3.4.21.76: Myeloblastin
This is an abbreviated version!
For detailed information about Myeloblastin, go to the full flat file.
Word Map on EC 3.4.21.76
-
3.4.21.76
-
ancas
-
myeloperoxidase
-
elastase
-
antineutrophil
-
autoantibody
-
anca-associated
-
cathepsin
-
pr3-anca
-
polyangiitis
-
autoimmune
-
granule
-
glomerulonephritis
-
mpo-anca
-
vasculitides
-
remission
-
autoantigens
-
anti-pr3
-
perinuclear
-
polymorphonuclear
-
cyclophosphamide
-
azurophilic
-
gpa
-
crescent
-
anti-mpo
-
anca-positive
-
lactoferrin
-
pauci-immune
-
churg-strauss
-
granulomatous
-
elafin
-
vasculitic
-
anti-myeloperoxidase
-
rituximab
-
small-vessel
-
antibody-associated
-
azurocidin
-
anti-proteinase
-
neutrophil-derived
-
polyarteritis
-
antinuclear
-
mpo-anca-associated
-
ethanol-fixed
-
goodpasture
-
drug development
-
diagnostics
-
chapel
-
medicine
-
analysis
-
nsp4
-
aspartate-specific
-
necrotising
-
nodosa
-
anti-gbm
-
anti-glomerular
- 3.4.21.76
-
ancas
- myeloperoxidase
- elastase
-
antineutrophil
- autoantibody
-
anca-associated
- cathepsin
-
pr3-anca
- polyangiitis
- autoimmune
- granule
- glomerulonephritis
-
mpo-anca
- vasculitides
-
remission
- autoantigens
- anti-pr3
-
perinuclear
-
polymorphonuclear
- cyclophosphamide
-
azurophilic
- gpa
-
crescent
-
anti-mpo
-
anca-positive
- lactoferrin
-
pauci-immune
-
churg-strauss
-
granulomatous
- elafin
-
vasculitic
-
anti-myeloperoxidase
- rituximab
-
small-vessel
-
antibody-associated
-
azurocidin
-
anti-proteinase
-
neutrophil-derived
- polyarteritis
-
antinuclear
-
mpo-anca-associated
-
ethanol-fixed
-
goodpasture
- drug development
- diagnostics
-
chapel
- medicine
- analysis
- nsp4
-
aspartate-specific
-
necrotising
- nodosa
- anti-gbm
-
anti-glomerular
Reaction
Hydrolysis of proteins, including elastin, by preferential cleavage: -Ala-/- > -Val-/- =
Synonyms
AGP7, C-ANCA antigen, hPR-3, human leukocyte proteinase 3, human PR3, human proteinase 3, Leukocyte proteinase 3, Leukocyte proteinase 4, membrane proteinase 3, membrane-associated proteinase 3, mP3, mPR3, myeloblastin, neutrophil protease PR3, neutrophil proteinase 3, neutrophil serine protease, neutrophilic serine protease proteinase 3, P29, p29b, PMNL proteinase, Pr 3, PR-3, PR3, protease 3, proteinase 3, Proteinase PR-3, Proteinase-3, proteinase3, PRTN3, SAP3, secreted aspartic proteinase 3, surface proteinase 3, Wegener autoantigen, Wegener's autoantigen, Wegener's granulomatosis autoantigen, Xenopus PR3, xPR-3
ECTree
3.4.21.76 MyeloblastinAdvanced search results
results (
results (Inhibitors
Inhibitors on EC 3.4.21.76 - Myeloblastin
Please wait a moment until all data is loaded. This message will disappear when all data is loaded.
