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Drug-Target Interaction

Drug

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PubChem ID:3698
Structure:
Synonyms:
(3,4'-BIPYRIDIN)-6(1H)-ONE, 5-AMINO-
3-Amino-5-(4-pyridinyl)-2(1H)-pyridinone
3-amino-5-pyridin-4-yl-1H-pyridin-2-one
5-25-15-00181 (Beilstein Handbook Reference)
5-Amino(3,4'-bipyridin)-6(1H)-one
5-Amino-(3,4'-bipyridin)-6(1H)-one
5-Amino-(3,4'-bipyridine)-6(1H)-one
5-amino-3,4'-bipyridin-6(1H)-one
60719-84-8
A4056_SIGMA
AC-12186
AC1L1GIK
Amcoral
Amcoral (TN)
Amrinon
Amrinona
Amrinona [INN-Spanish]
Amrinone
Amrinone (JAN/INN)
Amrinone [USAN:BAN:INN]
Amrinonum
Amrinonum [INN-Latin]
AWD 08-250
Bio-0795
BPBio1_001034
BRD-K45924332-001-04-4
BRN 0744819
BSPBio_000940
C10H9N3O
Cartonic
CAS-60719-84-8
CCG-39487
CCRIS 3794
CHEMBL12856
Cordarex
Cordemcura
D00231
DB01427
DivK1c_000136
EINECS 262-390-0
HMS1570O22
HMS2097O22
HMS2234F12
HMS3264E16
HMS500G18
I06-0688
IDI1_000136
Inamrinone
Inamrinone (USP)
Inamrinone lactate
Inamrinone [USAN:BAN:INN]
Inocor
KBio1_000136
KBio2_001830
KBio2_004398
KBio2_006966
KBio3_002052
KBioGR_001398
KBioSS_001830
LS-44658
MLS000069829
MLS001074083
NCGC00016896-01
NCGC00016896-02
NCGC00016896-03
NCGC00095984-01
NCGC00164379-01
NINDS_000136
Prestwick0_000800
Prestwick1_000800
Prestwick2_000800
Prestwick3_000800
Prestwick_44
SMR000058850
SPBio_002139
SPBio_002879
SPECTRUM1503084
Spectrum2_001980
Spectrum3_000956
Spectrum4_001069
Spectrum5_000999
Spectrum_001350
STK590307
STOCK5S-79086
UNII-JUT23379TN
WIN 40680
Win-40680
Wincoram
ZINC08673078
[3,4'-Bipyridin]-6(1H)-one, 5-amino-
ATC-Codes:
Side-Effects:
Side-EffectFrequency
thrombocytopenia0
hypersensitivity0
ascites0
hypotension0
chest pain0
abdominal pain0
fever0
pleurisy0
jaundice0
vomiting0
vasculitis0
esr increased0
anorexia0
nausea0
hemorrhage0
arrhythmia0
myositis0
pericarditis0

Target

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Uniprot ID:PDE4B_HUMAN
Synonyms:
cAMP-specific 3',5'-cyclic phosphodiesterase 4B
DPDE4
PDE32
EC-Numbers:3.1.4.17
Organism:Homo sapiens
Human
PDB IDs:1F0J 1JP1 1JP2 1RO6 1RO9 1ROR 1TB5 1XLX 1XLZ 1XM4 1XM6 1XMU 1XMY 1XN0 1XOS 1XOT 1Y2H 1Y2J 2CHM 2QYL 3D3P 3HC8 3HDZ
Structure:
3HDZ

Binding Affinities:

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

References:

9004165
Differential modulation of cytokine production by drugs: implications for therapy in heart failure.. A Matsumori; K Ono; Y Sato; T Shioi; Y Nose; S Sasayama (1996) Journal of molecular and cellular cardiology display abstract
We studied the effects of various phosphodiesterase (PDE) III inhibitors: amrinone, pimobendan and vesnarinone: a PDE IV inhibitor (Ro 20-1724) and a PDE V inhibitor (E-4021) on the production of cytokines which have been shown to depress myocardial function. Recently developed inotropic agents which inhibit PDE III activity have produced short-term hemodynamic benefits in patients with advanced heart failure, but long-term treatment with these agents has an adverse effect on survival. However, vesnarinone, which has been shown to improve survival dramatically, has an immunomodulating effect and inhibits the production of cytokines. Peripheral blood mononuclear cells obtained from healthy human subjects were stimulated with lipopolysaccharide and each PDE inhibitor was added. After 24 h of incubation, tumor necrosis factor alpha (TNF-alpha), interleukin 1 beta (IL-1 beta) and IL-6 in the culture supernatants were measured by an enzyme-linked immunosorbent assay. All three PDE III inhibitors, amrinone, pimobendan and vesnarinone, inhibited TNF-alpha production, but vesnarinone's inhibitory effect was the most prominent. Amrinone and pimobendan enhanced IL-1 beta production, whereas vesnarinone had no effect. Vesnarinone inhibited IL-6 production and pimobendan slightly decreased IL-6 production, whereas amrinone had no significant effect on IL-6 production. The PDE IV inhibitor, Ro 20-1724, decreased the production of IL-1 beta and TNF-alpha and also tended to inhibit IL-6 production; its modulation of cytokine production was similar to the effects of vesnarinone. Because 8Br-cAMP or 8Br-cGMP did not suppress cytokine production, the modulating effects were not considered to result from an increase in cAMP or cGMP. Differential modulation of cytokine production may play a role in the therapeutic effect in heart failure patients who are treated with drugs that have PDE-inhibitory actions. It may be important to study whether the use of dual inhibitors of PDE III and PDE IV is therapeutically more useful for the treatment of heart failure due to their immunomodulating properties.
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