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Enzyme Nomenclature
Information on EC 3.4.24.11 - neprilysin
for references in articles please use BRENDA:EC3.4.24.11
Word Map on EC 3.4.24.11
- 3.4.24.11
- angiotensin
-
natriuretic
- phosphoramidon
- renal
-
angiotensin-converting
- atrial
- thiorphan
- alzheimer
-
amyloid
- hypertension
-
aminopeptidase
-
neuropeptides
- bradykinin
- cardiovascular
- airway
-
opioids
-
endothelins
- captopril
-
tachykinins
-
abeta
-
vasoactive
- metallopeptidase
-
endothelin-converting
-
neurokinin
-
dipeptidyl
- capsaicin
-
renin-angiotensin-aldosterone
-
renin-angiotensin
- naloxone
-
conscious
-
endopeptidases
- bestatin
-
kinin
-
bronchoconstriction
- enalapril
- valsartan
-
diuresis
-
insulin-degrading
-
kininase
-
vasoconstrictor
- lisinopril
-
hfref
- met-enkephalin
-
bronchoconstrictors
-
3.4.15.1
- amastatin
-
angiotensin-1-7
-
lily
-
enzyme-1
- angioedema
- pharmacology
- molecular biology
- medicine
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The expected taxonomic range for this enzyme is: Eukaryota, Bacteria
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EC NUMBER 
COMMENTARY 
3.4.24.11
-
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RECOMMENDED NAME
GeneOntology No.
neprilysin
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REACTION
REACTION DIAGRAM
COMMENTARY
ORGANISM
UNIPROT
LITERATURE
preferential cleavage of polypeptides between hydrophobic residues, particularly with Phe or Tyr at P1'
-
-
-
-
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REACTION TYPE
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
hydrolysis of peptide bond
hydrolysis of peptide bond
-
-
endopeptidase; peptides, endopeptidase
-
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CAS REGISTRY NUMBER
COMMENTARY
82707-54-8
-
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ORGANISM
COMMENTARY
LITERATURE
UNIPROT
SEQUENCE DB
SOURCE
-
667149, 697782, 709710, 81608, 81609, 81610, 81623, 81625, 81627, 81628, 81630, 81631, 81632, 81633, 81634, 81635, 81636, 81643, 81644
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-
-
665146, 667485, 668277, 669935, 669988, 670407, 670479, 670735, 685448, 685866, 688516, 688534, 688546, 688557, 689382, 695993, 699653, 699683, 699695, 699967, 700415, 708333, 709162, 709710, 709757, 709761, 709805, 710107, 710522, 717346, 718018, 81603, 81604, 81605, 81606, 81607, 81609, 81612, 81613, 81614, 81616, 81618, 81642, 81643, 81644, 81646, 81648, 81649
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-
-
Uniprot
-
31018, 667856, 669913, 669936, 669945, 681904, 687524, 695460, 696023, 700419, 700436, 708427, 709107, 710357, 710623, 717067, 717699, 81639, 81644, 81646
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-
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GENERAL INFORMATION
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
evolution
malfunction
metabolism
physiological function
additional information
evolution
-
neprilysin is a plasma membrane glycoprotein of the neutral zinc metalloendopeptidase family
evolution
-
neprilysin is a zinc metalloendopeptidase belonging to the M13 family
evolution
-
neprilysin is a zinc metalloendopeptidase belonging to the M13 family
evolution
-
neprilysin is a zinc metalloendopeptidase belonging to the M13 family
evolution
-
the enzyme is a member of the M13 subgroup of the zinc-dependent endopeptidase family
evolution
-
the enzyme harbors an ectodomain, which contains the catalytic site and belongs to the M13 family of peptidases/proteases
malfunction
-
the role of NEP in neuropathy related to either insulin-deficient diabetes or diet-induced obesity using NEP deficient (-/-) mice is explored. Glucose disposal is impaired in both C57Bl/6 and NEP -/- mice fed a high fat diet. Thermal hypoalgesia and nerve conduction slowing are present in both streptozotocin-diabetic and high fat fed C57Bl/6 mice but not in NEP -/- mice exposed to either streptozotocin-induced diabetes or a high fat diet
malfunction
-
following overexpression of neprilysin using an adenovirus encoding neprilysin islet amyloid deposition and beta-cell apoptosis both decrease by 79%
malfunction
-
amyloid-beta concentrations are elevated in the brains of NEP knockout mice at all investigated age groups, but immunohistochemical analysis using monoclonal antibodies do not detect any amyloid-beta deposits even in old NEP knockout mice. Tests of learning and memory reveal that the ability to learn is not reduced in old NEP-deficient mice but instead have significantly improved. Data suggests a beneficial effect of pharmacological inhibition of cerebral NEP on learning and memory in mice due to the accumulation of peptides other than amyloid-beta degradable by NEP
malfunction
-
in NEP/NEP2 double-knockout mice, amyloid-beta peptide levels are marginally increased (1.5 to 2fold), compared with NEP-/-/NEP2+/+ controls. Treatment of these double-knockout mice with phosphoramidon results in elevations of amyloid-beta peptide, suggesting that yet other NEP-like amyloid-beta peptide -degrading endopeptidases are contributing to amyloid-beta peptide catabolism
malfunction
-
enzyme inhibition augmentes the maximum hemodynamic effects of pulmonary vasodilation by pulmonary vasodilative vasoactive intestinal peptide, VIP, aerosol, and also leads to a significant prolongation of these effects
malfunction
-
treatment of cells with TPI2155-14 and TPI2155-17, specific inhibitors for ADAM-17 protease, EC 3.4.24.86, results in a significant decrease in neprilysin activity in media, implicating a possible role for ADAM-17 in neprilysin release
malfunction
-
application of inhibitors to NEP in mouse brain produced dramatic elevations of endogenous amyloid beta peptide resulting in plaque deposition. But enzyme knockout mice show only a moderate increase in amyloid beta levels that are far from the levels needed to induce plaque deposition. This modest increase in amyloid beta peptide raises the possibility of alternative amyloid beta degrading-enzymes that are likewise sensitive to NEP-inhibitors
malfunction
-
application of inhibitors to NEP in rat brain produced dramatic elevations of endogenous amyloid beta peptide resulting in plaque deposition
malfunction
-
inhibitor N-phenethylphosphonyl-L-leucyl-L-tryptophane-treated mouse skin elastic fibers surrounding early anagen hair cycle phase hair bulbs seem to accumulate more than in vehicle-treated mouse skin
metabolism
-
the non-membrane bound form of neprilysin with catalytic activity has the potential to cleave substrates throughout the blood circulation with systemic effects. A likely role of exosomes and protease ADAM-17 in release of the enzyme, overview
metabolism
-
neprilysin-2 (NEP2), a NEP-like endopeptidase, cooperates with neprilysin (NEP) to control amyloid-beta peptide levels in the brain
metabolism
-
neprilysin-2 (NEP2), a NEP-like endopeptidase, cooperates with neprilysin (NEP) to control amyloid-beta peptide levels in the brain
metabolism
-
neprilysin-2 (NEP2), a NEP-like endopeptidase, cooperates with neprilysin (NEP) to control amyloid-beta peptide levels in the brain
physiological function
-
neprilysin decreases islet amyloid deposition by inhibiting human islet amyloid polypeptide fibril formation, rather than degrading human islet amyloid polypeptide
physiological function
-
inhibition of NEP by the opiorphin homologs influence the physiology of a wide variety of tissues by causing extended binding time of peptide agonists to their receptors such as G-protein-coupled receptors (GPCRs)
physiological function
-
inhibition of NEP by the opiorphin homologs influence the physiology of a wide variety of tissues by causing extended binding time of peptide agonists to their receptors such as G-protein-coupled receptors (GPCRs)
physiological function
-
CD10, a cell-surface neutral endopetidase, is involved in the maintenance of homeostasis, in neoplastic transformation, and in tumor progression through the enzymatic inactivation of bioactive peptides. CD10 is suggested to function as a tumor-suppressor gene, and to inactivate neuropeptide growth factors implicated in cancer progression; molecular interactions between arsenic microcrystals and membrane-bound CD10 to be implicated in arsenic-induced carcinogenesis
physiological function
-
a genetic case-control association study is performed investigating GT-repeat polymorphism in the NEP promoter region as well as 18 tag-SNPs in six linkage disequilibrium blocks in the NEP gene region in a large sample of complex regional pain syndrome patients. No significant genetic association is observed
physiological function
-
the enzyme inhibits the pulmonary vasodilation by pulmonary vasodilative vasoactive intestinal peptide, VIP, in lungs of subjects with pathophysiology of pulmonary hypertension (due to a deficiency in VIP) by rapid inactivation of VIP
physiological function
-
amyloid beta-induced death of hippocampal neuron of APP/PS1 mice is inhibited by human recombinant soluble enzyme, overview
physiological function
-
neprilysin is a neutral endopeptidase, is one of the major amyloid beta-degrading enzymes in the brain
physiological function
-
the role of neprilysin in regulating the hair cycle, a cyclic process of growing, regressing and resting phases, i.e. anagen, catagen, and telogen, respectively. The enzyme degrades elastin, which is associated with skin elasticity
physiological function
-
the role of neprilysin in regulating the hair cycle, a cyclic process of growing, regressing and resting phases, i.e. anagen, catagen, and telogen, respectively. The enzyme degrades elastin, which is associated with skin elasticity
physiological function
-
the role of neprilysin in regulating the hair cycle, a cyclic process of growing, regressing and resting phases, i.e. anagen, catagen, and telogen, respectively. The enzyme degrades elastin, which is associated with skin elasticity
physiological function
-
the enzyme degrades a number of physiological peptides that are involved in processes such as blood pressure regulation and nociception
additional information
-
protein-ligand docking calculations predict S2' subsite residues Arg102 and Arg110 of the enzyme to participate in specific interactions with amyloid beta peptide and are a target for modification of the enzyme for higher specificity against amyloid beta peptide
additional information
-
protease activities of the mature form of the enzyme do not differ between lipid rafts and nonlipid rafts. Cholesterol and other lipids regulate the localization of mature enzyme to lipid rafts, where the substrate amyloid beta peptide accumulates but does not modulate the protease activity of the enzyme
additional information
-
the enzyme is composed of an ectodomain, which contains the catalytic site, a transmembrane domain and a short intracellular domain. The structure of the ectodomain is composed of two largely alpha-helical domains that are arranged to form a central spherical water-filled core that contains the active site of the enzyme
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SUBSTRATE
PRODUCT
REACTION DIAGRAM
ORGANISM
UNIPROT
COMMENTARY
(Substrate)
(Substrate)
LITERATURE
(Substrate)
(Substrate)
COMMENTARY
(Product)
(Product)
LITERATURE
(Product)
(Product)
Reversibility
r=reversible
ir=irreversible
?=not specified
r=reversible
ir=irreversible
?=not specified
(7-methoxycoumarin-4-yl)acetyl-Arg-Pro-Pro-Gly-Phe-Ser-Ala-Phe-Lys-(2,4-dinitrophenyl) + H2O
(7-methoxycoumarin-4-yl)acetyl-Arg-Pro-Pro-Gly-Phe-Ser-Ala + Phe-Lys-(2,4-dinitrophenyl)
-
bradykinin-based quenched fluorescent substrate assay
-
-
?