top
INHIBITOR 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
IMAGE
(S)-4-isobutyl-2-[(p-chlorobenzylthio)methyl]-5-benzyl-1,2,5-thiadiazolidin-3-one 1,1-dioxide
-
-
(S)-4-isobutyl-2-[(phenylthio)methyl]-1,2,5-thiadiazolidin-3-one 1,1-dioxide
-
-
(S)-4-isobutyl-5-benzyl-2-chloromethyl-1,2,5-thiadiazolidin-3-one 1,1-dioxide
-
-
(S)-4-isobutyl-5-benzyl-2-[(phenylthio)methyl]-1,2,5-thiadiazolidin-3-one 1,1-dioxide
-
-
(S)-4-isobutyl-5-[(m-carboxyl)benzyl]-2-[(phenylsulfonyl)methyl]-1,2,5-thiadiazolidin-3-one 1,1-dioxide
-
-
(S)-4-isobutyl-5-[(m-carboxymethyl)benzyl]-2-[(phenylsulfonyl)methyl]-1,2,5-thiadiazolidin-3-one 1,1-dioxide
-
-
(S)-4-isobutyl-5-[(m-carboxymethyl)benzyl]-2-[(phenylthio)methyl]-1,2,5-thiadiazolidin-3-one 1,1-dioxide
-
-
(S)-4-isobutyl-N-[(4-chlorobenzylsulfonyl)methyl]-5-benzyl-1,2,5-thiadiazolidin-3-one 1,1-dioxide
-
-
1-acetyl-L-prolyl-L-tyrosyl-N-[1-[bis(4-chlorophenoxy)phosphoryl]ethyl]-L-alpha-asparagine
-
1-[11,21-dioxo-25-[(3aS,4S,6aR)-2-oxohexahydro-1H-thieno[3,4-d]imidazol-4-yl]-4,7,14,17-tetraoxa-10,20-diazapentacosanan-1-oyl]-L-prolyl-L-tyrosyl-N-[1-[bis(4-chlorophenoxy)phosphoryl]ethyl]-L-alpha-asparagine
-
1-[5-[(3aS,4S,6aR)-2-oxohexahydro-1H-thieno[3,4-d]imidazol-4-yl]pentanoyl]-L-prolyl-L-tyrosyl-N-[1-[bis(4-chlorophenoxy)phosphoryl]butyl]-L-alpha-asparagine
-
1-[5-[(3aS,4S,6aR)-2-oxohexahydro-1H-thieno[3,4-d]imidazol-4-yl]pentanoyl]-L-prolyl-L-tyrosyl-N-[1-[bis(4-chlorophenoxy)phosphoryl]ethyl]-L-alpha-asparagine
-
2,3-diethyl-5-([1-[(phenylsulfanyl)methyl]-1H-1,2,3-triazol-4-yl]methyl)-1,2,3,5-thiatriazolidin-4-one 1,1-dioxide
-
0.00862 mM inhibits by ca. 14%
2,3-diethyl-5-[[1-(2-oxo-2-phenylethyl)-1H-1,2,3-triazol-4-yl]methyl]-1,2,3,5-thiatriazolidin-4-one 1,1-dioxide
-
0.00862 mM inhibits by ca. 10%, fits into the Pr 3 active site well and engages in multiple interactions with the enzyme
2,3-diethyl-5-[[1-(4-methoxybenzyl)-1H-1,2,3-triazol-4-yl]methyl]-1,2,3,5-thiatriazolidin-4-one 1,1-dioxide
-
0.00862 mM inhibits by ca. 8%
2-(2,3-diethyl-1,1-dioxido-4-oxo-1,2,3,5-thiatriazolidin-5-yl)-N-phenylacetamide
-
0.00862 mM inhibits by ca. 13%
2-(2,3-diethyl-1,1-dioxido-4-oxo-1,2,3,5-thiatriazolidin-5-yl)-N-[2-(2-methoxyphenyl)ethyl]-3-phenylpropanamide
-
0.00862 mM inhibits by ca. 11%
2-(2,3-diethyl-1,1-dioxido-4-oxo-1,2,3,5-thiatriazolidin-5-yl)-N-[4-(morpholin-4-yl)phenyl]-3-phenylpropanamide
-
0.00862 mM inhibits by ca. 13%
4,5-bisbenzyl-2-[[(2-benzoxazolyl)thio]methyl]-1,2,5-thiadiazolidin-3-one-1,1-dioxide
-
-
4,5-bisbenzyl-2-[[(5-phenyl-1,3,4-oxadiazol-2-yl)thio]methyl]-1,2,5-thiadiazolidin-3-one-1,1-dioxide
-
-
4,5-bisbenzyl-2-[[(6-amino-2-benzoxazolyl)thio]methyl]-1,2,5-thiadiazolidin-3-one-1,1-dioxide
-
-
4-benzyl-5-methyl-2-[[(2-benzoxazolyl)thio]methyl]-1,2,5-thiadiazolidin-3-one-1,1-dioxide
-
-
4-isobutyl-5-methyl-2-[[(2-benzoxazolyl)thio]methyl]-1,2,5-thiadiazolidin-3-one-1,1-dioxide
-
-
4-isobutyl-5-methyl-2-[[(3-phenyl-1,2,4-oxadiazol-5-yl)thio]methyl]-1,2,5-thiadiazolidin-3-one-1,1-dioxide
-
-
4-isobutyl-5-methyl-2-[[(4,5-diphenyl-2-oxazolyl)thio]methyl]-1,2,5-thiadiazolidin-3-one-1,1-dioxide
-
-
