3.4.24.83: anthrax lethal factor endopeptidase
This is an abbreviated version!
For detailed information about anthrax lethal factor endopeptidase, go to the full flat file.
Word Map on EC 3.4.24.83
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3.4.24.83
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edema
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spore
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intoxication
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endosomal
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exotoxin
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metalloprotease
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inhalation
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inflammasome
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endocytosis
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toxin-induced
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anti-pa
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heptameric
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caspase-1
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sterne
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furin
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mapkks
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lt-induced
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tripartite
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diphtheria
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toxin-mediated
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spore-forming
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pyroptosis
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toxemia
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ring-shaped
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receptor-bound
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toxin-neutralizing
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zinc-dependent
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molecular biology
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cytolysis
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pa-binding
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medicine
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mkk
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bioterrorism
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diagnostics
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toxin-sensitive
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synthesis
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postexposure
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cell-binding
- 3.4.24.83
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edema
- spore
-
intoxication
- endosomal
-
exotoxin
- metalloprotease
-
inhalation
- inflammasome
-
endocytosis
-
toxin-induced
-
anti-pa
-
heptameric
- caspase-1
- sterne
- furin
- mapkks
-
lt-induced
-
tripartite
- diphtheria
-
toxin-mediated
-
spore-forming
-
pyroptosis
- toxemia
-
ring-shaped
-
receptor-bound
-
toxin-neutralizing
-
zinc-dependent
- molecular biology
-
cytolysis
-
pa-binding
- medicine
- mkk
-
bioterrorism
- diagnostics
-
toxin-sensitive
- synthesis
-
postexposure
-
cell-binding
Reaction
Preferred amino acids around the cleavage site can be denoted BBBBxHx-/-H, in which B denotes Arg or Lys, H denotes a hydrophobic amino acid, and x is any amino acid. The only known protein substrates are mitogen-activated protein (MAP) kinase kinases =
Synonyms
anthrax lethal factor, anthrax lethal factor protease, anthrax lethal toxin, anthrax LF, anthrax toxin lethal factor, Bacillus anthracis lethal toxin, lethal factor, lethal factor of anthrax toxin, lethal toxin, LeTx, LF, LTx
ECTree
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Inhibitors
Inhibitors on EC 3.4.24.83 - anthrax lethal factor endopeptidase
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(1E,6E)-4-(1,3-dithian-2-ylidene)-1,7-difuran-2-ylhepta-1,6-diene-3,5-dione