2-aminobenzoyl-ARFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-AR + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-DRFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-DR + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-FRFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-FR + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-HRFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-HR + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-IRFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-IR + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-KRFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-KR + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-LRFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-LR + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-NRFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-NR + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-RAFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-RA + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-RDFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-RD + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-REFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-RE + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-rGF-N-(2,4-dinitrophenyl)ethylenediamine + H2O
2-aminobenzoyl-D-Arg-Gly + Phe-N-(2,4-dinitrophenyl)ethylenediamine
-
-
-
-
ir
2-aminobenzoyl-RGFK(Dnp)-OH + H2O
2-aminobenzoyl-RG + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-RGFK-2,4-dinitrophenyl amide + H2O
2-aminobenzoyl-RG + FK-2,4-dinitrophenyl amide
-
-
-
-
ir
2-aminobenzoyl-RGFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-RG + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-rGL-N-(2,4-dinitrophenyl)ethylenediamine + H2O
2-aminobenzoyl-D-Arg-Gly + Leu-N-(2,4dinitrophenyl)ethylenediamine
-
-
-
-
ir
2-aminobenzoyl-rGV-N-(2,4-dinitrophenyl)ethylenediamine + H2O
2-aminobenzoyl-D-Arg-Gly + Val-N-(2,4-dinitrophenyl)ethylenediamine
-
-
-
-
ir
2-aminobenzoyl-RHFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-RH + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-RKFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-RK + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-RNFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-RN + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-RPFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-RP + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-RQFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-RQ + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-RRFK-2,4-dinitrophenyl amide + H2O
2-aminobenzoyl-RR + FK-2,4-dinitrophenyl amide
-
-
-
-
ir
2-aminobenzoyl-RRFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-RR + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-rRL-N-(2,4-dinitrophenyl)ethylenediamine + H2O
2-aminobenzoyl-D-Arg-L-Arg + Leu-N-(2,4-dinitrophenyl)ethylenediamine
-
-
-
-
ir
2-aminobenzoyl-RSFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-RS + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-rSL-N-(2,4-dinitrophenyl)ethylenediamine + H2O
2-aminobenzoyl-D-Arg-L-Ser + Leu-N-(2,4-dinitrophenyl)ethylenediamine
-
-
-
-
ir
2-aminobenzoyl-RTFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-RT + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-SRFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-SR + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-TRFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-TR + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-VRFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-VR + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-WRFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-WR + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
2-aminobenzoyl-YRFK-2,4-dinitrophenyl ester + H2O
2-aminobenzoyl-YR + FK-2,4-dinitrophenyl ester
-
-
-
-
ir
amyloid beta peptide Abeta42 + H2O
?
-
the peptide primarily undergoes degradation by NEP in vivo in the brain
-
-
?
amyloid beta peptide1-40 + H2O
amyloid beta peptide Asp1-Lys16 + amyloid beta peptide Asp1-Leu17 + amyloid beta peptide Asp1-Phe19
-
the wild-type enzyme cleaves Ab1-40 predominantly at Lys16-Leu17, Leu17-Val18 and Phe19-Phe20. The mutant G399V/G714K cleaves preferentially at Phe20-Ala21
main cleavage fragments after 60 min with the wild-type enzyme. After 360 min these fragments are degraded further, accompanied by the appearance of Val12-Leu17 and Tyr10-Leu17 fragments
-
?
amyloid beta(1-40) mutant A21G + H2O
?
-
Flemish variant of amyloid beta. Decreased degradation by neprilysin compared to either wild-type peptide or the other mutant peptides
-
-
?
glutaryl-Ala-Ala-Phe-2-naphthylamide + H2O
glutaryl-Ala-Ala + Phe-2-naphthylamide
-
-
-
?
glutaryl-Ala-Ala-Phe-4-methoxy-2-naphthylamide + H2O
glutaryl-Ala-Ala + Phe-4-methoxy-2-naphthylamide
glutaryl-Gly-Gly-Phe-2-naphthylamide + H2O
glutaryl-Gly-Gly + Phe-2-naphthylamide
-
-
-
?
glutaryl-Gly-Gly-Phe-2-naphthylamide + H2O
glutaryl-Gly-Gly-Phe + 2-naphthylamine
-
-
-
-
?
hippuryl-Arg-Arg-Ala-2-naphthylamide + H2O
hippuryl-Arg-Arg + Ala-2-naphthylamide
-
-
-
-
?
His-Lys-Thr-Asp-Ser-Phe-Val-Gly-Leu-Met-NH2 + H2O
His-Lys-Thr-Asp-Ser + Phe-Val-Gly + Leu-Met-NH2
leucine5-enkephalin + H2O
?
-
Tyr-Gly-Gly-Phe-Leu is cleaved at the Gly-Phe bond by the wild-type enzyme
-
-
?
N-(4-carboxy-1-oxobutyl)-L-alanyl-L-alanyl-N-(4-methoxy-2-naphthalenyl)-L-phenylalaninamide + H2O
N-(4-carboxy-1-oxobutyl)-L-alanyl-L-alanyl-L-phenylalanine + 4-methoxy-2-naphthylamine
-
-
-
-
?
N-benzyloxycarbonyl-Gly-Gly-Leu 2-naphthylamide + H2O
N-benzyloxycarbonyl-Gly-Gly + L-leucine 2-naphthylamide
-
-
-
?
N-formyl-L-Met-Leu-Phe + H2O
?
-
the enzyme may play an important role in modulating chemotactic response by cleavage of the chemotactic substance N-formyl-Met-Leu-Phe
-
-
-
Nalpha-benzoyl-Gly-Arg-Arg-Ala-2-naphthylamide + H2O
Nalpha-benzoyl-Gly-Arg-Arg + Ala-2-naphthylamide
-
-
-
?
Nalpha-benzoyl-Gly-Arg-Arg-Leu-2-naphthylamide + H2O
Nalpha-benzoyl-Gly-Arg-Arg + Leu-2-naphthylamide
-
-
-
?
Nalpha-benzoyl-Gly-Arg-Arg-Phe-2-naphthylamide + H2O
Nalpha-benzoyl-Gly-Arg-Arg + Phe-2-naphthylamide
-
-
-
?
Nalpha-benzoyl-Gly-Arg-Leu-2-naphthylamide + H2O
Nalpha-benzoyl-Gly-Arg + Leu-2-naphthylamide
-
-
-
?
Nalpha-benzoyl-Gly-Gly-Arg-Leu-2-naphthylamide + H2O
Nalpha-benzoyl-Gly-Gly-Arg + Leu-2-naphthylamide
-
-
-
?
