanillone, 4'-hydroxy-3'-methoxyacetophenone
apocynin
-
specific Nox inhibitor
apocynin
-
significantly attenuates hypoxia/reoxygenation-induced reactive oxygen species formation in porcine coronary artery endothelial cells and suppresses the hypoxia/reoxygenation-induced endothelial spheroid sprouting
bilirubin
-
bilirubin concentration-dependently reduces NADPH oxidase-dependent superoxide production stimulated by phorbol 12-myristate 13-acetate
bilirubin
-
bilirubin concentration-dependently reduces NADPH oxidase-dependent superoxide production stimulated by angiotensin II in vascular smooth muscle cells
diphenylene iodinium
-
inhibition of NAD(P)H oxidase, causes wild-type plants to phenocopy the isoform rdh2/Atrbohc mutant
diphenylene iodinium
-
treatment of NB-4 cells blocks basal generation of reactive oxygen species and arsenic trioxide-induced apoptosis
diphenylene iodinium
-
significant suppression of release of reactive oxygen species in astrocytes caused by calcium ionophores or opsonized zymosan
diphenylene iodinium
-
NaCl-induced increase in total Ca2+ in plasma membrane vesicles is partially abolished by the addition of diphenyleneiodinium
diphenylene iodinium chloride
-
enzyme inhibitor, pretreatment of cells completely blocks insulin-stimulated activation of hypoxia-inducible factor 1
diphenylene iodinium chloride
-
inhibition of enzyme, resulting in inhibitied growth and reactive oxygen species formation in tobacco pollen tube cultures
diphenylene iodinium chloride
-
inhibits NAD(P)H oxidase, effectively inhibits wound healing in potato tuber, and increases susceptibility to microbial infection and decay in 1-month-old tubers
diphenylene iodonium
-
blocks production of superoxide anion in sarcoplasmic reticulum of coronary arterial myocytes
diphenylene iodonium
-
significantly blunts both the generation of reactive oxygen species and induction of apoptosis induced by apigenin
diphenylene iodonium
-
inhibition of NADPH oxidase. In cells deficient for von Hippel-Lindau tumor suppressor gene, presence of diphenyleneiodonium decreases the expression of hypoxia-inducible factor 2alpha
diphenylene iodonium
-
directly inhibits the activity of enzyme component gp91phox/NOX2, the inhibitor targets the FAD binding sequence found in other flavoproteins and is therefore not specific for NOX2
diphenylene iodonium
-
paraquat-induced reactive oxygen species production is inhibited by NADPH oxidase inhibitors, apocynin and diphenylene iodonium. Apocynin and diphenylene iodonium also rescue cells from paraquat-induced toxicity. The inhibitors for protein kinase C delta or extracellular signal-regulated kinases ERK1/2 can partially attenuate paraquat-induced reactive oxygen species production and cell death
diphenylene iodonium
-
significantly inhibits RCC 786-O tumor formation in athymic mice
diphenylene iodonium
-
significantly reduces reactive oxygen species production, NADPH oxidase activity, and all the apoptotic events, and cell death induced by both 5 mM KCl and staurosporin
diphenylene iodonium
-
treatment blocks the induction of reactive oxygen species production by the dopaminergic toxin MPP+. Co-treatment with inhibitors aminoethylbenzenesulfonylfluoride, apocynin, or diphenylene iodinium significantly suppresses MPP*-induced cell death and attenuates MPP*-induced increases in caspase-3 enzymatic activity
diphenyleneiodonium
-
inhibition of NAD(P)H oxidase abolishes depolarisation of the neutrophil plasma membrane by electron current
diphenyleneiodonium
-
complete inhibition at 0.01 mM
diphenyleneiodonium
-
treatment significantly decreases angiotensin II-induced endothelin-1 RNA and peptide expression, superoxide production as well as collagen expression
diphenyleneiodonium
-
a nonspecific NOX inhibitor
diphenyleneiodonium
-
vascular mRNA expression of the proinflammatory cytokines IL-1, IL-6, and TNF-alpha and that of inducible nitric oxide synthase is significantly increased by both smoking and cigarette smoke extract exposure, which can be prevented by apocynin, diphenyleneiodinium, or scavenging of H2O2
diphenyleneiodonium
-
blocks up-regulation of epidermal growth factor receptor ligands and Akt activation by transforming growth factor-beta
diphenyleneiodonium
-
NAD(P)H oxidase inhibitor, complete inhibition at 0.001 mM
diphenyleneiodonium
-
significantly attenuates hypoxia/reoxygenation-induced reactive oxygen species formation in porcine coronary artery endothelial cells and suppresses the hypoxia/reoxygenation-induced endothelial spheroid sprouting
FLRGSSACCSTRVRRQL
-
-
FLRGSSACCSTRVRRQL
-
a peptide inhibitor derived from human gp91phox/NOX2
fulvene-5
-
-
fulvene-5
-
potent inhibitor of NADPH oxidase 4
gp91ds-tat
-
-
gp91ds-tat
-
peptidyl inhibitor. Treatment of engineered tissue blocks of a chamber model significantly reduces the level of reactive oxygen species and retards the tissue formation process. Vessels in treated tissues have smaller lumens than control
honokiol
-
submicromolar concentrations of honokiol suppress the increases of NADPH oxidase activity, Rac-1 phosphorylation, p22phox protein expression, and reactive oxygen species production in high glucose-stimulated HUVEC cells. Honokiol also suppresses high glucose-induced cyclooxygenase-2 upregulation and prostaglandin E2 production. Honokiol can reduce increased caspase-3 activity and the subsequent apoptosis and cell death triggered by high glucose medium