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(1Z,6E)-4-(1,3-dithian-2-ylidene)-1,7-difuran-2-ylhepta-1,6-diene-3,5-dione
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(2R)-2-[(4-fluoro-3-methoxybenzene-1-sulfonyl)(2-methylpropyl)amino]-N-hydroxy-3-methylbutanamide
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(2R)-2-[(4-fluoro-3-methylbenzene-1-sulfonyl)(2-methylpropyl)amino]-N-hydroxy-3-methylbutanamide
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(2R)-2-[(4-fluoro-3-methylbenzene-1-sulfonyl)[(4-nitrophenyl)methyl]amino]-N-hydroxypropanamide
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(2R)-N4-hydroxy-N1-[(2S)-3-(1H-indol-3-yl)-1-(methylamino)-1-oxopropan-2-yl]-2-(2-methylpropyl)butanediamide
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inhibitor identified by in silico high-throughput virtual screening protocol
(2S)-2-(3,4-dichlorophenyl)-N-hydroxy-3-(3-methylphenyl)propanamide
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(2S)-2-(4-fluoro-3,5-dimethylbenzyl)-6-[[1-(4-fluorophenyl)propyl]amino]-N-hydroxyhexanamide
i.e. PT-8541
(2S)-2-[(2R)-2-(4-fluorophenyl)-2-methoxyethyl]-6-[[1-(4-fluorophenyl)propyl]amino]-N-hydroxyhexanamide
i.e. PT-8420
(2S)-6-[(1R)-N-1-(4-fluorophenyl)propan]aminoamino-2-(4-fluoro-3,5-dimethylbenzyl)-N-hydroxyhexanamide
inhibitor provides protection against lethal infection when administered as a monotherapy. Two doses (10 mg/kg) administered at 2 h and 8 h after spore infection are sufficient to provide a significant survival benefit in infected mice
(2S)-6-[(4-fluorobenzyl)amino]-2-[(2R)-2-(4-fluorophenyl)-2-methoxyethyl]-N-hydroxyhexanamide
i.e. LFI4
(2S)-6-[N-1-(4-fluorophenyl)propan]amino-2-[(2R)-2-(4-fluorophenyl)-2-methoxyethyl]-N-hydroxyhexanamide
inhibitor provides protection against lethal infection when administered as a monotherapy. Two doses (10 mg/kg) administered at 2 h and 8 h after spore infection are sufficient to provide a significant survival benefit in infected mice
(3S)-N-hydroxy-4-methyl-3-([[(2R)-1-(methylamino)-1-oxo-4-phenylbutan-2-yl]amino]methyl)pentanamide
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inhibitor identified by in silico high-throughput virtual screening protocol
(5E)-5-(1,3-benzothiazol-2-ylimino)-1-(4-sulfophenyl)-4,5-dihydro-1H-pyrazole-3-carboxylic acid
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(5Z)-3-(4-hydroxyphenyl)-5-[[5-(4-nitrophenyl)furan-2-yl]methylidene]-2-thioxo-1,3-thiazolidin-4-one
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(5Z)-3-(4-methoxyphenyl)-2-thioxo-5-([5-[3-(trifluoromethyl)phenyl]furan-2-yl]methylidene)-1,3-thiazolidin-4-one
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(5Z)-3-(furan-2-ylmethyl)-5-[[5-(3-nitrophenyl)furan-2-yl]methylidene]-2-thioxo-1,3-thiazolidin-4-one
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(5Z)-3-(furan-2-ylmethyl)-5-[[5-(4-nitrophenyl)furan-2-yl]methylidene]-2-thioxo-1,3-thiazolidin-4-one
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(5Z)-5-[[5-(2-nitrophenyl)furan-2-yl]methylidene]-3-(2-phenylethyl)-2-thioxo-1,3-thiazolidin-4-one
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(5Z)-5-[[5-(3,4-dichlorophenyl)furan-2-yl]methylidene]-2-thioxo-1,3-thiazolidin-4-one
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(5Z)-5-[[5-(4-bromo-3-chlorophenyl)furan-2-yl]methylidene]-2-thioxo-1,3-thiazolidin-4-one
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(5Z)-5-[[5-(4-chlorophenyl)furan-2-yl]methylidene]-3-(furan-2-ylmethyl)-2-thioxo-1,3-thiazolidin-4-one
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(5Z)-5-[[5-(4-fluorophenyl)furan-2-yl]methylidene]-3-prop-2-en-1-yl-2-thioxo-1,3-thiazolidin-4-one
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1,4-dihydroxy-10-methoxy-5,8-dimethyl-3,7-dioxo-1,3-dihydro-7H-2,6,12-trioxabenzo[5,6]cyclohepta[1,2-e]indene-11-carbaldehyde
i.e. stictic acid
1-[(1S,2R,3S,4S,6S)-2-amino-6-[(6-amino-2,6-dideoxy-a-D-arabino-hexopyranosyl)oxy]-3,4-dihydroxycyclohexyl]guanidine