Nalpha-benzoyl-Gly-Lys-Arg-Arg-Leu-2-naphthylamide + H2O
Nalpha-benzoyl-Gly-Lys-Arg-Arg + Leu-2-naphthylamide
-
-
-
?
Nalpha-benzoyl-Gly-Lys-Lys-Arg-Arg-Leu-2-naphthylamide + H2O
Nalpha-benzoyl-Gly-Lys-Lys-Arg-Arg + Leu-2-naphthylamide
-
-
-
?
neuropeptide Y + H2O
truncated neuropeptide Y + C-terminal fragments of neuropeptide Y
-
-
neuropeptide Y 21-36 and 31-36 are the most abundant fragments generated in vivo
-
?
pulmonary vasodilative vasoactive intestinal peptide + H2O
?
-
rapid inactivation
-
-
?
pyroglutamyl-Leu-Asn-Phe-Thr-Pro-Asn-Trp-Gly-Thr-NH2 + H2O
pyroglutamyl-Leu-Asn + Phe-Thr-Pro-ASn-Trp-Gly-Thr-NH2
succinyl-Ala-Ala-Phe-4-methylcoumarin 7-amide + H2O
succinyl-Ala-Ala + Phe-4-methylcoumarin 7-amide
succinyl-Arg-Arg-Leu-2-naphthylamide + H2O
succinyl-Arg-Arg + Leu-2-naphthylamide
-
-
-
?
succinyl-Arg-Pro-Phe-His-Leu-Leu-Val-Tyr-7-amido-4-methylcoumarin + H2O
?
-
-
-
-
?
amyloid beta peptide1-40 + H2O
?
-
multiple cleavage sites, product peaks corresponding to Abeta1-16, Abeta1-17, Abeta10-17, Abeta20-28, Abeta20-29, and Abeta20-30. The C-terminal products result from the cleavages at K28-G29, G29-A30, and A30-I31. These products are derived from the trans-membrane region of the amyloid precursor protein (APP) from which Abeta is formed and are rather hydrophobic
-
-
?
Arg-Pro-Lys-Pro-Gln-Gln-Phe-Phe-Gly-Leu-Met-NH2 + H2O
?
-
-
-
-
?
Arg-Pro-Lys-Pro-Gln-Gln-Phe-Phe-Gly-Leu-Met-NH2 + H2O
?
-
-
-
-
?
Arg-Pro-Lys-Pro-Gln-Gln-Phe-Phe-Gly-Leu-Met-NH2 + H2O
?
-
i.e. substance P, seven peptides are produced
-
-
?
Asp-Tyr(SO3H)-Met-Gly-Trp-Met-Asp-PheNH2 + H2O
?
-
i.e. cholecystokinin-8, two distinct cleavage sites: Asp-Tyr(SO3H)-Met-Gly-/-Trp-Met-Asp-/-PheNH2, the splitting of the Asp7-Phe8NH2 bond proceeds 4-times more rapidly than the Gly4-Trp5 bond
-
-
?
Atrial natriuretic factor + H2O
?
-
human alpha atrial natriuretic peptide/cardiodilatin shows a single major cleavage site within the disulfide-linked loop between Cys and Phe in position 7 and 8
-
-
?
Atrial natriuretic factor + H2O
?
-
seven sites of hydrolysis: Arg4-Ser5, Cys7-Phe8, Arg11-Met12, Arg14-Ile15, Gly16-Ala17, Gly-20-Leu21, Ser25-Phe26. The initial attack takes place at a bond within the disulfide-linked loop and produces a peptide having the same amino acid composition as intact atrial natriuretic factor
-
-
?
Atrial natriuretic factor + H2O
?
-
dominant enzyme in the hydrolysis of atrial natriuretic factor
-
-
-
atrial natriuretic peptide + H2O
?
-
no activity with brain natriuretic peptide
-
-
?
D-Ala2-Leu5-enkephalin + H2O
Tyr-D-Ala-Gly + Phe-Leu
-
i.e. Tyr-D-Ala-Gly-Phe-Leu
-
?
D-Ala2-Leu5-enkephalin + H2O
Tyr-D-Ala-Gly + Phe-Leu
-
i.e. Tyr-D-Ala-Gly-Phe-Leu
-
-
?
D-Ala2-Leu5-enkephalin + H2O
Tyr-D-Ala-Gly + Phe-Leu
-
i.e. Tyr-D-Ala-Gly-Phe-Leu
-
-
?
D-Ala2-Leu5-enkephalin + H2O
Tyr-D-Ala-Gly + Phe-Leu
-
i.e. Tyr-D-Ala-Gly-Phe-Leu
-
-
?
D-Ala2-Leu5-enkephalin + H2O
Tyr-D-Ala-Gly + Phe-Leu
-
i.e. Tyr-D-Ala-Gly-Phe-Leu
-
-
?
D-Ala2-Leu5-enkephalin + H2O
Tyr-D-Ala-Gly + Phe-Leu
-
i.e. Tyr-D-Ala-Gly-Phe-Leu
-
-
?
gastrin G-17 + H2O
?
-
cleavage at four sites, Trp4-Leu5, Ala11-Tyr12, Gly13-Trp14 and Asp16-Phe17
-
-
?
gastrin G-17 + H2O
?
-
sulfated and unsulfated gastrin, cleavage is faster with the sulfated peptide
-
-
?
Glucagon + H2O
?
-
NEP24.11 is an important mediator of the degradation of both endogenous and exogenous glucagon in vivo
-
-
?
glutaryl-Ala-Ala-Phe-4-methoxy-2-naphthylamide + H2O
glutaryl-Ala-Ala + Phe-4-methoxy-2-naphthylamide
-
-
-
?
glutaryl-Ala-Ala-Phe-4-methoxy-2-naphthylamide + H2O
glutaryl-Ala-Ala + Phe-4-methoxy-2-naphthylamide
-
-
-
-
?
glutaryl-Ala-Ala-Phe-4-methoxy-2-naphthylamide + H2O
glutaryl-Ala-Ala + Phe-4-methoxy-2-naphthylamide
-
-
-
-
?
glutaryl-Ala-Ala-Phe-4-methoxy-2-naphthylamide + H2O
glutaryl-Ala-Ala + Phe-4-methoxy-2-naphthylamide
-
-
-
-
?
hippuryl-Arg-Arg-Leu-2-naphthylamide + H2O
hippuryl-Arg-Arg + Leu-2-naphthylamide
-
-
-
-
?
hippuryl-Arg-Arg-Leu-2-naphthylamide + H2O
hippuryl-Arg-Arg + Leu-2-naphthylamide
-
-
-
-
?
His-Lys-Thr-Asp-Ser-Phe-Val-Gly-Leu-Met-NH2 + H2O
His-Lys-Thr-Asp-Ser + Phe-Val-Gly + Leu-Met-NH2
-
-
-
-
?
His-Lys-Thr-Asp-Ser-Phe-Val-Gly-Leu-Met-NH2 + H2O
His-Lys-Thr-Asp-Ser + Phe-Val-Gly + Leu-Met-NH2
-
-
-
-
?
His-Lys-Thr-Asp-Ser-Phe-Val-Gly-Leu-Met-NH2 + H2O
His-Lys-Thr-Asp-Ser + Phe-Val-Gly + Leu-Met-NH2
-
-
-
-
?
His-Lys-Thr-Asp-Ser-Phe-Val-Gly-Leu-Met-NH2 + H2O
His-Lys-Thr-Asp-Ser + Phe-Val-Gly + Leu-Met-NH2
-
-
-
-
?
His-Lys-Thr-Asp-Ser-Phe-Val-Gly-Leu-Met-NH2 + H2O
His-Lys-Thr-Asp-Ser + Phe-Val-Gly + Leu-Met-NH2
-
i.e. neurokinin A, hydrolysis at two sites: Ser5-Phe6 and Gly8-Leu9
-
-
?
insulin B chain + H2O
?
-
multiple cleavage sites, product analysis and cleavage sites preferences of wild-type and mutant neprilysins, cleavage sites, overview
-
-
?
pyroglutamyl-Leu-Asn-Phe-Thr-Pro-Asn-Trp-Gly-Thr-NH2 + H2O
pyroglutamyl-Leu-Asn + Phe-Thr-Pro-ASn-Trp-Gly-Thr-NH2
-
-
-
?
pyroglutamyl-Leu-Asn-Phe-Thr-Pro-Asn-Trp-Gly-Thr-NH2 + H2O
pyroglutamyl-Leu-Asn + Phe-Thr-Pro-ASn-Trp-Gly-Thr-NH2
-
-
-
?
pyroglutamyl-Leu-Asn-Phe-Thr-Pro-Asn-Trp-Gly-Thr-NH2 + H2O
pyroglutamyl-Leu-Asn + Phe-Thr-Pro-ASn-Trp-Gly-Thr-NH2
-
-
-
?
succinyl-Ala-Ala-Phe-4-methylcoumarin 7-amide + H2O
succinyl-Ala-Ala + Phe-4-methylcoumarin 7-amide
-
-
-
?
succinyl-Ala-Ala-Phe-4-methylcoumarin 7-amide + H2O
succinyl-Ala-Ala + Phe-4-methylcoumarin 7-amide
-
-
-
-
?
succinyl-Ala-Ala-Phe-4-methylcoumarin 7-amide + H2O
succinyl-Ala-Ala + Phe-4-methylcoumarin 7-amide
-
-
-
?
succinyl-Ala-Ala-Phe-4-methylcoumarin 7-amide + H2O
succinyl-Ala-Ala + Phe-4-methylcoumarin 7-amide
-
-
-
-
?
succinyl-Ala-Ala-Phe-4-methylcoumarin 7-amide + H2O
succinyl-Ala-Ala + Phe-4-methylcoumarin 7-amide
-
-
-
?
