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Drug-Target Interaction

Drug

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PubChem ID:2754
Structure:
Synonyms:
2(1H)-Quinolinone,
2(1H)-Quinolinone, 3,4-dihydro-6-(4-(1-cyclohexyl-1H-tetrazol-5-yl)butoxy)-
2(1H)-Quionlinone, 6-(4-(1-cyclohexyl-1H-tetrazol-5-yl)butoxy)-3,4-dihydro-
3,4-Dihydro-6-(4-(1-cyclohexyl-1H-tetrazol-5-yl)butoxy)-2(1H)-quinolinone
6-(4-(1-Cyclohexyl-1H-tetrazol-5-yl)butoxy)-3,4-dihydro-2(1H)-quinolinone
6-(4-(1-Cyclohexyl-1H-tetrazol-5-yl)butoxy)-3,4-dihydrocarbostyril
6-(4-(1-Cyclohexyl-1H-tetrazol-5-yl)butoxyl)-3,4-dihydrocarobostyril
6-[4-(1-Cyclohexyl-1H-tetrazol-5-yl)-butoxy]-3,4-dihydro-2(1H)-quinolinone
6-[4-(1-cyclohexyltetrazol-5-yl)butoxy]-3,4-dihydro-1H-quinolin-2-one
73963-72-1
89332-50-3
BRN 3632107
BSPBio_002759
C045645
C0737_SIGMA
C20H27N5O2
CHEBI:31401
CILOSTAZOL
Cilostazol (JP15/USAN/INN)
Cilostazol [INN:JAN]
Cilostazole
Cilostazolum
Cilostazolum [INN-Latin]
CPD000058428
D01896
DB01166
EU-0100218
KBio3_002259
KBioGR_001184
Lopac-C-0737
Lopac0_000218
LS-142693
MLS000028470
MLS000758281
MLS000759507
MLS001076067
MLS002153891
NCGC00015207-01
NCGC00015207-02
NCGC00022153-02
NCGC00022153-04
NCGC00022153-05
NCGC00022153-06
NCGC00022153-07
OPC 13013
OPC 21
OPC-13013
OPC-21
Otsuka brand of cilostazol
Pharmacia brand of cilostazol
Pletaal
Pletal
Pletal (TN)
Pletal, Cilostazol
SAM001246734
SAM001247085
SMR000058428
SPBio_001256
SPECTRUM1505230
Spectrum2_001118
Spectrum3_001170
Spectrum4_000772
Spectrum5_001762
ST5408866
TL8005113
Tocris-1692
ZINC01552174

Target

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Uniprot ID:KAPCG_HUMAN
Synonyms:
cAMP-dependent protein kinase catalytic subunit gamma
PKA C-gamma
EC-Numbers:2.7.11.11
Organism:Homo sapiens
Human
PDB IDs:-

Binding Affinities:

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

References:

16822680
Protection from apoptotic cell death by cilostazol, phosphodiesterase type III inhibitor, via cAMP-dependent protein kinase activation.. Mi Jeong Kim; Jeong Hyun Lee; So Youn Park; Ki Whan Hong; Chi Dae Kim; Ki Young Kim; Won Suk Lee (2006) Pharmacological research : the official journal of the Italian Pharmacological Society display abstract
This study aimed to elucidate whether the effect of cilostazol to suppress apoptotic cell death is directly coupled to cAMP-dependent protein kinase activation in human umbilical vein endothelial cells (HUVECs). After exposure of HUVECs to LPS (1 microgml(-1)) for 18 h, the endothelial cells irregularly aggregated with loss of cobblestone appearance, which was reversed by cilostazol (1-100 microM), as well as by cilostamide (cilostazol analog), and cilostazol metabolites (OPC-13015 and OPC-31213), respectively. LPS-stimulated production of reactive oxygen species (ROS) was significantly reduced by cilostazol (0.1-10 microM). In line with these, LPS (1 microgml(-1))- and TNF-alpha (200 ngml(-1))-induced DNA fragmentation, assessed by agarose gel electrophoresis, was significantly reduced by treatment with cilostazol (10 microM) as well as by dibutyryl cAMP (100 microM). This effect was reversed by cAMP-dependent protein kinase inhibitor, Rp-cAMPs (200 microM). Further, LPS (1 microgml(-1))-induced decrease in Bcl-2 and increase in Bax protein expression were fully reversed by cilostazol (10 microM) and dibutyryl cAMP (100 microM), all of which were antagonized by Rp-cAMPs (200 microM). Taken together, cilostazol effectively protected HUVECs from LPS- and TNF-alpha-induced cell death associated with oligonucleosomal DNA fragmentation via activation of cAMP-dependent protein kinase.