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(1E,4E)-1,5-bis(3,4-dihydroxyphenyl)penta-1,4-dien-3-one
-
-
(1E,4E)-1,5-bis(3,5-di-tert-butyl-4-hydroxyphenyl)penta-1,4-dien-3-one
-
-
(1E,4E)-1,5-bis(3-bromo-4-hydroxy-5-methoxyphenyl)penta-1,4-dien-3-one
-
-
(1E,4E)-1,5-bis(4-hydroxy-3,5-dimethoxyphenyl)penta-1,4-dien-3-one
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(1E,4E)-1,5-bis(4-hydroxyphenyl)penta-1,4-dien-3-one
-
-
(1E,4Z,6E)-1,7-di-2-furyl-5-hydroxyhepta-1,4,6-trien-3-one
-
-
(1E,4Z,6E)-1-(2-bromophenyl)-5-hydroxy-7-(4-hydroxyphenyl)hepta-1,4,6-trien-3-one
-
-
(1E,4Z,6E)-1-[4-(dimethylamino)phenyl]-5-hydroxy-7-[5-(hydroxymethyl)-2-furyl]hepta-1,4,6-trien-3-one
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-
(1E,4Z,6E)-5-hydroxy-1,7-bis(4-hydroxy-3-methoxyphenyl)hepta-1,4,6-trien-3-one
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-
(1E,4Z,6E)-5-hydroxy-1,7-bis(5-methyl-2-furyl)hepta-1,4,6-trien-3-one
-
-
(1E,4Z,6E)-5-hydroxy-1-(4-hydroxy-3-methoxyphenyl)-7-(5-methyl-2-furyl)hepta-1,4,6-trien-3-one
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-
(1E,4Z,6E)-5-hydroxy-1-(4-hydroxy-3-methoxyphenyl)-7-[5-(hydroxymethyl)-2-furyl]hepta-1,4,6-trien-3-one
-
-
(1E,4Z,6E)-5-hydroxy-1-(4-hydroxyphenyl)-7-(2-thienyl)hepta-1,4,6-trien-3-one
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(1E,4Z,6E)-5-hydroxy-7-(4-hydroxy-3-methoxyphenyl)-1-(4-hydroxyphenyl)hepta-1,4,6-trien-3-one
-
-
(1E,4Z,6E)-5-hydroxy-7-(4-hydroxy-3-methoxyphenyl)-1-phenylhepta-1,4,6-trien-3-one
-
-
(1E,4Z,6E)-5-hydroxy-7-(4-hydroxyphenyl)-1-(3,4,5-trimethoxyphenyl)hepta-1,4,6-trien-3-one
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(1E,4Z,6E)-5-hydroxy-7-(4-hydroxyphenyl)-1-phenylhepta-1,4,6-trien-3-one
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-
(1E,4Z,6E)-5-hydroxy-7-[5-(hydroxymethyl)-2-furyl]-1-(3,4,5-trimethoxyphenyl)hepta-1,4,6-trien-3-one
-
-
(1E,4Z,6E)-5-hydroxy-7-[5-(hydroxymethyl)-2-furyl]-1-(4-methoxyphenyl)hepta-1,4,6-trien-3-one
-
-
(1E,4Z,6E)-5-hydroxy-7-[5-(hydroxymethyl)-2-furyl]-1-phenylhepta-1,4,6-trien-3-one
-
-
(2E,5E)-2,5-bis(3,4-dihydroxybenzylidene)cyclopentanone
-
-
(2E,5E)-2,5-bis(3-bromo-4-hydroxy-5-methoxybenzylidene)cyclopentanone
-
-
(2E,5E)-2,5-bis(4-hydroxybenzylidene)cyclopentanone
-
-
(2E,5E)-2,5-bis[(3,5-di-tert-butyl-4-hydroxyphenyl)methylidene]cyclopentanone
-
-
(2E,5E)-2,5-bis[(4-hydroxy-3,5-dimethoxyphenyl)methylidene]cyclopentanone
-
-
(2E,6E)-2,6-bis(3,4-dihydroxybenzylidene)cyclohexanone
-
-
(2E,6E)-2,6-bis(3-bromo-4-hydroxy-5-methoxybenzylidene)cyclohexanone
-
-
(2E,6E)-2,6-bis(4-hydroxybenzylidene)cyclohexanone
-
-
(2E,6E)-2,6-bis[(3,4-dimethoxyphenyl)methylidene]cyclohexanone
-
-
(2E,6E)-2,6-bis[(4-hydroxy-3,5-dimethoxyphenyl)methylidene]cyclohexanone
-
-
(2E,6E)-2-(4-hydroxybenzylidene)-6-(4-hydroxy-3-methoxybenzylidene)cyclohexanone
-
-
(2E,6E)-2-[(4-hydroxyphenyl)methylidene]-6-[(3,4,5-trimethoxyphenyl)methylidene]cyclohexanone
-
-
(3E,5E)-3,5-bis(3,4-dihydroxybenzylidene)piperidin-4-one
-
-
(3E,5E)-3,5-bis(3-bromo-4-hydroxy-5-methoxybenzylidene)piperidin-4-one
-
-
(3E,5E)-3,5-bis(4-hydroxybenzylidene)-4-oxopiperidinium
-
-
(3E,5E)-3,5-bis[(3,4-dimethoxyphenyl)methylidene]piperidin-4-one
-
-
(3E,5E)-3,5-bis[(4-hydroxy-3,5-dimethoxyphenyl)methylidene]piperidin-4-one
-
-
(3E,5E)-3-[(2,5-di-tert-butyl-4-hydroxyphenyl)methylidene]-5-[(3,5-di-tert-butyl-4-hydroxyphenyl)methylidene]piperidin-4-one
-
-
(4-ammoniothiophenolato)(2,2':6',2''-terpyridine)platinum(II) chloride
-
-
(4-ammoniothiophenolato)(4'-toyl-2,2':6',2''-terpyridine)platinum(II) nitrate
-
-
(4-hydroxylthiophenolato)(2,2':6',2''-terpyridine)platinum(II) chloride
-
-
(4-hydroxylthiophenolato)(4'-toyl-2,2':6',2''-terpyridine)platinum(II) chloride