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1-[([1,1'-biphenyl]-4-yl)methyl]-3-hydroxy-2-methylpyridine-4(1H)-thione
i.e. 94G5
2-([benzyl(ethyl)amino]methyl)-6-iodo-4-methylphenol
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inhibitor identified by in silico high-throughput virtual screening protocol
2-chloro-4-(5-[(Z)-[(3-cyano-4,5,6,7-tetrahydro-1-benzothiophen-2-yl)imino]methyl]furan-2-yl)benzoic acid
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2-chloro-4-(5-[(Z)-[4-oxo-3-(pyridin-3-ylmethyl)-2-thioxo-1,3-thiazolidin-5-ylidene]methyl]furan-2-yl)benzoic acid
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2-chloro-4-[5-[(Z)-(4-oxo-3-prop-2-en-1-yl-2-thioxo-1,3-thiazolidin-5-ylidene)methyl]furan-2-yl]benzoic acid
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2-chloro-4-[[(4Z)-4-[[4-(methylsulfanyl)phenyl]methylidene]-5-oxo-2-phenyl-4,5-dihydro-1H-imidazol-1-yl]sulfamoyl]benzoic acid
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2-chloro-5-[(4Z)-3-methyl-4-[[4-(1-methylethyl)phenyl]methylidene]-5-oxo-4,5-dihydro-1H-pyrazol-1-yl]benzoic acid
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2-chloro-5-[(4Z)-4-[[5-(4-chlorophenyl)furan-2-yl]methylidene]-3-methyl-5-oxo-4,5-dihydro-1H-pyrazol-1-yl]benzoic acid
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2-chloro-5-[[(4Z)-4-[[4-(methylsulfanyl)phenyl]methylidene]-5-oxo-2-phenylimidazolidin-1-yl]sulfamoyl]benzoic acid
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2-hydroxy-5-(5-[(Z)-[2-imino-4-oxo-3-(1,3-thiazol-2-yl)-1,3-thiazolidin-5-ylidene]methyl]furan-2-yl)benzoic acid
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2-hydroxy-5-[5-[(Z)-[2-imino-3-[imino(methylsulfanyl)methyl]-4-oxo-1,3-thiazolidin-5-ylidene]methyl]furan-2-yl]benzoic acid
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2-[[(2-amino-2-carboxyethyl)sulfanyl]methyl]-5-phenylfuran-3-carboxylic acid
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3,4-dihydroxy-N'-[(1Z)-(2-hydroxy-5-nitrophenyl)methylidene]benzohydrazide
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3-(5-[(Z)-[1-(3-chlorophenyl)-3,5-dioxopyrazolidin-4-ylidene]methyl]furan-2-yl)benzoic acid
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3-(benzyloxy)-1-(3,4-dichlorobenzene-1-sulfonyl)-N-hydroxypyrrolidine-2-carboxamide
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3-(N-hydroxycarboxamido)-2-isobutylpropanoyl-Trp-methylamide
inhibitor used for structure-based pharmacopore model
3-[(5E)-5-[(3-bromo-4-methoxyphenyl)methylidene]-4-oxo-2-thioxo-1,3-thiazolidin-3-yl]propanoic acid
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3-[(5Z)-5-[(3-bromo-4-methoxyphenyl)methylidene]-4-oxo-2-thioxo-1,3-thiazolidin-3-yl]propanoic acid
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3-[(5Z)-5-[[5-(2-nitrophenyl)furan-2-yl]methylidene]-4-oxo-2-thioxo-1,3-thiazolidin-3-yl]propanoic acid
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3-[(5Z)-5-[[5-(4-chlorophenyl)furan-2-yl]methylidene]-4-oxo-2-thioxo-1,3-thiazolidin-3-yl]propanoic acid
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3-[(5Z)-5-[[5-(4-nitrophenyl)furan-2-yl]methylidene]-4-oxo-2-thioxo-1,3-thiazolidin-3-yl]propanoic acid
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4-(5-[(Z)-[3-(4-nitrophenyl)-4-oxo-2-thioxo-1,3-thiazolidin-5-ylidene]methyl]furan-2-yl)benzoic acid
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4-methyl-N-[(1R)-1-[5-(naphthalen-1-yl)-2-(prop-2-en-1-yl)tetrahydrofuran-3-yl]ethyl]benzenesulfonamide
i.e. SM157, non-competitive inhibition
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4-phenylaminocarbonylbis-demethoxycurcumin
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inhibitory potency is comparable with curcumin, while showing improved solubility and stability
4-[(5Z)-5-[[5-(3-nitrophenyl)furan-2-yl]methylidene]-4-oxo-2-thioxo-1,3-thiazolidin-3-yl]butanoic acid
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4-[(5Z)-5-[[5-(4-bromophenyl)furan-2-yl]methylidene]-4-oxo-2-thioxo-1,3-thiazolidin-3-yl]butanoic acid