Tyr-Gly-Gly-Phe-Met + H2O
Tyr-Gly-Gly + Phe-Met
-
i.e. methionine enkephalin
-
-
?
Tyr-Gly-Gly-Phe-Met + H2O
Tyr-Gly-Gly + Phe-Met
-
i.e. methionine enkephalin
-
-
?
Tyr-Gly-Gly-Phe-Met + H2O
Tyr-Gly-Gly + Phe-Met
-
i.e. methionine enkephalin
-
-
?
additional information
?
-
-
NEP-1 plays an important role in the regulation of nematode locomation. NEP-1 is a central component that controls the neuronal innervation of pharyngeal pumping in Caenorhabditis elegans
-
-
-
additional information
?
-
-
the enzyme may play an important role as regulator of plasma-derived peptides in the nephron
-
-
-
additional information
?
-
-
elevation of the enzyme activity in serum from underground coal miners exposed to chronic inhalation of coal mine dust particles. The enzyme reflects the chronic pulmonary inflammatory state induced by coalmine dust exposure, and so may be a marker of lung injury
-
-
-
additional information
?
-
-
the enzyme is involved in the processing of other peptide hormones
-
-
-
additional information
?
-
-
the enzyme is responsible for the difference in metabolism of sulfated and unsulfated gastrin in human circulation
-
-
-
additional information
?
-
-
the enzyme is the major inactivator of enkephalin in brain
-
-
-
additional information
?
-
-
the enzyme may participate in the regulation of blood pressure and water and sodium excretion through inactivation of kinins
-
-
-
additional information
?
-
-
induction of neutral endopeptidase (NEP) activity of SK-N-SH cells by natural compounds from green tea. Caffeine leads to an increase in specific cellular neutral endopeptidase activity more than theophylline, theobromine or theanine. The combination of epigallocatechin and epigallocatechingallate with caffeine, theobromine or theophylline induces cellular neutral endopeptidase activity. The enhancement of cellular neutral endopeptidase activity by green tea extract and its natural products might be correlated with an elevated level of intracellular cyclic adenosine monophosphate
-
-
-
additional information
?
-
-
neutral endopeptidase 24.11/CD10 suppresses the progression of ovarian carcinomas
-
-
-
additional information
?
-
-
hydrolysis of polypeptides between hydrophobic residues
-
-
-
additional information
?
-
-
a quenched fluorogenic peptide substrate containing the first seven residues of the Abeta peptide plus a C-terminal Cysteine residue is synthesized to detect neprilysin activity. A fluorophore is attached to the C-terminal Cysteine and its fluorescence is quenched by a quencher linked to the N-terminus of the peptide
-
-
?
additional information
?
-
-
the enzyme degrades a wide range of peptide substrates, physiologically relevant peptides are such as enkephalins, tachykinins, and natriuretic peptides
-
-
-
additional information
?
-
-
the enzyme directly interacts with phosphatidylserine and cardiolipin but not with cholesterol
-
-
-
additional information
?
-
-
the enzyme has broader substrate specificity and is a peptidase capable of cleaving a variety of physiological peptides
-
-
-
additional information
?
-
-
human neprilysin-2 has a more restricted substrate specificity compared to human neprilysin with less activity against several vasoactive peptides
-
-
-
additional information
?
-
-
catabolism of atrial and brain natriuretic peptide is independent of neutral endopeptidase. One or more other peptidase degrade atrial natriuretic peptide or brain natriuretic peptide in the heart, lungs and kidney
-
-
-
additional information
?
-
-
nicastrin controls neprilysin at a transcriptional level by contributing to the production of the beta-amyloid precursor protein intracellular domain with the gamma-secretase complex
-
-
-
additional information
?
-
-
the enzyme is the major inactivator of enkephalin in brain
-
-
-
additional information
?
-
-
the enzyme may participate in the regulation of blood pressure and water and sodium excretion through inactivation of kinins
-
-
-
additional information
?
-
-
the enzyme is the major inactivator of enkephalin in brain
-
-
-
additional information
?
-
-
the enzyme may participate in the regulation of blood pressure and water and sodium excretion through inactivation of kinins
-
-
-
additional information
?
-
-
in sepsis, the local concentration and action of adrenomedullin in tissue may be differentially regulated by NEP
-
-
-
additional information
?
-
-
neutral endopeptidase inhibition has natriuretic and aquaretic actions in cirrhosis without any effect on blood pressure and kidney perfusion due to a significant overexpression of thgis enzyme in renal cortex
-
-
-
additional information
?
-
-
physiological role in metabolism of insect peptides at the synapse
-
-
-
additional information
?
-
-
could play an important role in the hydrolysis of neuropeptides
-
-
-
additional information
?
-
-
the enzyme may participate in the regulation of blood pressure and water and sodium excretion through inactivation of kinins
-
-
-
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
NATURAL SUBSTRATES
NATURAL PRODUCTS
REACTION DIAGRAM
ORGANISM
UNIPROT
COMMENTARY
(Substrate)
(Substrate)
LITERATURE
(Substrate)
(Substrate)
COMMENTARY
(Product)
(Product)
LITERATURE
(Product)
(Product)
REVERSIBILITY
r=reversible
ir=irreversible
?=not specified
r=reversible
ir=irreversible
?=not specified
amyloid beta peptide Abeta42 + H2O
?
-
the peptide primarily undergoes degradation by NEP in vivo in the brain
-
-
?
Atrial natriuretic factor + H2O
?
-
dominant enzyme in the hydrolysis of atrial natriuretic factor
-
-
-
Glucagon + H2O
?
-
NEP24.11 is an important mediator of the degradation of both endogenous and exogenous glucagon in vivo
-
-
?
leucine5-enkephalin + H2O
?
-
Tyr-Gly-Gly-Phe-Leu is cleaved at the Gly-Phe bond by the wild-type enzyme
-
-
?
N-formyl-L-Met-Leu-Phe + H2O
?
-
the enzyme may play an important role in modulating chemotactic response by cleavage of the chemotactic substance N-formyl-Met-Leu-Phe
-
-
-
neuropeptide Y + H2O
truncated neuropeptide Y + C-terminal fragments of neuropeptide Y
-
-
neuropeptide Y 21-36 and 31-36 are the most abundant fragments generated in vivo
-
?
pulmonary vasodilative vasoactive intestinal peptide + H2O
?
-
rapid inactivation
-
-
?
additional information
?
-
-
NEP-1 plays an important role in the regulation of nematode locomation. NEP-1 is a central component that controls the neuronal innervation of pharyngeal pumping in Caenorhabditis elegans
-
-
-
additional information
?
-
-
the enzyme may play an important role as regulator of plasma-derived peptides in the nephron
-
-
-
additional information
?
-
-
elevation of the enzyme activity in serum from underground coal miners exposed to chronic inhalation of coal mine dust particles. The enzyme reflects the chronic pulmonary inflammatory state induced by coalmine dust exposure, and so may be a marker of lung injury
-
-
-
additional information
?
-
-
the enzyme is involved in the processing of other peptide hormones
-
-
-
additional information
?
-
-
the enzyme is responsible for the difference in metabolism of sulfated and unsulfated gastrin in human circulation
-
-
-
additional information
?
-
-
the enzyme is the major inactivator of enkephalin in brain
-
-
-
additional information
?
-
-
the enzyme may participate in the regulation of blood pressure and water and sodium excretion through inactivation of kinins
-
-
-
additional information
?
-
-
induction of neutral endopeptidase (NEP) activity of SK-N-SH cells by natural compounds from green tea. Caffeine leads to an increase in specific cellular neutral endopeptidase activity more than theophylline, theobromine or theanine. The combination of epigallocatechin and epigallocatechingallate with caffeine, theobromine or theophylline induces cellular neutral endopeptidase activity. The enhancement of cellular neutral endopeptidase activity by green tea extract and its natural products might be correlated with an elevated level of intracellular cyclic adenosine monophosphate
-
-
-
additional information
?
-
-
neutral endopeptidase 24.11/CD10 suppresses the progression of ovarian carcinomas
-
-
-
additional information
?
-
-
the enzyme degrades a wide range of peptide substrates, physiologically relevant peptides are such as enkephalins, tachykinins, and natriuretic peptides
-
-
-
additional information
?