4-isobutyl-5-methyl-2-[[(5-phenyl-1,3,4-oxadiazol-2-yl)thio]methyl]-1,2,5-thiadiazolidin-3-one-1,1-dioxide
-
-
4-isobutyl-5-methyl-2-[[(5-phenyl-2-benzoxazoyl)thio]methyl]-1,2,5-thiadiazolidin-3-one-1,1-dioxide
-
-
4-isobutyl-5-methyl-2-[[2-benzothiazolthio]methyl]-1,2,5-thiadiazolidin-3-one-1,1-dioxide
-
-
4-methyl-N-[5-[(3aS,4S,6aR)-2-oxohexahydro-1H-thieno[3,4-d]imidazol-4-yl]pentanoyl]-L-norleucyl-L-tyrosyl-N-[1-[bis(4-chlorophenoxy)phosphoryl]ethyl]-L-alpha-asparagine
-
5-benzyl-4-isobutyl-2-[[(2-benzoxazolyl)thio]methyl]-1,2,5-thiadiazolidin-3-one-1,1-dioxide
-
-
5-benzyl-4-isobutyl-2-[[(3-phenyl-1,2,4-oxadiazol-5-yl)thio]methyl]-1,2,5-thiadiazolidin-3-one-1,1-dioxide
-
-
5-benzyl-4-isobutyl-2-[[(4,5-diphenyl-2-oxazolyl)thio]methyl]-1,2,5-thiadiazolidin-3-one-1,1-dioxide
-
-
5-benzyl-4-isobutyl-2-[[(5-phenyl-1,3,4-oxadiazol-2-yl)thio]methyl]-1,2,5-thiadiazolidin-3-one-1,1-dioxide
-
-
5-benzyl-4-isobutyl-2-[[(5-phenyl-2-benzoxazoyl)thio]methyl]-1,2,5-thiadiazolidin-3-one-1,1-dioxide
-
-
5-benzyl-4-isobutyl-2-[[2-benzothiazolthio]methyl]-1,2,5-thiadiazolidin-3-one-1,1-dioxide
-
-
Abz-VADnV[PSI](COCH2)ADYQ-EDDnp
best inhibitor, selective for proteinase 3, displays a competitive and reversible inhibition mechanism
alpha-1-Proteinase inhibitor
inhibits the enzyme, inhibition is implicated by anti-neutrophil cytoplasmic antibodies with proteinase 3 specificity
-
alpha1-proteinase
-
does not inhibit when PR3 is bound to the outer cell surface of neutrophils
-
anti-neutrophil cytoplasmic antibodies with proteinase 3 specificity
screening: a great majority of PR3-ANCA has inhibitory capacity towards the enzyme, overview. PR3-ANCA with inhibitory properties bind to the active site surface of proteinase 3. Epitopes of inhibitory PR3-ANCA are not masked by elafin
-
biotin-Val-Tyr-Asp-NvaP(O-C6H4-4-Cl)2
occupancy of the S1 subsite of PR3 by a NVA residue and of the S4-S5 subsites by a biotinylated Val residue enhances the second-order inhibition constant toward PR3 by more than 10 times as compared to the best phosphonate PR3 inhibitor reported. The inhibitor shows no significant inhibitory activity toward human neutrophil elastase and resists proteolytic degradation in sputa from cystic fibrosis patients. It also inhibits macaque PR3 but not the PR3 from rodents
N-(1,3-benzodioxol-5-yl)-2-(2,3-diethyl-1,1-dioxido-4-oxo-1,2,3,5-thiatriazolidin-5-yl)-3-phenylpropanamide
-
0.00862 mM inhibits by ca. 23%
N-[5-[(3aS,4S,6aR)-2-oxohexahydro-1H-thieno[3,4-d]imidazol-4-yl]pentanoyl]-L-leucyl-L-tyrosyl-N-[1-[bis(4-chlorophenoxy)phosphoryl]ethyl]-L-alpha-asparagine
-
N-[5-[(3aS,4S,6aR)-2-oxohexahydro-1H-thieno[3,4-d]imidazol-4-yl]pentanoyl]-L-norleucyl-L-tyrosyl-N-[1-[bis(4-chlorophenoxy)phosphoryl]ethyl]-L-alpha-asparagine
-
N-[5-[(3aS,4S,6aR)-2-oxohexahydro-1H-thieno[3,4-d]imidazol-4-yl]pentanoyl]-L-valyl-L-tyrosyl-N-[1-[bis(4-chlorophenoxy)phosphoryl]butyl]-L-alpha-asparagine
-
N-[5-[(3aS,4S,6aR)-2-oxohexahydro-1H-thieno[3,4-d]imidazol-4-yl]pentanoyl]-L-valyl-L-tyrosyl-N-[1-[bis(4-chlorophenoxy)phosphoryl]ethyl]-L-alpha-asparagine
-
protein 3-specific MCPR3-7 antibody