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4-[5-[(E)-(5-cyano-2-hydroxy-4-methyl-6-oxopyridin-3(6H)-ylidene)methyl]furan-2-yl]benzenesulfonamide
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4-[5-[(Z)-(3-benzyl-4-oxo-2-thioxo-1,3-thiazolidin-5-ylidene)methyl]furan-2-yl]benzoic acid
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4-[5-[(Z)-[4-oxo-2-thioxo-3-[3-(trifluoromethyl)phenyl]-1,3-thiazolidin-5-ylidene]methyl]furan-2-yl]benzoic acid
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4-[[(4-chlorophenyl)carbamoyl]amino]-N-(5-ethyl-1,3,4-thiadiazol-2-yl)benzenesulfonamide
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5-(4-carboxy-3-chlorophenyl)-2-[(Z)-[(3-cyano-4,5,6,7-tetrahydro-1-benzothiophen-2-yl)imino]methyl]furan-3-carboxylic acid
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5-bromo-2-(5-[(Z)-[1-(3-carboxyphenyl)-5-oxo-3-(trifluoromethyl)-1,5-dihydro-4H-pyrazol-4-ylidene]methyl]furan-2-yl)benzoic acid
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5-bromo-2-(5-[(Z)-[1-(3-carboxyphenyl)-5-oxo-3-(trifluoromethyl)-1,5-dihydro-4H-pyrazol-4-ylidene]methyl]uran-2-yl)benzoic acid
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5-chloro-2-[5-[(E)-(1,5-dioxo-6,7,8,9-tetrahydro-5H-[1]benzothieno[3,2-e][1,3]thiazolo[3,2-a]pyrimidin-2(1H)-ylidene)methyl]furan-2-yl]benzoic acid
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5-[4-[(E)-2-[(2R,3R,3'R)-3'-(3,5-dihydroxyphenyl)-6'-hydroxy-2,2'-bis(4-hydroxyphenyl)-2,2',3,3'-tetrahydro-3,4'-bi-1-benzofuran-5-yl]ethenyl]-6-hydroxy-2-(3-hydroxyphenyl)-2,3-dihydro-1-benzofuran-3-yl]benzene-1,3-diol
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8-[(E)-[[4-(2,3-dihydro-1,3-thiazol-2-ylsulfamoyl)phenyl]imino]methyl]-4H-1,3-benzodioxine-6-carboxylic acid
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C-terminal dimer of the protective antigen binding domain of anthrax lethal factor
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C-terminal trimer of the protective antigen binding domain of anthrax lethal factor
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celastrol
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celastrol, a quinine methide triterpene derived from a plant extract used in herbal medicine, inhibits lethal toxin-induced death of RAW264.7 murine macrophages. Celastrol does not prevent cleavage of mitogen activated protein kinase kinase 1. Celastrol confers almost complete protection when it is added up to 1.5 h after intoxication, indicating that it can rescue cells in the late stages of intoxication. Celastrol inhibits the proteasome-dependent degradation of proteins in RAW264.7 cells. Celastrol blocks stimulation of IL-18 processing, indicating that celastrol acts upstream of inflammasome activation
curcumin
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inhibits by both decreasing catalytic capacity and increasing substrate affinity
fluvastatin
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statins attenuate lethal factor action action. statin treatment maintains macrophage cell viability above 60% of untreated control cells even after 9 h of lethal toxin treatment. Statins decrease mitogen-activated protein kinase cleavage
In2LF
i.e. Ac-Gly-Tyr-betaAla-(L-Arg)8-Val-Leu-Arg-CONHOH, competitive inhibitor
mevastatin
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statins attenuate lethal factor action action. statin treatment maintains macrophage cell viability above 60% of untreated control cells even after 9 h of lethal toxin treatment. Statins decrease mitogen-activated protein kinase cleavage
N'1,N'4-bis[(1E)-(2-hydroxy-5-methylphenyl)methylidene]benzene-1,4-dicarbohydrazide
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N'1-[(1E)-(2-hydroxyphenyl)methylidene]-N'4-[(1Z)-(2-hydroxyphenyl)methylidene]benzene-1,4-dicarbohydrazide
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N'1-[(1E)-(5-fluoro-2-hydroxyphenyl)methylidene]-N'4-[(1Z)-(5-fluoro-2-hydroxyphenyl)methylidene]benzene-1,4-dicarbohydrazide