-
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(4-methylpyrimidine-2-thiolato-kappaS)(1,3,5-triaza-7-phosphatricyclo[3.3.1.13,7]decane-kappaP)gold
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-
(4-methylpyrimidine-2-thiolato-kappaS)[1,1'-(1,3,7-triaza-5-phosphabicyclo[3.3.1]nonane-3,7-diyl-kappaP)diethanone]gold
-
-
(N-acetyl-4-aminothiophenolato)(2,2':6',2''-terpyridine)platinum(II) chloride
-
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(N-acetyl-4-aminothiophenolato)(4'-toyl-2,2':6',2''-terpyridine)platinum(II) nitrate
-
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(pyridine-2-thiolato-kappaS)(1,3,5-triaza-7-phosphatricyclo[3.3.1.13,7]decane-kappaP)gold
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(pyridine-2-thiolato-kappaS)[1,1'-(1,3,7-triaza-5-phosphabicyclo[3.3.1]nonane-3,7-diyl-kappaP)diethanone]gold
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(pyrimidine-2-thiolato-kappaS)(1,3,5-triaza-7-phosphatricyclo[3.3.1.13,7]decane-kappaP)gold
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1,1'-sulfanediylbis(2,4-dinitrobenzene)
1,1'-sulfanediylbis[2-nitro-4-(trifluoromethyl)benzene]
1,2-[bis(1,2-benzisoselenazolone-3(2H)-ketone)]ethane
-
apoptosis induced by the inhibitor is through Bcl-2/Bax and caspase-3 pathways
1,3-dinitro-5-(trifluoromethyl)benzene
1,4-dihydroxyanthroquinone
-
1,8-dihydroxyanthroquinone
-
1-chloro-2,4-dinitrobenzene
1-Fluoro-2,4-dinitrobenzene
1-methyl-1-propyl-2-imidazolyl disulfide
15-deoxy-D-12,14-PGJ2
-
0.06 mM, IC50: 0.00036 mM
2,2'-(ethane-1,2-diyl)di(1,2-benzoselenazol-3(2H)-one)
-
IC50 value for HEK-293T cells 3.4 microg/ml
2,2'-(hexane-1,6-diyl)di(1,2-benzoselenazol-3(2H)-one)
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IC50 value for HEK-293T cells 2.5 microg/ml
2-aminothiazolium [trans-tetrachlorobis(2-aminothiazole)ruthenate(III)]
-
2-benzoyloxycinnamaldehyde
2-benzyloxycinnamaldehyde
2-chloro-1,3-dinitro-5-(trifluoromethyl)benzene
2-hydroxymethyl-5-methoxy-1-methyl-3-[(2,4,6-trifluorophenoxy)methyl]indole-4,7-dione
2-hydroxymethyl-5-methoxy-1-methyl-3-[(4-nitrophenoxy)methyl]indole-4,7-dione
2-hydroxymethyl-6-methoxy-1-methyl-3-[(4-nitrophenoxy)methyl]indole-4,7-dione
3,4-estronequinone
-
0.032 mM, IC50: 0.02 mM
3-(4-[[2-(1-hydroxy-4-oxocyclohexa-2,5-dien-1-yl)-1H-indol-1-yl]sulfonyl]phenyl)propanoic acid
-
-
3-(4-[[6-fluoro-2-(1-hydroxy-4-oxocyclohexa-2,5-dien-1-yl)-1H-indol-1-yl]sulfonyl]phenyl)propanoic acid
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4,5-dinitro-1,3-benzodioxole
4,6-dinitro-2,1,3-benzothiadiazole
4-(1,3-benzothiazol-2-yl)-4-hydroxycyclohexa-2,5-dien-1-one
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4-(1,3-benzoxazol-2-yl)-4-hydroxycyclohexa-2,5-dien-1-one
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4-(1-benzothien-2-yl)-4-hydroxycyclohexa-2,5-dien-1-one
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4-(5-fluoro-1,3-benzothiazol-2-yl)-4-hydroxycyclohexa-2,5-dien-1-one
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-
4-azobenzene sulfonic acid
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63% residual activity at 5 mM
4-hydroxy-2-nonenal
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0.005-0.025 mM, IC50: 0.0038 mM, irreversible inhibition; 0.05 mM, remarkable lost inhibition
4-hydroxy-4-[1-(phenylsulfonyl)-1H-indol-2-yl]cyclohexa-2,5-dien-1-one
-
-
4-hydroxynonenal
-
0.06 mM, IC50: 0.012 mM
4-nitro-2,1,3-benzothiadiazole
4-[6-fluoro-1-(phenylsulfonyl)-1H-indol-2-yl]-4-hydroxycyclohexa-2,5-dien-1-one
-
-
5,5'-dithiobis(2-nitrobenzoate)
-
above 0.1 mM
5-fluoro-2-hydroxycinnamaldehyde
5-methoxy-1,2-dimethyl-3-[1-oxo-2-(2,4,6-trifluorophenyl)ethyl]indole-4,7-dione
