Home
Drugs
Targets
Pathways
Ontologies
Cyp450s
Adv.search
Help/FAQ

Drug-Target Interaction

Drug

show drug details
PubChem ID:77999
Structure:
Synonyms:
122320-73-4
2,4-Thiazolidinedione,
2,4-Thiazolidinedione, 5-((4-(2-(methyl-2-pyridinylamino)ethoxy)phenyl)methyl)-
2,4-Thiazolidinedione, 5-004-02-((((methyl-2-pyridinylamino)ethoxy)phenyl)methyl)-
2,4-thiazolidinedione, 5-[[4-[2-(methyl-2-pyridinylamino)ethoxy]phenyl]methyl]-
2,4-Thiazolidinedione, 5-[[4-[2-(methyl-2-pyridinylamino)ethoxy]phenyl]methyl]- (9CI)
5-((4-(2-(methyl-2-pyridinylamino)ethoxy)phenyl)methyl)-2,4-thiazolidinedione
5-((4-(2-Methyl-2-(pyridinylamino)ethoxy)phenyl)methyl)-2,4-thiazolidinedione-2-butenedioate
5-(4-{2-[methyl(pyridin-2-yl)amino]ethoxy}benzyl)-1,3-thiazolidine-2,4-dione
5-[4-[2-(N-Methyl-N-(2-pyridyl)amino)ethoxy]benzyl]thiazolidine-2,4-dione
5-[[4-[2-(methyl-(2-pyridyl)amino)ethoxy]phenyl]methyl] thiazolidine-2,4-dione
5-[[4-[2-(methyl-pyridin-2-ylamino)ethoxy]phenyl]methyl]-1,3-thiazolidine-2,4-dione
Avandaryl
Avandia
BB_SC-4138
Brl 49653
Brl-49653
BRL49653
BSPBio_002693
C18H19N3O3S
CHEBI:50122
DB00412
IDMB (1uM BRL49653, 1uM Dexamethasone, 0.5uM IBMX, 10ug/mL Insulin)
KBio2_002183
KBio2_004751
KBio2_007319
KBio3_001913
KBioGR_001609
KBioSS_002183
LS-151340
NCGC00095124-01
NCGC00095124-02
NCGC00095124-03
RGZ
Rosi
Rosigilitazone
Rosigliazone maleate
Rosiglitazone
rosiglitazone (Avandia)
Rosiglitazone maleate
Rosiglitazone [INN:BAN]
Rosiglizole
RSG
S00306
SPBio_001142
SPECTRUM1504263
Spectrum2_001241
Spectrum3_000997
Spectrum4_001125
Spectrum5_001464
Spectrum_001703
TDZ 01
[3H]rosiglitazone
ATC-Codes:
Side-Effects:
Side-EffectFrequency
abdominal pain0.0010
hyperbilirubinemia0.0010
hyperglycemia0.0010
hypoglycemia0.0010
influenza0.0010
nasopharyngitis0.0010
nausea0.0010
pain0.0010
pleural effusions0.0010
pruritus0.0010
pulmonary edema0.0010
sinusitis0.0010
stevens - johnson syndrome0.0010
upper respiratory tract infection0.0010
urticaria0.0010
vomiting0.0010
hepatic failure0.0010
hepatitis0.0010
congestive heart failure0.0010
cardiac failure0.0010
anaphylactic reaction0.0010
anemia0.0010
angioedema0.0010
back pain0.0010
cough0.0010
type 2 diabetes0.0010
diabetic ketoacidosis0.0010
diarrhea0.0010
dizziness0.0010
dysmenorrhea0.0010
headache0.0010
edema0.0010
rash0.0010
weight gain0
fatigue0
hypertension0
arthralgia0
constipation0
myocardial infarction0
myocardial ischemia0

Target

show target details
Uniprot ID:CASP3_MOUSE
Synonyms:
Apopain
CASP-3
Caspase-3
CPP-32
Cysteine protease CPP32
LICE
SCA-1
SREBP cleavage activity 1
Yama protein
EC-Numbers:3.4.22.56
Organism:Mouse
Mus musculus
PDB IDs:-

Binding Affinities:

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

References:

18560759
Rosiglitazone counteracts palmitate-induced beta-cell dysfunction by suppression of MAP kinase, inducible nitric oxide synthase and caspase 3 activities.. S Meidute Abaraviciene; I Lundquist; A Salehi (2008) Cellular and molecular life sciences : CMLS display abstract
Chronic exposure of pancreatic islets to elevated levels of palmitate leads to beta-cell dysfunction. We examined possible involvement of mitogenactivated protein kinases (MAPKs) and caspase-3 in palmitate-induced beta-cell dysfunction and tested the influence of the anti-diabetic drug rosiglitazone (ROZ). Palmitate amplified glucose-stimulated augmentation of intracellular free calcium ([Ca2+]i) and insulin secretion in incubated islets. ROZ suppressed this amplification, whereas it modestly augmented glucose-induced increase in these events. ROZ suppressed short-term palmitate-induced phosphorylation of pro-apoptotic MAPKs, i.e., SAPK/JNK and p38. Long-term islet culturing with palmitate induced inducible nitric oxide synthase (iNOS) and activated SAPK/JNK-p38. ROZ counteracted these effects. Both palmitate and cytokines activated caspase-3 in MIN6c4-cells and isolated islets. ROZ suppressed palmitate- but not cytokine-induced caspase-3 activation. Finally, after palmitate culturing, ROZ reversed the inhibitory effect on glucose-stimulated insulin release. We suggest that ROZ counteracts palmitateinduced deleterious effects on beta-cell function via suppression of iNOS, pro-apoptotic MAPKs and caspase-3 activities, as evidenced by restoration of glucose-stimulated insulin release.