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N,N''',N'''''',N'''''''''-[[(1R,3S,4S,6R)-4,6-dicarbamimidamidocyclohexane-1,3-diyl]bis(oxybenzene-1,2,4-triyl)]tetraguanidine
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N,N'''-[(1R,3S)-4-(2,4-dicarbamimidamidonaphthalen-1-yl)-6-hydroxycyclohexane-1,3-diyl]diguanidine
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N,N'''-[(1R,3S)-4-(2-amino-1H-benzimidazol-7-yl)-6-hydroxycyclohexane-1,3-diyl]diguanidine
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N,N'''-[(1R,3S,4R,5R,6S)-4-[(2,6-dicarbamimidamido-2,6-dideoxy-a-D-glucopyranosyl)oxy]-5,6-dihydroxycyclohexane-1,3-diyl]diguanidine
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N,N'''-[(1R,3S,4R,6R)-4-(2-carbamimidamidophenyl)-6-hydroxycyclohexane-1,3-diyl]diguanidine
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N,N'''-[(1R,3S,4R,6R)-4-(4-carbamimidamidonaphthalen-1-yl)-6-hydroxycyclohexane-1,3-diyl]diguanidine
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N,N'''-[(1R,3S,4R,6R)-4-(4-carbamimidamidophenyl)-6-hydroxycyclohexane-1,3-diyl]diguanidine
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N,N'''-[(1R,3S,4S,6R)-4-(3-carbamimidamidopyridin-2-yl)-6-hydroxycyclohexane-1,3-diyl]diguanidine
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N,N'''-[(1R,3S,4S,6R)-4-(5-carbamimidamidopyridin-2-yl)-6-hydroxycyclohexane-1,3-diyl]diguanidine
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N,N'''-[(1S,2R,3S,4S,6S)-6-[(6-amino-2-carbamimidamido-2,6-dideoxy-a-D-glucopyranosyl)oxy]-3,4-dihydroxycyclohexane-1,2-diyl]diguanidine
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N,N'''-[4-[(1R,2S,4R,5R)-2,4-dicarbamimidamido-5-hydroxycyclohexyl]benzene-1,3-diyl]diguanidine
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N,N'-bis(4-amino-2-methylquinolin-6-yl)urea
i.e. NSC12155, competitive inhibition
N-2-benzyl-N-2-[(4-fluoro-3-methylphenyl)sulfonyl]-N-hydroxy-D-alaninamide
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N-2-[4-(aminomethyl)benzyl]-N-2-[(4-fluoro-3-methylphenyl)sulfonyl]-N-hydroxy-D-alaninamide
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N-hydroxy-N2-[[3-(methoxymethyl)phenyl]sulfonyl]-N2-(2-methylpropyl)-D-valinamide
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N-terminal dimer of the protective antigen binding domain of anthrax lethal factor
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N-terminal trimer of the protective antigen binding domain of anthrax lethal factor
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N-[([1,1'-biphenyl]-4-yl)methyl]-3-hydroxy-4-sulfanylidene-4H-pyran-2-carbothioamide
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N-[([1,1'-biphenyl]-4-yl)methyl]-3-hydroxy-6-methyl-4-sulfanylidene-4H-pyran-2-carboxamide
i.e. AM-2S
N-[3-(1,3-benzothiazol-2-yl)-4-methylthiophen-2-yl]-4-chlorobenzene-1-sulfonamide
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N-[3-(1,3-benzothiazol-2-yl)thiophen-2-yl]-4'-methoxy[1,1'-biphenyl]-4-sulfonamide
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N2-[(4-fluoro-3-methylphenyl)sulfonyl]-N-hydroxy-N-2-(4-nitrobenzyl)-D-alaninamide
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NH4Cl
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blocks mitogen-activated protein kinase kinase 3 proteolysis in anthrax lethal toxin-treated macrophages
simvastatin
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statins attenuate lethal factor action action. statin treatment maintains macrophage cell viability above 60% of untreated control cells even after 9 h of lethal toxin treatment. Statins decrease mitogen-activated protein kinase cleavage
verapamil
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blocks mitogen-activated protein kinase kinase 3 proteolysis in anthrax lethal toxin-treated macrophages
[(5Z)-5-([5-[2-chloro-5-(trifluoromethyl)phenyl]furan-2-yl]methylidene)-4-oxo-2-thioxo-1,3-thiazolidin-3-yl]acetic acid
