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Drug-Target Interaction

Drug

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PubChem ID:4549
Structure:
Synonyms:
(NPPB)
107254-86-4
2-PHENPROPYLAMINO-5-NITROBENZOIC ACID
5 nitro 2 (3 phenylpropylamino)benzoic acid
5-NITRO-2-(3-PHENYLPROPYLAMINO)-BENZOIC ACID
5-Nitro-2-(3-phenylpropylamino)benzoic acid
5-nitro-2-[(3-phenylpropyl)amino]benzoic acid
AC1L1IEV
AC1Q20U0
AR-1G9096
Benzoic acid, 5-nitro-2-((3-phenylpropyl)amino)-
Bio1_000124
Bio1_000613
Bio1_001102
BRD-K89272762-001-02-8
BRD-K89272762-001-04-4
Brit J Pharmacol 117: 175 (1996)
BSPBio_001423
BSPBio_003195
C058176
C13705
CBiol_001838
CCG-39187
CHEMBL1256759
DivK1c_000619
EU-0100857
HMS1791H05
HMS1989H05
HMS2235P03
HMS3262L15
HMS501O21
IDI1_000619
IN1196
KBio1_000619
KBio2_002309
KBio2_004877
KBio2_007445
KBio3_002695
KBioGR_000715
KBioSS_002311
Lopac-N-4779
Lopac0_000857
LS-186884
LS-187538
MLS000859983
N 4779
N4779_SIGMA
NCGC00015740-01
NCGC00015740-02
NCGC00015740-03
NCGC00015740-04
NCGC00015740-05
NCGC00015740-06
NCGC00015740-07
NCGC00015740-08
NCGC00015740-09
NCGC00015740-10
NCGC00024671-01
NCGC00024671-02
NCGC00024671-03
NCGC00024671-04
NCGC00024671-05
NCGC00024671-06
NCGC00024671-07
NCGC00024671-08
NINDS_000619
NPPB
SMR000326842
SPBio_001433
Spectrum2_001477
Spectrum3_001518
Spectrum4_000338
Spectrum5_001244
Spectrum_001814
Tocris-0593
UPCMLD-DP143
UPCMLD-DP143:001
UPCMLD-DP143:002

Target

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Uniprot ID:ICE_DROME
Synonyms:
Caspase
drICE
EC-Numbers:3.4.22.-
Organism:Drosophila melanogaster
Fruit fly
PDB IDs:-

Binding Affinities:

Ki: Kd:Ic 50:Ec50/Ic50:
----

References:

11981408
Amelioration of myocardial global ischemia/reperfusion injury with volume-regulatory chloride channel inhibitors in vivo.. Kazuhiro Mizoguchi; Hajime Maeta; Akira Yamamoto; Masahiro Oe; Hiroaki Kosaka (2002) Transplantation display abstract
BACKGROUND: Recently, the apoptotic volume decrease was suggested to be regulated by volume regulatory Cl- channels in cultured cell lines. We thus examined whether inhibition of volume-regulatory Cl- channels is cardioprotective, like caspase inhibition, by hindering the apoptosis of cardiomyocytes induced by global ischemia/reperfusion (I/R) in vivo. METHODS: We performed global ischemia for 8 min at 37 degrees C or 4 degrees C in isolated rat hearts, followed by 24-hr reperfusion via heterotopic heart transplantation. The heart tissue was examined by means of the terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) method, genomic DNA electrophoresis, and caspase-3 activity. Two blockers of volume-regulatory Cl- channels, 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) and 5-nitro-2-(3-phenylpropylamino)-benzoate (NPPB), and a broad-spectrum caspase inhibitor, benzoyloxycarbonyl-Asp-CH2OC(O)-2,6-dichlorobenzene (Z-Asp-DCB), were administered intravenously. Triphenyltetrazolium chloride (TTC) staining and ultrasound cardiography were performed to examine myocardial viability. The TTC-unstained region was assessed by means of horseradish peroxidase (HRP) infiltration and the TUNEL method. RESULTS: The transplanted hearts showed TUNEL-positivity and DNA laddering with a peak at 24 hr during reperfusion after ischemia at 37 degrees C, but not at 4 degrees C. NPPB and DIDS were as potent as Z-Asp-DCB for recovery of cardiac function and for blocking the appearance of TUNEL-positivity, DNA laddering, caspase 3 activity, and a TTC-unstained area. TTC-unstained areas were composed of either TUNEL- and slightly HRP-positive or TUNEL-negative and strongly HRP-positive cardiomyocytes. CONCLUSION: The present results demonstrated that myocardial DNA fragmentation, caspase activation, and loss of cardiac function after global I/R were blocked by NPPB and DIDS, similar to in the case of Z-Asp-DCB. These results suggest that inhibition of volume-regulatory Cl- channels is also effective for preventing cardiac I/R injury.