N-ethylmaleimide
-
weak inhibition
N-[2-(4-hydroxy-phenyl)-ethyl]-2-(2, 5-dimethoxy-phenyl)-3-(3-methoxy-4-hydroxy-phenyl)-acrylamide
-
i.e. FLZ, squamosamide derivative. FLZ inhibits the translocation of the cytosolic subunit p47phox to the membrane and thus inhibits the activation of NAD(P)H oxidase. In vivo, FLZ significantly protects against 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine-induced dopaminergic neuronal loss
N-[2-(4-hydroxy-phenyl)-ethyl]-2-(2, 5-dimethoxy-phenyl)-3-(3-methoxy-4-hydroxy-phenyl)-acrylamide
-
i.e. FLZ, squamosamide derivative, mediates anti-inflammatory and neuroprotective effects in both lipopolysaccharide-and 1-methyl-4-phenylpyridinium-mediated models of Parkinson's disease. FLZ inhibits the translocation of the cytosolic subunit p47phox to the membrane and thus inhibits the activation of NAD(P)H oxidase
neopterin
-
significantly blunts both the generation of reactive oxygen species and induction of apoptosis induced by apigenin
Phenylarsine oxide
-
-
Phenylarsine oxide
-
partial inactivation and desensitization of activity to Ca2+, effect is completely reversed by addition of 2,3-dimercaptopropanol
RGVHFIF
-
-
RGVHFIF
-
a peptide inhibitor derived from human gp91phox/NOX2
rosiglitazone
-
activates 5'-AMP-activated protein kinase which, in turn, prevents hyperactivity of NAD(P)H oxidase induced by high glucose, possibly through protein kinase C inhibition. Rosiglitazone protects endothelial cells against glucose-induced oxidative stress with an 5'-AMP-activated protein kinase-dependent and a PPARgamma-independent mechanism
rosiglitazone
-
treatment of animals for 1 week significantly reduces aortic superoxide production and the mRNA expression of enzyme subunits Nox-1, Nox-2, and Nox-4
RSRKRLSQDAYRRNSVRF
-
inhibits NADPH oxidase activation
RSRKRLSQDAYRRNSVRF
-
a peptide inhibitor derived from human p47phox
VAS2870
-
-
VAS2870
-
inhibition of NOX2 and NOX4
VAS3947
-
i.e. 3-benzyl-7-(2-oxazolyl)thio-1,2,3-triazolo[4,5-d]pyrimidine, specific low micromolar NADPH oxidase inhibitor
VAS3947
-
i.e. 3-benzyl-7-(2-oxazolyl)thio-1,2,3-triazolo[4,5-d]pyrimidine, specific low micromolar NADPH oxidase inhibitor
additional information
-
metronidazole has no measurable inhibitory effect on the NADPH oxidase activity of RdxA
-
additional information
-
unidentified inhibitor found in 3000 g particulate fraction from patients with Grave's disease
-
additional information
-
epicatechin is a superoxide anion scavenger, but not inhibitory to NAD(P)H oxidase. HUVEC cells are able to convert (-)-epicatechin to its inhibitory O-methyl esters. IC50-values of (-)epicatechin and (+)catechin are above 0.1 mM in cell lysates
-
additional information
-
presence of Candida albicans inhibits by contrasting the assembly of the enzyme on dedritic cell's plasma membrane
-
additional information
-
trimer hydroxylated quinone is the major active compound in AOP-1, with strong inhibitory activity against vascular endothelial cell NADPH oxidase with an IC50 of 0.000031 mM at 22°C, pH not specified in the publication
-
additional information
-
Francisella tularensis inhibits NADPH oxidase activity in a cell-free assay; the regulatory factor fevR is essential for NADPH oxidase inhibition, whereas iglI and iglJ, candidate secretion system effectors, and the acid phosphatase acpA are not
-
additional information
-
V204A mutant is a competitive inhibitor of wild-type p67phox
-
additional information
-
knockout of adenosine A2A receptor significantly decreases NADPH-dependent superoxide anion production in mouse hearts compared to age-matched wild-type controls, accompanied by a significant decrease in catalytic subunit Nox2 protein expression, and down-regulation of ERK1/2, p38MAPK, and JNK phosphorylation. In wild-type mice, intraperitoneal injection of the selective adenosine A2A receptor antagonist SCH58261 inhibits phosphorylation of regulatory subunit p47phox, which is accompanied by a down-regulated cardiac reactive oxygen species production, and decreased JNK and ERK1/2 activation
-
additional information
-
K+ depletion increases superoxide levels, phosphorylation of c-Jun, expression of c-Src, and tyrosine phosphorylation of ROMK channel in renal cortex and outer medulla in wild-type mice. Low K+ intake decreases mean product of channel number and open probability of ROMK channels. In mice lacking the NAD(P)H oxidase subunit gp91phox, the effects of low K intake are significantly attenuated
-
additional information
-
treatment of animals by oral administration of isoobtusilactone A for two weeks does not result in significant difference between control animals and treated animals with respect to the body weight gain, the body weight ratio of liver, spleen and kidney, haematological and clinical chemistry parameters
-
additional information
-
trimer hydroxylated quinone is the major active compound in AOP-1, with strong inhibitory activity against vascular endothelial cell NADPH oxidase with an IC50 of 0.000031 mM at 22°C, pH not specified in the publication
-
additional information
-
mGluR5 activation inhibits microglial NADPH oxidase activity
-
additional information
-
-
-
additional information
-
inhibition by addition of hexokinase and glucose to remove ATP
-
additional information
-
non-iodinated lipid aldehydes inhibit depending on their chain length, maximum inhibition with dodecanal and tridecanal, no inhibition with octanal
-