-
-
the enzyme directly interacts with phosphatidylserine and cardiolipin but not with cholesterol
-
-
-
additional information
?
-
-
the enzyme has broader substrate specificity and is a peptidase capable of cleaving a variety of physiological peptides
-
-
-
additional information
?
-
-
catabolism of atrial and brain natriuretic peptide is independent of neutral endopeptidase. One or more other peptidase degrade atrial natriuretic peptide or brain natriuretic peptide in the heart, lungs and kidney
-
-
-
additional information
?
-
-
nicastrin controls neprilysin at a transcriptional level by contributing to the production of the beta-amyloid precursor protein intracellular domain with the gamma-secretase complex
-
-
-
additional information
?
-
-
the enzyme is the major inactivator of enkephalin in brain
-
-
-
additional information
?
-
-
the enzyme may participate in the regulation of blood pressure and water and sodium excretion through inactivation of kinins
-
-
-
additional information
?
-
-
the enzyme is the major inactivator of enkephalin in brain
-
-
-
additional information
?
-
-
the enzyme may participate in the regulation of blood pressure and water and sodium excretion through inactivation of kinins
-
-
-
additional information
?
-
-
in sepsis, the local concentration and action of adrenomedullin in tissue may be differentially regulated by NEP
-
-
-
additional information
?
-
-
neutral endopeptidase inhibition has natriuretic and aquaretic actions in cirrhosis without any effect on blood pressure and kidney perfusion due to a significant overexpression of thgis enzyme in renal cortex
-
-
-
additional information
?
-
-
physiological role in metabolism of insect peptides at the synapse
-
-
-
additional information
?
-
-
could play an important role in the hydrolysis of neuropeptides
-
-
-
additional information
?
-
-
the enzyme may participate in the regulation of blood pressure and water and sodium excretion through inactivation of kinins
-
-
-
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
METALS and IONS
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
Zinc
Zn2+
additional information
additional information
-
Pb2+ slightly modifies the recombinant enzyme conformation, but does not affect the enzyme activity
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
INHIBITORS
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
IMAGE
(2R)-2-([1-[(5-ethyl-1,3,4-thiadiazol-2-yl)carbamoyl]cyclopentyl]methyl)pentanoic acid
-
-
(2R)-2-[(1-[[(1S)-1-carboxy-2-(3-phenyl-1,2,4-oxadiazol-5-yl)ethyl]carbamoyl]cyclopentyl)methyl]-5-oxopentanoic acid
-
-
(2R)-2-[(1-[[(1S)-1-carboxy-2-(4-ethyl-1,3-oxazol-2-yl)ethyl]carbamoyl]cyclopentyl)methyl]pentanoic acid
-
-
(2R)-2-[(1-[[(1S)-1-carboxy-2-(4-phenyl-1,3-oxazol-2-yl)ethyl]carbamoyl]cyclopentyl)methyl]-5-oxopentanoic acid
-
-
(2R)-2-[(1-[[(1S)-1-carboxy-2-(4-phenyl-1,3-oxazol-2-yl)ethyl]carbamoyl]cyclopentyl)methyl]pentanoic acid
-
-
(2R)-2-[(1-[[(1S)-1-carboxy-2-(5-phenyl-1,3,4-oxadiazol-2-yl)ethyl]carbamoyl]cyclopentyl)methyl]-5-oxopentanoic acid
-
-
(2R)-2-[(1-[[(1S)-1-carboxy-2-(5-phenyl-1,3-oxazol-2-yl)ethyl]carbamoyl]cyclopentyl)methyl]-5-oxopentanoic acid
-
-
(2R)-2-[(1-[[(1S)-1-carboxy-2-(5-phenyl-1,3-oxazol-2-yl)ethyl]carbamoyl]cyclopentyl)methyl]pentanoic acid
-
-
(2R)-2-[[1-([(1S)-1-carboxy-2-[4-(2-methylpropyl)-1,3-oxazol-2-yl]ethyl]carbamoyl)cyclopentyl]methyl]pentanoic acid
-
-
(2R)-2-[[1-([(1S)-1-carboxy-2-[5-(4-chlorophenyl)-1,3-oxazol-2-yl]ethyl]carbamoyl)cyclopentyl]methyl]-5-oxopentanoic acid
-
-
(2S)-2-[(1-[[2-(hydroxymethyl)-2,3-dihydro-1H-inden-2-yl]carbamoyl]cyclopentyl)methyl]-4-methoxybutanoic acid
-
-
(2S)-2-[(1-[[3-(4-chlorophenyl)propyl]carbamoyl]cyclopentyl)methyl]-4-methoxybutanoic acid
-
-
(2S)-2-[(1-[[3-(4-fluorophenyl)propyl]carbamoyl]cyclopentyl)methyl]-4-methoxybutanoic acid
-
-
(2S)-2-[[(2S)-1-[[(1S)-2-(biphenyl-4-yl)-1-carboxyethyl]amino]-5-methyl-1-oxohexan-2-yl]amino]-4-phenylbutanoic acid (non-preferred name)
-
-
(2S)-4-methoxy-2-([1-[(1-methyl-2-phenylethyl)carbamoyl]cyclopentyl]methyl)butanoic acid
-
-
(2S)-4-methoxy-2-[(1-[[(1R,2S)-2-(4-methoxyphenyl)cyclopropyl]carbamoyl]cyclopentyl)methyl]butanoic acid
-
-
(S)-N-[2-(phosphonomethylamino)-3-(4-biphenylyl)-propionyl]-3-aminopropionic acid
-
effects of neutral endopeptidase in acute inflammation in the lung are studied using a newly developed murine model of smoke and burn injury using NEP antagonist CGS-24592. Smoke and burn-induced lung injury and inflammation in mice pretreated with CGS-24592 is exacerbated, leading to more plasma extravasation and severe airway inflammation
2-(1-heptylcarbamoyl-cyclopentylmethyl)-4-methoxy-butyric acid tert-butyl ester
-
-
2-([1-[(1,3-benzodioxol-5-ylmethyl)carbamoyl]cyclopentyl]methyl)pentanoic acid
-
IC50: 1500 nM
2-([1-[(1-benzyl-2-hydroxyethyl)carbamoyl]cyclopentyl]methyl)pentanoic acid
-
IC50: 384 nM
2-([1-[(1-benzyl-6-oxo-1,6-dihydropyridin-3-yl)carbamoyl]cyclopentyl]methyl)pentanoic acid
-
IC50: 313 nM
2-([1-[(1-ethyl-1H-1,2,3-triazol-4-yl)carbamoyl]cyclopentyl]methyl)pentanoic acid
-
IC50: 82 nM
2-([1-[(3-ethylpyridin-2-yl)carbamoyl]cyclopentyl]methyl)pentanoic acid
-
IC50: 1710 nM
2-([1-[(4-benzylpyridin-2-yl)carbamoyl]cyclopentyl]methyl)pentanoic acid
-
IC50: 96 nM
2-([1-[(4-butylpyridin-2-yl)carbamoyl]cyclopentyl]methyl)pentanoic acid
-
IC50: 184 nM
2-([1-[(4-carbamoylcyclohexyl)carbamoyl]cyclopentyl]methyl)pentanoic acid
-
IC50: 150 nM
2-([1-[(5-benzyl-1,3,4-thiadiazol-2-yl)carbamoyl]cyclopentyl]methyl)pentanoic acid
-
IC50: 30 nM
2-([1-[(5-ethyl-1,3,4-thiadiazol-2-yl)carbamoyl]cyclopentyl]methyl)-4-phenylbutanoic acid
-
IC50: 46 nM
2-([1-[(5-ethyl-1,3,4-thiadiazol-2-yl)carbamoyl]cyclopentyl]methyl)-5-methylhexanoic acid
-
IC50: 120 nM
2-([1-[(5-ethyl-1,3,4-thiadiazol-2-yl)carbamoyl]cyclopentyl]methyl)hexanoic acid
-
IC50: 84 nM
2-([1-[(5-ethyl-1,3,4-thiadiazol-2-yl)carbamoyl]cyclopentyl]methyl)pentanoic acid
-
IC50: 60 nM
2-([1-[(5-methyl-1,3,4-thiadiazol-2-yl)carbamoyl]cyclopentyl]methyl)pentanoic acid
-
IC50: 176 nM
2-([1-[(5-phenyl-1,3,4-thiadiazol-2-yl)carbamoyl]cyclopentyl]methyl)pentanoic acid
-
IC50: 283 nM
2-([1-[(6-methoxypyridazin-3-yl)carbamoyl]cyclopentyl]methyl)pentanoic acid
-
IC50: 374 nM
2-([1-[5-(1-benzyl-6-oxo-1,6-dihydropyridin-3-yl)-1,3,4-oxadiazol-2-yl]cyclopentyl]methyl)pentanoic acid
-
IC50: 1139 nM
2-methoxymethyl-3-[1-(trans-2-phenyl-cyclopropylcarbamoyl)-cyclopentyl]-propionic acid tert-butyl ester
-
-
2-[(1-[[(1R)-1-phenylethyl]carbamoyl]cyclopentyl)methyl]pentanoic acid
-
IC50: 530 nM
2-[(1-[[(1R)-3-(dimethylcarbamoyl)cyclohexyl]carbamoyl]cyclopentyl)methyl]pentanoic acid
-
IC50: 297 nM
2-[(1-[[(1R,2R)-2-benzylcyclohexyl]carbamoyl]cyclopentyl)methyl]pentanoic acid
-
IC50: 195 nM
2-[(1-[[(1R,2S)-2-propylcyclohexyl]carbamoyl]cyclopentyl)methyl]pentanoic acid
-
IC50: 890 nM
2-[(1-[[(3R)-1-benzylpyrrolidin-3-yl]carbamoyl]cyclopentyl)methyl]pentanoic acid
-
IC50: 1060 nM
2-[(1-[[(3R)-1-carbamoylpyrrolidin-3-yl]carbamoyl]cyclopentyl)methyl]pentanoic acid
-
IC50: 213 nM
2-[(1-[[(5-methyl-1,3,4-thiadiazol-2-yl)methyl]carbamoyl]cyclopentyl)methyl]pentanoic acid
-
IC50: 700 nM
2-[(1-[[1-(hydroxymethyl)cyclopentyl]carbamoyl]cyclopentyl)methyl]pentanoic acid
-