5-methoxy-1-methyl-3-[(2,4,6-trifluorophenoxy)methyl]indole-4,7-dione
5-methoxy-1-methyl-3-[(4-nitrophenoxy)methyl]indole-4,7-dione
5-nitro-2,1,3-benzothiadiazole
6-methoxy-1-methyl-3-[(2,4,6-trifluorophenoxy)methyl]indole-4,7-dione
6-methoxy-1-methyl-3-[(4-nitrophenoxy)methyl]indole-4,7-dione
allyl isothiocyanate
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0.0205 mM, 50% inhibition after 30 min preincubation in assay with 5,5'-dithiobis(2-nitrobenzoic acid) as substrate
arsenic trioxide
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irreversible. Both the N-terminal redox-active dithiol and the C-terminal selenothiol-active site of reduced TrxR may participate in the reaction with the inhibitor. The inhibition of MCF-7 cell growth by arsenic trioxide is correlated with irreversible inactivation of thioredoxin reductase, which subsequently led to thioredoxin oxidation
Benzyl isothiocyanate
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0.0033 mM, 50% inhibition after 30 min preincubation in assay with 5,5'-dithiobis(2-nitrobenzoic acid) as substrate
bis-demethoxy curcumin
-
-
chaetocin
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competitive inhibitor with anticancer effects, complete inhibition at 0.015 mM
chloro[N(4)-ortho-chlorophenyl-2-acetylpyridinethiosemicarbazonato]gold(III)dichloroaurate(I)
-
in addition, the complex is highly cytotoxic to MCF-7 and HT29 cells
Cr6+
-
hexavalent chromium causes pronounced inhibition of TrxR, the inhibition of TrxR is not reversed by removal of residual Cr6+ or by NADPH. In cells treated with 0.025 or 0.050 mM Cr6+ for 90 min, TrxR activity is inhibited by 71 and 77%, respectively, while after 180 min of the same treatments, TrxR is inhibited by 97 and 85%, respectively
cyclophosphamide
-
250 mg/kg reduces activity reversibly to 25% at 3h after treatment
diallyl disulfide
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0.38 mM, 50% inhibition after 30 min preincubation in assay with 5,5'-dithiobis(2-nitrobenzoic acid) as substrate
dichloro[N(4)-ortho-chlorophenyl-2-acetylpyridinethiosemicarbazonato]antimony(III)
-
in addition, the complex is highly cytotoxic to MCF-7 and HT29 cells
diphenylene iodonium
-
IC50: 0.001 mM
Glyoxal
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93% residual activity at 5 mM
gold acetate
-
500 nM, 50% inhibition
gold sodium thiomalate
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500 nM, 50% inhibition
ifosfamide
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inhibition of thioredoxin reductase activity in malignant cells by ifosfamide is highly associated with its anticancer effect and the mechanism of ifosfamide systemic toxicity may be related to multi-organ inhibition of thioredoxin reductase activity
Iodine
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86% residual activity at 5 mM
leukotriene A4 methyl ester
-
0.06 mM, IC50: 0.513 mM
metronidazole
-
metronidazole-modified recombinant enzyme displays considerably reduced thioredoxin reductase activity. By reducing metronidazole, the enzyme renders itself and associated thiol-containing proteins vulnerable to adduct formation
myricetin
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0.05 mM, strong inhibitory effect, IC50: 0.62 mM
NAD+
-
NAD+ acts as poor competitive inhibitor respect to both NADPH and NADH
p-chloromercuribenzoate
-
with NADPH
palmarumycin CP1
-
0.001 mM, the naphthoquinone spiroketal fungal metabolite palmarumycin CP1 is a potent inhibitor of thioredoxin reductase-1, IC50: 0.00035 mM
palmitoyl-CoA
covalent inhibition of TrxR1/hTrx1 by palmitoyl-CoA. The palmitoyl-CoA/TrxR1 reaction is NADPH-dependent and produces palmitoylated TrxR1 at an active site selenocysteine residue