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[(5Z)-5-[[5-(2-nitrophenyl)furan-2-yl]methylidene]-4-oxo-2-thioxo-1,3-thiazolidin-3-yl]acetic acid
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[(5Z)-5-[[5-(3,4-dichlorophenyl)furan-2-yl]methylidene]-4-oxo-2-thioxo-1,3-thiazolidin-3-yl]acetic acid
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[(5Z)-5-[[5-(3-chloro-4-methoxyphenyl)furan-2-yl]methylidene]-4-oxo-2-thioxo-1,3-thiazolidin-3-yl]acetic acid
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[(5Z)-5-[[5-(3-chloro-4-sulfamoylphenyl)furan-2-yl]methylidene]-4-oxo-2-thioxo-1,3-thiazolidin-3-yl]acetic acid
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[(5Z)-5-[[5-(3-nitrophenyl)furan-2-yl]methylidene]-4-oxo-2-thioxo-1,3-thiazolidin-3-yl]acetic acid
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[(5Z)-5-[[5-(4-bromophenyl)furan-2-yl]methylidene]-4-oxo-2-thioxo-1,3-thiazolidin-3-yl]acetic acid
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[(5Z)-5-[[5-(4-chloro-2-nitrophenyl)furan-2-yl]methylidene]-4-oxo-2-thioxo-1,3-thiazolidin-3-yl]acetic acid
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[(5Z)-5-[[5-(4-chlorophenyl)furan-2-yl]methylidene]-4-oxo-2-thioxo-1,3-thiazolidin-3-yl]acetic acid
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[(5Z)-5-[[5-(4-iodophenyl)furan-2-yl]methylidene]-4-oxo-2-thioxo-1,3-thiazolidin-3-yl]acetic acid
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[4-[(5Z)-5-(furan-2-ylmethylidene)-4-oxo-2-thioxo-1,3-thiazolidin-3-yl]phenyl]acetic acid
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i.e. L915
(2R)-2-[(4-fluoro-3-methylbenzene-1-sulfonyl)amino]-N-hydroxy-2-(oxan-4-yl)acetamide
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peptides that can block toxin assembly. Minimal peptide sequence TYWWLD can be used to develop potent polyvalent inhibitors of anthrax toxin
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additional information
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complete caspase-1 inhibition is required to block antrax lethal toxin-mediated necrosis
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additional information
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Ca2+-free medium completely prevents mitogen-activated protein kinase kinase 3 proteolysis in anthrax lethal toxin-treated macrophages
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additional information
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statin-mediated effects on lethal toxin action are attributable to disruption of Rho GTPases. The Rho GTPase-inactivating toxin, toxin B, does not significantly affect lethal toxin binding or internalization, suggesting that the Rho GTPases regulate trafficking and/or localization of lethal toxin once internalized
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additional information
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fusion protein of N-terminal 27 amino acids deletion of protective antigen-binding domain of anthrax lethal factor Delta27LFn and protective antigen-binding domain of edema factor is a 62-fold more potent toxin inhibitor than protective antigen-binding domain of anthrax lethal factor or protective antigen-binding domain of edema factor in a cell model of intoxication, and this increased activity corresponds to a 39-fold higher protective antigen-binding affinity by Biacore analysis. The fusion protein can protect the highly susceptible Fischer 344 rats from anthrax lethal toxin challenge
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additional information
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micromolar-level anthrax lethal factor inhibition can be attained by compounds with non-hydroxamate zinc-binding groups that exhibit monodentate zinc chelation as long as key hydrophobic interactions with at least two anthrax lethal factor subsites are retained
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