IC50: 1710 nM
2-[(1-[[2-(hydroxymethyl)-2,3-dihydro-1H-inden-2-yl]carbamoyl]cyclopentyl)methyl]pentanoic acid
-
IC50: 96 nM
2-[(1-[[4-(dimethylcarbamoyl)cyclohexyl]carbamoyl]cyclopentyl)methyl]pentanoic acid
-
IC50: 370 nM
2-[(1-[[5-(2-methylpropyl)-1,3,4-thiadiazol-2-yl]carbamoyl]cyclopentyl)methyl]pentanoic acid
-
IC50: 124 nM
2-[(1-[[5-(cyclopropylmethyl)-1,3,4-thiadiazol-2-yl]carbamoyl]cyclopentyl)methyl]pentanoic acid
-
IC50: 38 nM
2-[(3-iodo-4-hydroxy)phenylmethyl]-4-N-[3-hydroxyamino-3-oxo-1(phenylmethyl)propyl]amino-4-oxobutanoic acid
-
i.e. RB104, use of the inhibitor in detecting nanogram quantities of the enzyme by inhibitor gel electrophoresis
2-[(3-iodohydroxy)phenylmethyl]-4-N-[3-hydroxyamino-3-oxo-1-phenylmethylpropyl]-amino-4-oxobutanoic acid
-
i.e. RB104, highly selective and potent inhibitor
2-[1-(2-hydroxymethyl-indan-2-ylcarbamoyl)-cyclopentylmethyl]-4-methoxy-butyric acid tert-butyl ester
-
-
2-[1-(4-butyl-pyridin-2-ylcarbamoyl)-cyclopentylmethyl]-4-methoxybutyric acid benzyl ester
-
-
2-[1-(5-ethyl-[1,3,4]thiadiazol-2-ylcarbamoyl)-cyclopentylmethyl]-pentanoic acid
-
-
2-[1-[2-(trans-4-chlorophenyl)-cyclopropylcarbamoyl]-cyclopentylmethyl]-4-methoxy-butyric acid tert-butyl ester
-
-
2-[1-[3-(4-chloro-phenyl)-propylcarbamoyl]-cyclopentylmethyl]-4-methoxy-butyric acid tert-butyl ester
-
-
2-[1-[3-(4-fluoro-phenyl)-propylcarbamoyl]-cyclopentylmethyl]-4-methoxy-butyric acid tert-butyl ester
-
-
2-[[1-(1,3,4-thiadiazol-2-ylcarbamoyl)cyclopentyl]methyl]pentanoic acid
-
IC50: 377 nM
2-[[1-(2,3-dihydro-1H-inden-2-ylcarbamoyl)cyclopentyl]methyl]pentanoic acid
-
IC50: 313 nM
2-[[1-(5-benzyl-1,3,4-oxadiazol-2-yl)cyclopentyl]methyl]pentanoic acid
-
IC50: 3100 nM
2-[[1-(pyridin-2-ylcarbamoyl)cyclopentyl]methyl]pentanoic acid
-
IC50: 1500 nM
3-[1-[(5-ethyl-1,3,4-thiadiazol-2-yl)carbamoyl]cyclopentyl]propanoic acid
-
IC50: 237 nM
3-[1-[2-(trans-4-chlorophenyl)-cyclopropylcarbamoyl]-cyclopentyl]-2-methoxymethyl-propionic acid tert-butyl ester
-
-
4-hydroxy-nonenal
-
intracellular neprilysin develops 4-hydroxy-nonenal adducts after 24 h of 4-hydroxy-nonenal treatment. 4-Hydroxy-nonenal-modified neprilysin shows decreased catalytic activity, which is associated with elevations in amyloid beta1-40 in SH-SY5Y and H4 APP695wt cells. Incubation of cells with amyloid beta1-42 also induces 4-hydroxy-nonenal adduction of neprilysin
4-methoxy-2-(1-phenethylcarbamoyl-cyclopentylmethyl)-butyric acid benzyl ester
-
-
4-methoxy-2-[1-(3-phenyl-propylcarbamoyl)-cyclopentylmethyl]-butyric acid tert-butyl ester
-
-
4-methoxy-2-[1-(trans-2-pentyl-cyclopropylcarbamoyl)-cyclopentylmethyl]-butyric acid tert-butyl ester
-
-
4-methoxy-2-[1-(trans-2-phenyl-cyclopropylcarbamoyl)-cyclopentylmethyl]-butyric acid tert-butyl ester
-
-
4-methoxy-2-[1-[(trans-2-(4-fluorophenyl)-cyclopropylcarbamoyl)]-cyclopentylmethyl]-butyric acid tert-butyl ester
-
-
4-methoxy-2-[1-[(trans-2-(4-methoxy-phenyl)-cyclopropylcarbamoyl)]-cyclopentylmethyl]-butyric acid tert-butyl ester
-
-
4-methoxy-2-[1-[2-(4-methoxy-phenoxy)-ethylcarbamoyl]-cyclopentylmethyl]-butyric acid tert-butyl ester
-
-
4-methoxy-2-[1-[2-(4-methoxy-phenyl)-ethylcarbamoyl]-cyclopentylmethyl]-butyric acid tert-butyl ester
-
-
4-methoxy-2-[1-[3-(4-methoxy-phenyl)-propylcarbamoyl]-cyclopentylmethyl]-butyric acid tert-butyl ester
-
-
AHU-377
-
LCZ696 comprises molecular moieties of valsartan, and of the NEP inhibitor prodrug AHU377 ((2R,4S)-5-biphenyl-4-yl-5-(3-carboxy-propionylamino)-2-methyl-pentanoic acid ethyl ester) (1:1 molar ratio). Oral administration of LCZ696 causes dose-dependent increases in atrial natriuretic peptide immunoreactivity due to NEP inhibition in Sprague-Dawley rats and provides sustained, dose-dependent blood pressure reductions in hypertensive double-transgenic rats
amyloid beta1-42
-
incubation of cells with amyloid beta1-42 induces 4-hydroxy-nonenal adduction of neprilysin. In an apparent compensatory response, amyloid beta-treated cells show increased neprilysin mRNA and protein expression. Despite elevations in neprilysin protein, the activity is significantly lower compared with the neprilysin protein level
-
candoxatril
-
treatment increases plasma atrial natriuretic peptide levels and leads to significantly higher levels of atrial tissue cyclic GMP as well as plasma cyclic GMP. Candoxatril suppresses the shortening of atrial effective refractory period and monophasic action potential duration in the rapid atrial pacing model
cis-4-[([1-[(2S)-2-carboxy-3-(2-methoxyethoxy)propyl]cyclopentyl]carbonyl)amino]cyclohexanecarboxylic acid
-
-
DL-[N-(3-mercapto-2-benzylpropanoyl)]glycine
-
following neprilysin inhibition, islet amyloid deposition and beta-cell apoptosis increase by 54 and 75%, respectively
Hg2+
-
0.001-0.05 mM, modifies the recombinant enzyme conformation, and highly reduces the enzyme activity. Hg2+ incubation increases NEP protein levels, but does not change NEP mRNA levels nor the levels of the amyloid intracellular domain peptide, a protein fragment with transcriptional activity. The Hg2+-induced inhibition of the enzyme activity may be mediated by a conformational change resulting in reduced amyloid beta1-42 degradation
Insulin B chain
-
inhibits the activity with substrate N-(4-carboxy-1-oxobutyl)-L-alanyl-L-alanyl-N-(4-methoxy-2-naphthalenyl)-L-phenylalaninamide
LCZ696
-
LCZ696 is a dual-acting angiotensin II-receptor and neprilysin inhibitor (ARNI) in a single molecule: angiotensin-receptor blockade via its valsartan molecular moiety, and neprilysin inhibition via its AHU377 molecular moiety. In a randomized, double-blind, placebo-controlled, active comparator study it is shown that compared with valsartan, dual-acting LCZ696 provides complementary and fully additive reduction of blood pressure
N-([1-[(2S)-2-carboxy-3-[[N2-(methylsulfonyl)-L-lysyl]amino]propyl]cyclopentyl]carbonyl)-L-tyrosine
-
-
N-[5-fluoresceinyl]-N'-[6-(3-mercapto-2-benzyl-1-oxopropyl)amino-1-hexyl]thiocarbamide
-
the inhibitor is a very potent probe for detecting membrane-bound enzyme for biological studies or diagnostic applications. Particularly useful for detecting the membrane-bound enzyme by flow cytometry
N-[N-[1(5)-carboxy-3-(4-hydroxyphenyl)propyl]-(5)-phenylalanyl]-(5)-isoserine
-
-
SCH48446
-
i.e. the diiodo analog of N-[N-[1(5)-carboxy-3-(4-hydroxyphenyl)propyl]-(5)-phenylalanyl]-(5)-isoserine
-
tert-butyl 2-([1-[(5-benzyl-1,3,4-thiadiazol-2-yl)carbamoyl]cyclopentyl]methyl)-4-methoxybutanoate
-
-
valsartan
-
LCZ696 comprises molecular moieties of valsartan, and of the NEP inhibitor prodrug AHU377 ((2R,4S)-5-biphenyl-4-yl-5-(3-carboxy-propionylamino)-2-methyl-pentanoic acid ethyl ester) (1:1 molar ratio). Oral administration of healthy volunteers is associated with increases in plasma cGMP, renin concentration and activity, and angiotensin II, providing evidence for NEP inhibition and angiotensin receptor blockade
amyloid beta
-
amyloid beta reduces global DNA methylation whilst increasing neprilysin DNA methylation and further suppressing the neprilysin expression in mRNA and protein levels. Amyloid beta induces epigenetic effects, implying that DNA methylation may be part of a vicious cycle involving the reduction in neprilysin expression along with a resultant increase in amyloid beta accumulation, and that amyloiud beta may induce global DNA hypo-methylation