phenethyl isothiocyanate
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0.075 mM, 50% inhibition after 30 min preincubation in assay with 5,5'-dithiobis(2-nitrobenzoic acid) as substrate
phenyl mercuric acetate
-
stabilizes enzyme in one of two possible conformations
Prostaglandin A2
-
0.06 mM, IC50: 0.068 mM
pseudohypericin
strong inhibitor of isoform TrxR1
PX-911
-
0.001 mM, a water-soluble prodrug of a palmarumycin CP1 analogue, IC50: 0.0032 mM
PX-916
-
0.001 mM, a water-soluble prodrug of a palmarumycin CP1 analogue, potent inhibitor of purified human thioredoxin reductase-1, IC50: 0.00028 mM
PX-960
-
0.001 mM, a water-soluble prodrug of a palmarumycin CP1 analogue, IC50: 0.00027 mM
quercetin
-
0.05 mM, strong inhibitory effect, IC50: 0.97 mM
reactive oxygen species
-
0.1 mM, ROS generated by xanthine/xanthine oxidase enhance the inhibitory effect of flavonoids
-
sodium aurothiomalate
-
0.1 mM
sodium aurothiosulfate
-
100 nM, 50% inhibition
sulforaphane
-
0.04 mM, 50% inhibition after 30 min preincubation in assay with 5,5'-dithiobis(2-nitrobenzoic acid) as substrate
theaflavin-3'-monogallate
-
theaflavin-3,3'-digallate
-
theaflavin-3-monogallate
-
trans-[bis(2-amino-5-methylthiazole)tetrachlororuthenate(III)]
selective inhibition of TrxR1
triphenyl phosphine gold chloride
-
75 nM, 50% inhibition
trisodium (4,5-dihydro-1,3-thiazole-2-thiolato-kappaS2)[3,3',3''-(phosphanetriyl-kappaP)tribenzenesulfonato(3-)]aurate(3-)
-
-
trisodium [3,3',3''-(phosphanetriyl-kappaP)tribenzenesulfonato(3-)](pyrimidine-2-thiolato-kappaS)aurate(3-)
-
-
Zinc
-
0.05 mM, 50% inhibition
[(iPr2Im)2Au]Cl
-
mainly inhibits isoform TrxR2, about 30% residual activity after 8 h at 0.005 mM or 0.05 mM
[Au(d2pype)2]Cl
-
mainly inhibits isoform TrxR1, about 30% residual activity after 8 h at 0.005 mM, about 10% residual activity after 8 h at 0.05 mM
[Au(d2pypp)2]Cl
-
about 30% residual activity after 8 h at 0.005 mM, about 10% residual activity after 8 h at 0.05 mM
[Pt(2,2'-bipyridine)(ethylenediamine)]Cl2
-
the platinum(II) complex acts as an inhibitor by binding with the active site of the enzyme
1,1'-sulfanediylbis(2,4-dinitrobenzene)
-
IC50: 0.004 mM
1,1'-sulfanediylbis(2,4-dinitrobenzene)
-
IC50: 0.0005 mM
1,1'-sulfanediylbis[2-nitro-4-(trifluoromethyl)benzene]
-
IC50: 0.15 mM
1,1'-sulfanediylbis[2-nitro-4-(trifluoromethyl)benzene]
-
IC50: 0.02 mM
1,3-dinitro-5-(trifluoromethyl)benzene
-
IC50: 0.2 mM
1,3-dinitro-5-(trifluoromethyl)benzene
-
IC50: 0.03 mM
1-chloro-2,4-dinitrobenzene
-
i.e. DNCB; irreversible, with NADPH, alkylation of the active site cysteine disulfide, strong increase in oxidation activity of the enzyme against NADPH
1-chloro-2,4-dinitrobenzene
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i.e. DNCB; mitochondrial isoform
1-chloro-2,4-dinitrobenzene
-
0.01 mM, irreversible inhibition
1-chloro-2,4-dinitrobenzene
-
-
1-chloro-2,4-dinitrobenzene
-
i.e. DNCB; irreversible, with NADPH, alkylation of the active site cysteine disulfide, strong increase in oxidation activity of the enzyme against NADPH
1-chloro-2,4-dinitrobenzene
-
1-chloro-2,4-dinitrobenzene
-
0.1 mM
1-chloro-2,4-dinitrobenzene
-
uncompetitive inhibition
1-chloro-2,4-dinitrobenzene
-
TrxR inhibition by 1-chloro-2,4-dinitrobenzene results in generation of reactive oxygen species and subsequent activation of stress-inducible kinases without impairment of the cellular antioxidant status or mitochondrial function
1-chloro-2,4-dinitrobenzene
-
1-chloro-2,4-dinitrobenzene
-
-
1-Fluoro-2,4-dinitrobenzene
-
irreversible, with NADPH, alkylation of the active site cysteine disulfide, strong increase in oxidation activity of the enzyme against NADPH
1-Fluoro-2,4-dinitrobenzene
-