the monoclonal antibody interfers with the activity of proteinase 3 by an allosteric mechanism. It can change its conformation and impair interactions with alpha1-proteinase inhibitor. The conformation of the S1 pocket of the enzyme is not changed significantly after binding of MCPR3-7, but rather the S1' subsite of the enzyme is changed
-
trappin
80% inhibition, oxidized with N-chlorosuccinimide: 19% inhibition
-
[4-[(2,3-diethyl-1,1-dioxido-4-oxo-1,2,3,5-thiatriazolidin-5-yl)methyl]-1H-1,2,3-triazol-1-yl]acetic acid
-
0.00862 mM inhibits by ca. 11%
(E)-4-(N-(2-(1-(hydroxyimino)butyl)phenyl)sulfamoyl)phenyl pivalate
-
(E)-4-(N-(2-(1-(hydroxyimino)ethyl)phenyl)sulfamoyl)phenyl pivalate
the compound has several beneficial effects in inflammatory disease and lipopolysacchride-induced edema, overview
(E)-4-(N-(2-(1-(hydroxyimino)ethyl)phenyl)sulfamoyl)phenyl pivalate
shows dual inhibitory effects on neutrophil elastase and proteinase 3. The compound significantly attenuates histological changes in lung tissue from mice with LPS-induced acute lung injury (ALI)
(E)-4-(N-(2-(1-(hydroxyimino)methyl)phenyl)sulfamoyl)phenyl pivalate
-
(E)-4-(N-(2-(1-(hydroxyimino)propyl)phenyl)sulfamoyl)phenyl pivalate
-
(E)-4-(N-(2-(1-(methoxyimino)ethyl)phenyl)sulfamoyl)phenyl pivalate
-
(Z)-4-(N-(2-(1-(methoxyimino)ethyl)phenyl)sulfamoyl)phenyl pivalate
-
4-(N-(2-(2-hydroxyethylcarbamoyl)phenyl)sulfamoyl)phenyl pivalate
-
4-(N-(2-acetylphenyl)sulfamoyl)phenyl 2-methylpropane-2-sulfinate
-
4-(N-(2-formylphenyl)sulfamoyl)phenyl 2-methylpropane-2-sulfinate
-
alpha1-antitrypsin
MeOSuc-AAPV-4-nitroanilide as substrate, 1% Triton X-100 (w/v), 20% dimethylformamide (v/v), pH 8.0, IC50 = 0.98 M
-
alpha1-antitrypsin
-
inhibition of bilayer-bound PR3 is more important than that observed for the soluble form of the enzyme
-
alpha1-antitrypsin
MeOSuc-AAPV-4-nitroanilide as substrate, 1% Triton X-100 (w/v), 20% dimethylformamide (v/v), pH 8.0, IC50 = 0.74 M
-
alpha1-protease inhibitor
-
membrane-bound Pr3 is inhibited almost as rapidly as the soluble Pr3, but inhibition is not complete after 1 h. No interaction between constitutive membrane-bound Pr3 and the inhibitor
-
alpha1-protease inhibitor
-
purified human alpha1-protease inhibitor inhibits gibbon PR3 and forms a covalently linked complex with it
-
Alpha1-proteinase inhibitor
the inhibition is highly dependent on the proper conformation of an exposed reactive center loop, which serves as a pseudosubstrate. Inhibitor mutant E342K is less effective due to an altered conformation of the reactive center loop
-
Eglin c
MeOSuc-AAPV-4-nitroanilide as substrate, 1% Triton X-100 (w/v), 20% dimethylformamide (v/v), pH 8.0, IC50 = 117 M
Eglin c
MeOSuc-AAPV-4-nitroanilide as substrate, 1% Triton X-100 (w/v), 20% dimethylformamide (v/v), pH 8.0, IC50 = 3.3 M
elafin
55% inhibition, oxidized with N-chlorosuccinimide: 10% inhibition
-
elafin
MeOSuc-AAPV-4-nitroanilide as substrate, 1% Triton X-100 (w/v), 20% dimethylformamide (v/v), pH 8.0, IC50 = 1.9 M
-
elafin
-
does not inhibit when PR3 is bound to the outer cell surface of neutrophils
-
elafin
-
membrane-bound Pr3 is inhibited almost as rapidly as the soluble Pr3, but inhibition is not complete after 1 h. No interaction between constitutive membrane-bound Pr3 and the inhibitor