-
amyloid beta
-
infusion with amyloid beta(25-35) induces decrease of somatostatin-like immunoreactive content, somatostatin mRNA levels, phosphorylated-cAMP-response element binding protein CREB content and neprilysin levels
-
candoxatrilat
-
application restores vagal reflex bradycardia in old rats to levels similar to those in young neutral endopeptidase inhibitor-treated rats
Leu5-enkephalin
-
hydrolysis of succinyl-Ala-Ala-Phe-4-methylcoumarin 7-amide
Met5-enkephalin
-
hydrolysis of succinyl-Ala-Ala-Phe-4-methylcoumarin 7-amide
N-phenethylphosphonyl-L-leucyl-L-tryptophan
-
NPLT, synthesis of the phosphoramidon derivative with enhanced permeability into the skin that shows inability to inhibit type I and type IV collagenase, but inhibits fibroblast elastase
N-phenethylphosphonyl-L-leucyl-L-tryptophan
-
NPLT, synthesis of the phosphoramidon derivative with enhanced permeability into the skin that shows inability to inhibit type I and type IV collagenase, but inhibits fibroblast elastase
N-phenethylphosphonyl-L-leucyl-L-tryptophan
-
NPLT, synthesis of the phosphoramidon derivative with enhanced permeability into the skin that shows inability to inhibit type I and type IV collagenase, but inhibits fibroblast elastase
phosphoramidon
-
the inhibitor induces a dramatic increase in amyloid-beta peptide levels
phosphoramidon
-
neprilysin inhibition potentiates substance P-mediated neutrophil oxygen radical production and may promote other inflammatory activities during magnesium deficiency. Magnesium deficiency plus treatment with phosphoramidon reduces neprilysin activity by 48%, phosphoramidon or magnesium deficiency alone only reduce its activity by 26% and 15%, respectively
phosphoramidon
-
the inhibitor induces a dramatic increase in amyloid-beta peptide levels
thiorphan
-
-
thiorphan
-
the inhibitor induces a dramatic increase in amyloid-beta peptide levels
thiorphan
-
plasma and lung A-type natriuretic peptide levels in rats treated with lipopolysaccharide are significantly higher than those in the control group, but are significantly decreased by thiorphan administration. Natriuretic peptide receptor-A mRNA levels do not differ significantly among the groups. Natriuretic peptide receptor-C mRNA levels in animals treated with lipopolysaccharide plus thiorphan group are significantly higher than those in the other groups
thiorphan
-
the inhibitor induces a dramatic increase in amyloid-beta peptide levels
additional information
-
both staurosporine-stimulated caspase-3 activation, p53 and neprilysin expression and activity are not affected by over-expression or depletion of presenilin complex component TMP21
-
additional information
-
no inhibition by 4-(2-butylbenzyl)-5-(4-hydroxybenzyl)-1-[1-(2-[[6-(4-hydroxybenzyl)-2,3-dioxopiperazin-1-yl]methyl]pyrrolidin-1-yl)-3-(naphthalen-2-yl)propan-2-yl]piperazine-2,3-dione and 4-(cyclopentylmethyl)-5-(4-hydroxybenzyl)-1-[1-(2-[[6-(4-hydroxybenzyl)-2,3-dioxopiperazin-1-yl]methyl]pyrrolidin-1-yl)-3-(naphthalen-2-yl)propan-2-yl]piperazine-2,3-dione
-
additional information
-
application of aldosterone, atrial natriuretic peptide, asymmetric dimethylarginine, and angiotensin peptides fail to cause down-regulation of renal neprilysin expression in vitro
-
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
ACTIVATING COMPOUND
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
IMAGE
androgen
-
androgens positively regulate neural expression of neprilysin in adult male rats
-
dihydrotestosterone
-
induces a time-dependent increase in neprilysin expression. Dihydrotestosterone also significantly decreases levels of amyloid beta in androgen receptor-expressing cells transfected with amyloid precursor protein, but does not affect levels of either full-length or non-amyloidogenic, soluble amyloid precursor protein. The dihydrotestosterone-induced decrease of amyloid beta is blocked by pharmacological inhibition of neprilysin. The dihydrotestosterone-mediated increase in neprilysin expression and decrease in amyloid beta levels are not observed in rat pheochromocytoma cell 12 lacking androgen receptor and blocked in androgen receptor-expressing cells by the antagonists, cyproterone acetate and flutamide
estrogen
-
estrogen stimulates degradation of beta-amyloid peptide by up-regulating neprilysin
minocycline
-
minocycline abrogates the amyloid beta(25-35)-induced decrease of somatostatin-like immunoreactive content, somatostatin mRNA levels, phosphorylated-cAMP-response element binding protein CREB content and neprilysin levels. Minocycline alone enhances these targets
additional information
-
both staurosporine-stimulated caspase-3 activation, p53 and neprilysin expression and activity are not affected by over-expression or depletion of presenilin complex component TMP21
-
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
KM VALUE [mM]
SUBSTRATE
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
IMAGE
0.024
alpha-endorphin
-
wild-type enzyme, pH and temperature not specified in the publication
0.0086
angiotensin
-
wild-type enzyme, pH and temperature not specified in the publication
0.0062
Arg-vasopressin
-
wild-type enzyme, pH and temperature not specified in the publication
0.053
endothelin-1
-
wild-type enzyme, pH and temperature not specified in the publication
0.013
gamma-endorphin
-
wild-type enzyme, pH and temperature not specified in the publication
0.15
gastri-releasing peptide
-
wild-type enzyme, pH and temperature not specified in the publication
0.024
GLP-1
-
wild-type enzyme, pH and temperature not specified in the publication
-
0.025
glucagon
-
wild-type enzyme, pH and temperature not specified in the publication
0.011 - 0.087
N-(4-carboxy-1-oxobutyl)-L-alanyl-L-alanyl-N-(4-methoxy-2-naphthalenyl)-L-phenylalaninamide
0.0093
Neurokinin A
-
wild-type enzyme, pH and temperature not specified in the publication
0.022
neurokinin B
-
wild-type enzyme, pH and temperature not specified in the publication
0.02
nociceptin
-
wild-type enzyme, pH and temperature not specified in the publication
0.0074
somatostatin 14
-
wild-type enzyme, pH and temperature not specified in the publication
0.031
somatostatin 28
-
wild-type enzyme, pH and temperature not specified in the publication
additional information
additional information
-
Michaelis-Menten profiles and steady-state kinetic parameters for cleavage of amyloid beta peptide1-40 and off-target peptide by wild-type and mutant enzymes, overview
-
0.014
amyloid beta peptide1-40
-
mutant G399V/G714K, pH and temperature not specified in the publication
-
0.042
amyloid beta peptide1-40
-
mutant G714K, pH and temperature not specified in the publication
-
0.055
amyloid beta peptide1-40
-
mutant G399V, pH and temperature not specified in the publication
-
0.104
amyloid beta peptide1-40
-
wild-type enzyme, pH and temperature not specified in the publication
-
0.032
bradykinin
-
wild-type enzyme, pH and temperature not specified in the publication
0.011
N-(4-carboxy-1-oxobutyl)-L-alanyl-L-alanyl-N-(4-methoxy-2-naphthalenyl)-L-phenylalaninamide
-
pH 6.5, 37°C, mutant NEPS546A