irreversible, with NADPH, alkylation of the active site cysteine disulfide, strong increase in oxidation activity of the enzyme against NADPH
1-methyl-1-propyl-2-imidazolyl disulfide
-
1-methyl-1-propyl-2-imidazolyl disulfide
-
2-benzoyloxycinnamaldehyde
-
-
2-benzoyloxycinnamaldehyde
-
-
2-benzoyloxycinnamaldehyde
-
-
2-benzyloxycinnamaldehyde
-
-
2-benzyloxycinnamaldehyde
-
-
2-chloro-1,3-dinitro-5-(trifluoromethyl)benzene
-
IC50: 0.1 mM
2-chloro-1,3-dinitro-5-(trifluoromethyl)benzene
-
IC50: 0.008 mM
2-hydroxycinnamaldehyde
-
-
2-hydroxycinnamaldehyde
-
-
2-hydroxymethyl-5-methoxy-1-methyl-3-[(2,4,6-trifluorophenoxy)methyl]indole-4,7-dione
-
maximum inhibition is achieved 5 min after addition of 0.003 mM
2-hydroxymethyl-5-methoxy-1-methyl-3-[(2,4,6-trifluorophenoxy)methyl]indole-4,7-dione
-
maximum inhibition is achieved 5 min after addition of 0.003 mM
2-hydroxymethyl-5-methoxy-1-methyl-3-[(4-nitrophenoxy)methyl]indole-4,7-dione
-
-
2-hydroxymethyl-5-methoxy-1-methyl-3-[(4-nitrophenoxy)methyl]indole-4,7-dione
-
-
2-hydroxymethyl-6-methoxy-1-methyl-3-[(4-nitrophenoxy)methyl]indole-4,7-dione
-
-
2-hydroxymethyl-6-methoxy-1-methyl-3-[(4-nitrophenoxy)methyl]indole-4,7-dione
-
-
2-pentoxycinnamaldehyde
-
-
2-pentoxycinnamaldehyde
-
-
4,5-dinitro-1,3-benzodioxole
-
IC50: 0.08 mM
4,5-dinitro-1,3-benzodioxole
-
IC50: 0.01 mM
4,6-dinitro-2,1,3-benzothiadiazole
-
IC50: 0.002 mM
4,6-dinitro-2,1,3-benzothiadiazole
-
IC50: 0.01 mM
4-nitro-2,1,3-benzothiadiazole
-
IC50: 0.05 mM
4-nitro-2,1,3-benzothiadiazole
-
IC50: 0.002 mM
4-Vinylpyridine
-
irreversible
4-Vinylpyridine
-
irreversible
5-fluoro-2-hydroxycinnamaldehyde
-
-
5-fluoro-2-hydroxycinnamaldehyde
-
-
5-fluoro-2-hydroxycinnamaldehyde
-
-
5-methoxy-1,2-dimethyl-3-[1-oxo-2-(2,4,6-trifluorophenyl)ethyl]indole-4,7-dione
-
-
5-methoxy-1,2-dimethyl-3-[1-oxo-2-(2,4,6-trifluorophenyl)ethyl]indole-4,7-dione
-
-
5-methoxy-1-methyl-3-[(2,4,6-trifluorophenoxy)methyl]indole-4,7-dione
-
-
5-methoxy-1-methyl-3-[(2,4,6-trifluorophenoxy)methyl]indole-4,7-dione
-
-
5-methoxy-1-methyl-3-[(4-nitrophenoxy)methyl]indole-4,7-dione
-
-
5-methoxy-1-methyl-3-[(4-nitrophenoxy)methyl]indole-4,7-dione
-
-
5-nitro-1,3-benzodioxole
-
IC50: 0.2 mM
5-nitro-1,3-benzodioxole
-
0.1 mM, 10% inhibition
5-nitro-2,1,3-benzothiadiazole
-
IC50: 0.09 mM
5-nitro-2,1,3-benzothiadiazole
-
IC50: 0.01 mM
6,7-dinitroquinoxaline
-
IC50: 0.14 mM
6,7-dinitroquinoxaline
-
IC50: 0.002 mM
6-methoxy-1-methyl-3-[(2,4,6-trifluorophenoxy)methyl]indole-4,7-dione
-
-
6-methoxy-1-methyl-3-[(2,4,6-trifluorophenoxy)methyl]indole-4,7-dione
-
-
6-methoxy-1-methyl-3-[(4-nitrophenoxy)methyl]indole-4,7-dione
-
-
6-methoxy-1-methyl-3-[(4-nitrophenoxy)methyl]indole-4,7-dione
-
-
6-nitroquinoxaline
-
IC50: 0.2 mM
6-nitroquinoxaline
-
IC50: 0.04 mM
Ag+
-
enzyme activity is moderately reduced (50%) by 1 mM
Ag+
-
silver ions bind to the active sites of thioredoxin reductase with dissociation constants of 0.0014 mM and stoichiometries of 1 Ag+ ion per protein
arsenite
-
-
auranofin
-
-
auranofin
-
15 nM, complete inhibition
auranofin
-
inhibition of thioredoxin reductase by auranofin induces apoptosis in cisplatin-resistant human ovarian cancer cells
auranofin
-
about 10% residual activity at 400 nM in the presence of NADPH, less than 5% residual activity at 400 nM for 5,5'-dithiobis(2-nitrobenzoic acid) reduction, about 80% residual activity at 400 nM for juglone reduction
auranofin
-
efficient inhibition, about 20% residual activity after 8 h at 0.005 mM, about 7% residual activity after 8 h at 0.05 mM
auranofin
-
irreversibe inhibition
auranofin
-
5-10 nM, 50% inhibition, complete inhibition above 15 nM
auranofin
-