-
elafin
-
is inhibited by purified human elafin, a canonical low molecular weight inhibitor of human PR3
-
elafin
MeOSuc-AAPV-4-nitroanilide as substrate, 1% Triton X-100 (w/v), 20% dimethylformamide (v/v), pH 8.0, IC50 = 0.99 M
-
ethyl 2-(4-(3,3,3-trifluoro-2,2-dimethylpropanoyloxy)benzamido)benzoate
-
MeO-Suc-AAPA-chloromethyl ketone
-
irreversible inhibitor, inhibits about 90% of the activity after 2 h. Membrane-bound Pr3 remains bound to the membrane when inhibited by the chloromethyl ketone inhibitor
methyl 2-(4-(3,3,3-trifluoro-2,2-dimethylpropanoyloxy)benzamido)benzoate
-
methyl 2-(4-(3,3,3-trifluoro-2,2-dimethylpropanoyloxy)phenylsulfonamide)benzoate
-
methyl 2-(4-(3,3,3-trifluoro-2,2-dimethylpropanoyloxy)phenylsulfonamide)benzoate
-
-
propyl 2-(4-(3,3,3-trifluoro-2,2-dimethylpropanoyloxy)benzamido)benzoate
-
sivelestat
acetylating, nonpeptidic inhibitor, sivelestat, developed for the treatment of acute lung injury (ALI )in Japan
SLPI
MeOSuc-AAPV-4-nitroanilide as substrate, 1% Triton X-100 (w/v), 20% dimethylformamide (v/v), pH 8.0, limited inhibition, more than 75% of activity remained in the presence of the highest concentration of inhibitor
SLPI
MeOSuc-AAPV-4-nitroanilide as substrate, 1% Triton X-100 (w/v), 20% dimethylformamide (v/v), pH 8.0, limited inhibition, more than 75% of activity remained in the presence of the highest concentration of inhibitor
Val15-aprotinin
MeOSuc-AAPV-4-nitroanilide as substrate, 1% Triton X-100 (w/v), 20% dimethylformamide (v/v), pH 8.0, limited inhibition, more than 75% of activity remained in the presence of the highest concentration of inhibitor
-
Val15-aprotinin
MeOSuc-AAPV-4-nitroanilide as substrate, 1% Triton X-100 (w/v), 20% dimethylformamide (v/v), pH 8.0, IC50 = 447 M
-
additional information
-
substituted isocoumarins, peptide-phosphonates and chloromethyl ketones inhibit proteinase 3 less potently than human neutrophil elastase, by 1-2 orders of magnitude
-
additional information
-
not: alpha1-anti-chymotrypsin; secretory leukocyte proteinase inhibitor
-
additional information
-
aprotinin; cysteine, aspartic, or metalloproteinase inhibitors; secretory leukocyte proteinase inhibitor
-
additional information
-
membrane-bound enzyme is resistant to inhibition by physiologic proteinase inhibitors
-
additional information
low molecular weight serine protease inhibitors, but only partially by inhibitors of larger molecular weight such as alpha1-protease inhibitor
-
additional information
-
low molecular weight serine protease inhibitors, but only partially by inhibitors of larger molecular weight such as alpha1-protease inhibitor
-
additional information
transcription of PR3 is downregulated upon granulocyte and monocyte maturation
-
additional information
-
transcription of PR3 is downregulated upon granulocyte and monocyte maturation
-
additional information
-
hydrolysis of N-methoxysuccinyl-Ala-Ala-Pro-Val-pNA by neutrophil PR3 is reduced by 40% as a result of deglycosylation
-
additional information
-