0.051
N-(4-carboxy-1-oxobutyl)-L-alanyl-L-alanyl-N-(4-methoxy-2-naphthalenyl)-L-phenylalaninamide
-
pH 6.5, 37°C, wild-type enzyme and mutant NEPF563V
0.073
N-(4-carboxy-1-oxobutyl)-L-alanyl-L-alanyl-N-(4-methoxy-2-naphthalenyl)-L-phenylalaninamide
-
pH 6.5, 37°C, mutant NEPS546T
0.074
N-(4-carboxy-1-oxobutyl)-L-alanyl-L-alanyl-N-(4-methoxy-2-naphthalenyl)-L-phenylalaninamide
-
pH 6.5, 37°C, mutant NEPS546E
0.081
N-(4-carboxy-1-oxobutyl)-L-alanyl-L-alanyl-N-(4-methoxy-2-naphthalenyl)-L-phenylalaninamide
-
pH 6.5, 37°C, mutant NEPF563L
0.083
N-(4-carboxy-1-oxobutyl)-L-alanyl-L-alanyl-N-(4-methoxy-2-naphthalenyl)-L-phenylalaninamide
-
pH 6.5, 37°C, mutant NEPF563I
0.087
N-(4-carboxy-1-oxobutyl)-L-alanyl-L-alanyl-N-(4-methoxy-2-naphthalenyl)-L-phenylalaninamide
-
pH 6.5, 37°C, mutant NEPF563M
0.016
neurotensin
-
wild-type enzyme, pH and temperature not specified in the publication
0.016
Substance P
-
wild-type enzyme, pH and temperature not specified in the publication
0.054
succinyl-Ala-Ala-Phe-4-methylcoumarin 7-amide
-
enzyme from cerebrospinal fluid
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
TURNOVER NUMBER [1/s]
SUBSTRATE
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
IMAGE
8.9
alpha-endorphin
-
wild-type enzyme, pH and temperature not specified in the publication
8.2
angiotensin
-
wild-type enzyme, pH and temperature not specified in the publication
2.8
Arg-vasopressin
-
wild-type enzyme, pH and temperature not specified in the publication
0.68
endothelin-1
-
wild-type enzyme, pH and temperature not specified in the publication
4.8
gamma-endorphin
-
wild-type enzyme, pH and temperature not specified in the publication
26
gastri-releasing peptide
-
wild-type enzyme, pH and temperature not specified in the publication
3.3
GLP-1
-
wild-type enzyme, pH and temperature not specified in the publication
-
4.5
glucagon
-
wild-type enzyme, pH and temperature not specified in the publication
17
Neurokinin A
-
wild-type enzyme, pH and temperature not specified in the publication
20
neurokinin B
-
wild-type enzyme, pH and temperature not specified in the publication
13
neurotensin
-
wild-type enzyme, pH and temperature not specified in the publication
11
nociceptin
-
wild-type enzyme, pH and temperature not specified in the publication
32
somatostatin 14
-
wild-type enzyme, pH and temperature not specified in the publication
9.1
somatostatin 28
-
wild-type enzyme, pH and temperature not specified in the publication
0.83
amyloid beta peptide1-40
-
wild-type enzyme, pH and temperature not specified in the publication
-
1.9
amyloid beta peptide1-40
-
mutant G714K, pH and temperature not specified in the publication
-
2.1
amyloid beta peptide1-40
-
mutant G399V/G714K, pH and temperature not specified in the publication
-
2.7
amyloid beta peptide1-40
-
mutant G399V, pH and temperature not specified in the publication
-
16
bradykinin
-
wild-type enzyme, pH and temperature not specified in the publication
18
Substance P
-
wild-type enzyme, pH and temperature not specified in the publication
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
kcat/KM VALUE [1/mMs-1]
SUBSTRATE
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
IMAGE
390
alpha-endorphin
-
wild-type enzyme, pH and temperature not specified in the publication
970
angiotensin
-
wild-type enzyme, pH and temperature not specified in the publication
450
Arg-vasopressin
-
wild-type enzyme, pH and temperature not specified in the publication
480
bradykinin
-
wild-type enzyme, pH and temperature not specified in the publication
13
endothelin-1
-
wild-type enzyme, pH and temperature not specified in the publication
380
gamma-endorphin
-
wild-type enzyme, pH and temperature not specified in the publication
170
gastri-releasing peptide
-
wild-type enzyme, pH and temperature not specified in the publication
140
GLP-1
-
wild-type enzyme, pH and temperature not specified in the publication
-
180
glucagon
-
wild-type enzyme, pH and temperature not specified in the publication
1700
Neurokinin A
-
wild-type enzyme, pH and temperature not specified in the publication
920
neurokinin B
-
wild-type enzyme, pH and temperature not specified in the publication
820
neurotensin
-
wild-type enzyme, pH and temperature not specified in the publication
570
nociceptin
-
wild-type enzyme, pH and temperature not specified in the publication
4400
somatostatin 14
-
wild-type enzyme, pH and temperature not specified in the publication
160
somatostatin 28
-
wild-type enzyme, pH and temperature not specified in the publication
1100
Substance P
-
wild-type enzyme, pH and temperature not specified in the publication
8
amyloid beta peptide1-40
-
wild-type enzyme, pH and temperature not specified in the publication
-
45
amyloid beta peptide1-40
-
mutant G714K, pH and temperature not specified in the publication
-
49
amyloid beta peptide1-40
-
mutant G399V, pH and temperature not specified in the publication
-
150
amyloid beta peptide1-40
-
mutant G399V/G714K, pH and temperature not specified in the publication
-
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
Ki VALUE [mM]
INHIBITOR
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
IMAGE
1.08
Tat peptide 5118
-
preincubated neprilysin with 20 microg/ml peptide 5118 and then diluted 10fold into the assay
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
IC50 VALUE [mM]
INHIBITOR
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
IMAGE
0.00000237
(2R)-2-([1-[(5-ethyl-1,3,4-thiadiazol-2-yl)carbamoyl]cyclopentyl]methyl)pentanoic acid
Canis lupus familiaris
-
-
0.0000019
(2R)-2-[(1-[[(1S)-1-carboxy-2-(3-phenyl-1,2,4-oxadiazol-5-yl)ethyl]carbamoyl]cyclopentyl)methyl]-5-oxopentanoic acid
Homo sapiens
-
pH and temperature not specified in the publication
0.000022
(2R)-2-[(1-[[(1S)-1-carboxy-2-(4-ethyl-1,3-oxazol-2-yl)ethyl]carbamoyl]cyclopentyl)methyl]pentanoic acid
Homo sapiens
-
pH and temperature not specified in the publication
0.0000048
(2R)-2-[(1-[[(1S)-1-carboxy-2-(4-phenyl-1,3-oxazol-2-yl)ethyl]carbamoyl]cyclopentyl)methyl]-5-oxopentanoic acid
Homo sapiens
-
pH and temperature not specified in the publication
0.000007
(2R)-2-[(1-[[(1S)-1-carboxy-2-(4-phenyl-1,3-oxazol-2-yl)ethyl]carbamoyl]cyclopentyl)methyl]pentanoic acid
Homo sapiens
-
pH and temperature not specified in the publication
0.000006
(2R)-2-[(1-[[(1S)-1-carboxy-2-(5-phenyl-1,3,4-oxadiazol-2-yl)ethyl]carbamoyl]cyclopentyl)methyl]-5-oxopentanoic acid
Homo sapiens
-
pH and temperature not specified in the publication
0.0000003
(2R)-2-[(1-[[(1S)-1-carboxy-2-(5-phenyl-1,3-oxazol-2-yl)ethyl]carbamoyl]cyclopentyl)methyl]-5-oxopentanoic acid
Homo sapiens
-
pH and temperature not specified in the publication
0.0000006
(2R)-2-[(1-[[(1S)-1-carboxy-2-(5-phenyl-1,3-oxazol-2-yl)ethyl]carbamoyl]cyclopentyl)methyl]pentanoic acid
Homo sapiens
-
pH and temperature not specified in the publication
0.00002
(2R)-2-[[1-([(1S)-1-carboxy-2-[4-(2-methylpropyl)-1,3-oxazol-2-yl]ethyl]carbamoyl)cyclopentyl]methyl]pentanoic acid
Homo sapiens
-
pH and temperature not specified in the publication
0.0000003 - 0.000005
(2R)-2-[[1-([(1S)-1-carboxy-2-[5-(4-chlorophenyl)-1,3-oxazol-2-yl]ethyl]carbamoyl)cyclopentyl]methyl]-5-oxopentanoic acid
<