about 10% residual activity at 400 nM in the presence of NADPH, less than 5% residual activity at 400 nM for 5,5'-dithiobis(2-nitrobenzoic acid) reduction, about 80% residual activity at 400 nM for juglone reduction
auranofin
-
protects cerebellar granular neurons from the action of different doses of tetanus neurotoxin, about 1 microM auranofinF confers a full protection against tetnus neurotoxin intoxication. Auranofin protects cerebellar granular neurons from the cleavage of VAMP-2 induced by botulinum neurotoxi B and the cleavage of syntaxin 1A induced by botulinum neurotoxin C
aurothioglucose
-
IC50: 120 nM
aurothioglucose
-
0.02 mM
aurothioglucose
-
about 90% residual activity after 8 h at 0.005 mM, about 80% residual activity after 8 h at 0.05 mM
Ca2+
-
-
Ca2+
-
non-reversible by EDTA
calveolin
overexpression of caveolin 1 inhibits TrxR activity by about 50% whereas a lack of caveolin 1 activates TrxR, both in vitro and in vivo
-
calveolin
-
overexpression of caveolin 1 inhibits TrxR activity by about 50% whereas a lack of caveolin 1 activates TrxR, both in vitro and in vivo
-
Cd2+
-
enzyme activity is drastically reduced (70%) by 1 mM
cisplatin
-
cisplatin
-
i.e. cis-diamminedichloroplatinum(II), about 3% residual activity at 400 nM in the presence of NADPH, about 10% residual activity at 400 nM for 5,5'-dithiobis(2-nitrobenzoic acid) reduction, about 90% residual activity at 400 nM for juglone reduction
cisplatin
-
about 40% residual activity after 8 h at 0.005 mM or 0.05 mM
cisplatin
-
at pharmacological doses inhibits TrxR activity in both ascitic hepatoma 22 cells and kidney, leading to suppression of H22 cells proliferation along with nephrotoxicity. Amifostine, a clinical used cytoprotective agent, protected against CDDP-induced TrxR inactivation in kidney but not in H22 cells
cisplatin
-
heat shock protein 27 protects L929 cells from cisplatin-induced apoptosis by enhancing Akt activation and abating suppression of thioredoxin reductase activity
cisplatin
complete inhibition after 1 h at 0.5 mM
cisplatin
-
i.e. cis-diamminedichloroplatinum(II), about 3% residual activity at 400 nM in the presence of NADPH, about 10% residual activity at 400 nM for 5,5'-dithiobis(2-nitrobenzoic acid) reduction, about 90% residual activity at 400 nM for juglone reduction
Cu2+
-
strong inhibition
Cu2+
-
enzyme activity is drastically reduced (70%) by 1 mM
curcumin
-
curcumin
-
IC50: 0.0036 mM
curcumin
-
irreversible inhibition
ebselen
-
competitive, inhibitor reacts with the active site dithiol
ebselen
-
reversible competitive inhibitor of the enzyme from Escherichia coli. Ebselen can form a stable selenosulfide bond with the attacking cysteine in Escherichia coli thioredoxin reductase which cannot easily be resolved by the other cysteine in the active site. The binding blocks the electron transfer from Escherichia coli TrxR to Trx, and ultimately to the downstream substrates of thioredoxin. Ebselen is an excellent substrate for mammalian thioredoxin system
ES936
-
i.e. 5-methoxy-1,2-dimethyl-3-[(4-nitrophenoxy)methyl]indole-4,7-dione, potent inhibitor
ES936
-
i.e. 5-methoxy-1,2-dimethyl-3-[(4-nitrophenoxy)methyl]indole-4,7-dione, potent inhibitor
gold
-
potent inhibitor, the inhibition of TrxR1 by the metal compound is not markedly influenced by the presence of EDTA
gold
-
potent inhibitor, the inhibition of TrxR1 by the metal compound is not markedly influenced by the presence of EDTA
Hg2+
-
Hg2+
-
enzyme activity is drastically reduced (70%) by 1 mM
Hg2+
potently inhibits (at concentrations of 5-50 nM) TrxR1 activity in both cell-free and intracellular assays
Hg2+
-
in the presence of NADPH, a ratio of 2 HgCl2 molecules to 1 TrxR dimer leads to a virtually inactive enzyme. On treatment with 0.005 mM selenite and NADPH, TrxR inactivated by HgCl2 displays almost full recovery of activity