peptide-specific T-cell responses, exemplary for PRTN358 and PRTN3235, can be inhibited by anti-HLA-DR antibodies, but not by an anti-HLAABC antibody
-
additional information
synthesis and pharmacological characterization of 2-aminobenzaldehyde oxime analogues as dual inhibitors of neutrophil elastase and proteinase 3, structureactivity relationship analysis, overview
-
additional information
-
synthesis and pharmacological characterization of 2-aminobenzaldehyde oxime analogues as dual inhibitors of neutrophil elastase and proteinase 3, structureactivity relationship analysis, overview
-
additional information
design of ketomethylene-based enzyme inhibitors that show low micromolar IC50 values. Molecular dynamics simulations show that the interactions between enzyme and ketomethylene-containing inhibitors are similar to those with the corresponding substrates. N- and C-terminal FRET groups are important for securing high inhibitory potency toward the enzyme
-
additional information
-
design of ketomethylene-based enzyme inhibitors that show low micromolar IC50 values. Molecular dynamics simulations show that the interactions between enzyme and ketomethylene-containing inhibitors are similar to those with the corresponding substrates. N- and C-terminal FRET groups are important for securing high inhibitory potency toward the enzyme
-
additional information
PR3 inhibitors belong either to the group of peptide analogues (whose structure is directed by the sequence of the substrates) or to non-peptidyl inhibitors, including oxazolidine-2,4-diones, 3,1-benzoxazin-4-ones, isocoumarins, N-hydroxysuccinimides, thiatriazolidines, oximes, Kojic acid derivatives. Analysis of aminophosphonates as potent and selective PR3 inhibitors, overview. Synthesis of alpha-aminoalkylphosphonate diaryl esters. No inhibition by Pro-Tyr-Asp-AlaP(O-C6H4-4-Cl)2
-
additional information
synthesis of a series 2-aminobenzaldehyde oxime and 2-aminobenzoate analogues, their inhibitory effects on neutrophilic serine proteases (NsPs), i.e. cathepsin G, proteinase 3 (Pr3), and human neutrophil elastase (HNE), are determined. A hydroxyl oxime moiety plays an important role in ligand-enzyme affinity through hydrogen bonding, structure-activity relationships, overview. Most of the compounds have a potent and dual inhibitory effect on human neutrophil elastase and Pr3
-
additional information
-
synthesis of a series 2-aminobenzaldehyde oxime and 2-aminobenzoate analogues, their inhibitory effects on neutrophilic serine proteases (NsPs), i.e. cathepsin G, proteinase 3 (Pr3), and human neutrophil elastase (HNE), are determined. A hydroxyl oxime moiety plays an important role in ligand-enzyme affinity through hydrogen bonding, structure-activity relationships, overview. Most of the compounds have a potent and dual inhibitory effect on human neutrophil elastase and Pr3
-
additional information
potencies of peptidyl di(chlorophenyl)-phosphonate ester inhibitors, kinetics and molecular docking and modeling, overview
-
additional information
-
potencies of peptidyl di(chlorophenyl)-phosphonate ester inhibitors, kinetics and molecular docking and modeling, overview
-