Hg2+
-
in the presence of NADPH, a ratio of 2 HgCl2 molecules to 1 TrxR dimer leads to a virtually inactive enzyme. On treatment with 0.005 mM selenite and NADPH, TrxR inactivated by HgCl2 displays almost full recovery of activity
iodoacetate
-
irreversible
iodoacetate
-
irreversible
juglone
-
K2PdCl4
-
strong and irreversible inhibition, about 30% residual activity at 400 nM in the presence of NADPH, less than 10% residual activity at 400 nM for 5,5'-dithiobis(2-nitrobenzoic acid) reduction, about 90% residual activity at 400 nM for juglone reduction
K2PdCl4
-
strong and irreversible inhibition, about 30% residual activity at 400 nM in the presence of NADPH, less than 10% residual activity at 400 nM for 5,5'-dithiobis(2-nitrobenzoic acid) reduction, about 90% residual activity at 400 nM for juglone reduction
K2PdCl6
-
irreversible inhibition
K2PdCl6
-
irreversible inhibition
K2PtCl4
-
irreversible inhibition, about 5% residual activity at 400 nM in the presence of NADPH, complete inhibition of 5,5'-dithiobis(2-nitrobenzoic acid) reduction at 400 nM, about 90% residual activity at 400 nM for juglone reduction
K2PtCl4
-
irreversible inhibition, about 5% residual activity at 400 nM in the presence of NADPH, complete inhibition of 5,5'-dithiobis(2-nitrobenzoic acid) reduction at 400 nM, about 90% residual activity at 400 nM for juglone reduction
K2PtCl6
-
irreversible inhibition
K2PtCl6
-
irreversible inhibition
KAuCl4
-
irreversible inhibition, about 10% residual activity at 400 nM in the presence of NADPH, less than 5% residual activity at 400 nM for 5,5'-dithiobis(2-nitrobenzoic acid) reduction, about 70% residual activity at 400 nM for juglone reduction
KAuCl4
-
irreversible inhibition, about 10% residual activity at 400 nM in the presence of NADPH, less than 5% residual activity at 400 nM for 5,5'-dithiobis(2-nitrobenzoic acid) reduction, about 70% residual activity at 400 nM for juglone reduction
menadione
-
methylmercury
-
in the case of methylmercury, a ratio of 16 molecules per dimer leads to a virtually inactive enzyme
methylmercury
-
a single administration of methylmercury (1, 5, and 10 mg/kg) causes a marked inhibition of kidney TrxR activity, while significant inhibition is observed in the liver 24 h after exposure to 5 and 10 mg/kg. In the brain, methylmercury does not inhibit TrxR activity. Methylmercury can bind to selenocysteine residues present in the catalytic site of TrxR, in turn causing enzyme inhibition that can compromise the redox state of cells
methylmercury
-
in the case of methylmercury, a ratio of 16 molecules per dimer leads to a virtually inactive enzyme
N-ethylmaleimide
-
46% residual activity at 5 mM
N-ethylmaleimide
-
reaction only with the reduced enzyme
NADP+
-
better competitive inhibitor than NAD+
NADP+
-
product inhibition
oxaliplatin
-
palladium
-
potent inhibitor, the inhibition of TrxR1 by the metal compound is not markedly influenced by the presence of EDTA
palladium
-
potent inhibitor, the inhibition of TrxR1 by the metal compound is not markedly influenced by the presence of EDTA
platinum
-
the inhibition of TrxR1 by the metal compound is not markedly influenced by the presence of EDTA
platinum
-
the inhibition of TrxR1 by the metal compound is not markedly influenced by the presence of EDTA
theaflavin
-
trans,trans-curcumin
-
0.01-0.05 mM, IC50: 0.0015 mM, irreversible inhibition
trans,trans-curcumin
-
IC50: 0.0036 mM, irreversible inhibition after incubation at room temperature for 2 h in vitro
trans-cinnamaldehyde
-
-
Zn2+
-
strong inhibition
Zn2+
-
enzyme activity is drastically reduced (70%) by 1 mM
Zn2+
-
0.1-0.2 mM and above
Zn2+
-
0.1-0.2 mM and above
additional information
-
no inhibition with dinitrohalobenzene analogues: 1,4-dichlorobenzene, 1-chloro-4-nitrobenzene, 1-chloro-3,4-dinitrobenzene, 1-chloro-2,5-dinitrobenzene
-
additional information
-
not inhibited by 1-chloro-2,4-dinitrobenzene
-
additional information
-
not inhibited by trans-cinnamaldehyde and 2-hydroxycinnamaldehyde after 1 h of incubation
-
additional information
-
no inhibition with dinitrohalobenzene analogues: 1,4-dichlorobenzene, 1-chloro-4-nitrobenzene, 1-chloro-3,4-dinitrobenzene, 1-chloro-2,5-dinitrobenzene
-
additional information
-
no inhibition by Ca2+ or Co2+
-
additional information
transfection of HeLa cells with siRNA targeted against TrxR1 effectively decreases TrxR1 protein levels and activity relative to control cells. Trx1 oxidation is not an inevitable consequence of TrxR1 inhibition
-
additional information
-
hypoxanthine/xanthine oxidase system and H2O2 in rheumatoid arthritis cells decrease thioredoxin reductase activity, which is found to be unchanged in osteoarthritis cells. H2O2 and superoxide anion cause a time-dependent accumulation of oxidized thioredoxin reductase and induces the formation of carbonyl groups in thioredoxin reductase protein in rheumatoid arthritis cells rather than osteoarthritis cells, and oxidizes the selenocysteine of the active site. The oxidation in thioredoxin reductase protein is irreversible in rheumatoid arthritis cells but not in osteoarthritis cells
-
additional information
-
2-[(1-methylpropyl)dithio]-1H-imidazole (IV-2) causes the oxidation of cysteine residues from both thioredoxin reductase and thioredoxin, with only the latter leading to irreversible inhibition of protein function
-
additional information
-
SecTRAPs (selenium compromised thioredoxin reductase-derived apoptotic proteins) can be formed from the selenoprotein thioredoxin reductase by targeting of its selenocysteine residue with electrophiles, or by its removal through C-terminal truncation. SecTRAPs are devoid of thioredoxin reductase activity but can induce rapid cell death in cultured cancer cell lines by a gain of function. Human and rat SecTRAPs induce cell death in human A549 and HeLa cells
-
additional information
black tea extract and theaflavins (mixture of theaflavin, theaflavin-3-monogallate, theaflavin-3'-monogallate and theaflavin-3,3'-digallate) inhibit the purified TrxR1 with IC50 44 mg/ml and 21 mg/ml, respectively. Kinetics of theaflavins exhibit a mixed type of competitive and non-competitive inhibition, with Kis 4 mg/ml and Kii 26 mg/ml against coenzyme NADPH, and with Kis 12 mg/ml and Kii 27 mg/ml against substrate 5,5'-dithiobis(2-nitrobenzoic acid)
-
additional information
-
not inhibited by 2-methoxycinnamaldehyde and cinnamic acid
-
additional information
-
tetrahydrocurcumin has no significant effect on TxnRd activity at doses of up to 0.05 mM
-
additional information
-
no inhibition by Ca2+ or Co2+
-
additional information
-
the enzyme is not inhibited by dimedone even at 150fold excess
-
additional information
-
quinols irreversible inhibit mammalian TrxR by targeting the penultimate C-terminal selenocysteine residue
-
additional information
SecTRAPs (selenium compromised thioredoxin reductase-derived apoptotic proteins) can be formed from the selenoprotein thioredoxin reductase by targeting of its selenocysteine residue with electrophiles, or by its removal through C-terminal truncation. SecTRAPs are devoid of thioredoxin reductase activity but can induce rapid cell death in cultured cancer cell lines by a gain of function. Human and rat SecTRAPs induce cell death in human A549 and HeLa cells
-
additional information
-
not inhibited by 2-methoxycinnamaldehyde and cinnamic acid after 1 h of incubation
-