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Drug-Target Interaction

Drug

show drug details
PubChem ID:123631
Structure:
Synonyms:
"gefitini; iressa"
184475-35-2
4-(3'-Chloro-4'-fluoroanilino)-7-methoxy-6-(3-morpholinopropoxy)quinazolin
4-(3'-Chloro-4'-fluoroanilino)-7-methoxy-6-(3-morpholinopropoxy)quinazoline
4-Quinazolinamine, N-(3-chloro-4-fluorophenyl)-7-methoxy-6-(3-(4-morpholinyl)propoxy)-
4-Quinazolinamine, N-(3-chloro-4-fluorophenyl)-7-methoxy-6-(3-4-morpholin)propoxy)-
6-(3-morpholinopropoxy)-N-(3-chloro-4-fluorophenyl)-7-methoxyquinazolin-4-amine
BCB03_000781
C419708
CCRIS 9011
CHEBI:49668
CU-00000000396-1
D01977
DB00317
Gefitini; Iressa
Gefitinib
Gefitinib (JAN/USAN/INN)
Gefitinib [USAN]
IRE
Iressa
Iressa (TN)
Irressat
K00240
KBioSS_002241
LS-139916
N-(3-Chloro-4-fluoro-phenyl)-7-methoxy-6-(3-morpholin-4-ylpropoxy)quinazolin-4-amine
N-(3-chloro-4-fluorophenyl)-7-methoxy-6-(3-(4-morpholinyl)propoxy)-4-quinazolinamide
N-(3-chloro-4-fluorophenyl)-7-methoxy-6-(3-(4-morpholinyl)propoxy)-4-quinazolinamine
N-(3-chloro-4-fluorophenyl)-7-methoxy-6-(3-morpholin-4-ylpropoxy)quinazolin-4-amine
N-(3-Chloro-4-fluorophenyl)-7-methoxy-6-(3-morpholinopropoxy)quinazolin-4-amine
N-(3-chloro-4-fluorophenyl)-7-methoxy-6-[3-(morpholin-4-yl)propoxy]quinazolin-4-amine
NCGC00159455-02
NCGC00159455-03
nchembio.117-comp18
nchembio866-comp14
NSC715055
STOCK6S-52331
ZD 1839
ZD-1839
ZD-1839, Iressa, Gefitinib
ZD1839
ZINC19632614
ATC-Codes:
Side-Effects:
Side-EffectFrequency
rash0.21499999
diarrhea0.19199999
acne0.125
dry skin0.065
nausea0.051999997
vomiting0.048
pruritus0.04
anorexia0.035
asthenia0.03
interstitial lung disease0.0010
toxic epidermal necrolysis0.0010
allergic reactions0.0010
eye pain0.0010
idiopathic pulmonary fibrosis0.0010
ulcer0.0010
interstitial pneumonia0.0010
pneumonitis0.0010
pancreatitis0.0010
cough0.0010
dyspnea0.0010
epistaxis0.0010
erythema multiforme0.0010
angioedema and urticaria0.0010
fever0.0010
hematuria0.0010
haemorrhage0.0010
ischemia0.0010
deep thrombophlebitis0
bundle branch block0
dry eyes0
mouth ulceration0
gastrointestinal hemorrhage0
peripheral edema0
exfoliative dermatitis0
dermatitis0
hypotension0
constitutional symptoms0
hemoptysis0
electrolyte imbalance0
tumor0
melena0
infection0
shock0
pleural effusion0
hypokalemia0
fatigue0
respiratory failure0
heart disease0
hypoxia0
conjunctivitis0
arrhythmia0
hypomagnesemia0
mediastinal disorders0
stevens - johnson syndrome0
thrombocytopenia0
stomatitis0
amblyopia0
sgot increased0
seborrhea0
constipation0
paronychia0
alopecia0
pain0
neutropenia0
nail disorder0
anemia0
dry mouth0
blepharitis0
urticaria0
abdominal pain0
dehydration0
atrial fibrillation0
pneumoconiosis0
edema0
vascular disorders0
weight loss0

Target

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Uniprot ID:PK3C3_HUMAN
Synonyms:
Phosphatidylinositol 3-kinase catalytic subunit type 3
Phosphatidylinositol 3-kinase p100 subunit
Phosphoinositide-3-kinase class 3
PI3-kinase type 3
PI3K type 3
PtdIns-3-kinase type 3
EC-Numbers:2.7.1.137
Organism:Homo sapiens
Human
PDB IDs:-

Binding Affinities:

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

References:

11585753
The tyrosine kinase inhibitor ZD1839 ("Iressa") inhibits HER2-driven signaling and suppresses the growth of HER2-overexpressing tumor cells.. M M Moasser; A Basso; S D Averbuch; N Rosen (2001) Cancer research display abstract
The epidermal growth factor receptor (EGFR) is commonly overexpressed in many human tumors and provides a new target for anticancer drug development. ZD1839 ("Iressa"), a quinazoline tyrosine kinase inhibitor selective for the EGFR, has shown good activity in preclinical studies and in the early phase of clinical trials. However, because it remains unclear which tumor types are the best targets for treatment with this agent, the molecular characteristics that correlate with tumor sensitivity to ZD1839 have been studied. In a panel of human breast cancer and other epithelial tumor cell lines, HER2-overexpressing tumors were particularly sensitive to ZD1839. Growth inhibition of these tumor cell lines was associated with the dephosphorylation of EGFR, HER2, and HER3, accompanied by the loss of association of HER3 with phosphatidylinositol 3-kinase, and down-regulation of Akt activity. These studies suggest that HER2-overexpressing tumors are particularly susceptible to the inhibition of HER family tyrosine kinase signaling and suggest novel strategies to treat these particularly aggressive tumors.
15604992
PLC and PI3K pathways are important in the inhibition of EGF-induced cell migration by gefitinib ('Iressa', ZD1839).. Tadahiko Shien; Hiroyoshi Doihara; Humikata Hara; Hirotoshi Takahashi; Seiji Yoshitomi; Naruto Taira; Youiti Ishibe; Jyun Teramoto; Motoi Aoe; Nobuyoshi Shimizu (2004) Breast cancer (Tokyo, Japan) display abstract
BACKGROUND: Expression of epidermal growth factor receptor (EGFR) by human breast cancer tissues is associated with poor clinical response. The EGFR tyrosine kinase inhibitor (EGFR-TKI), gefitinib ('Iressa', ZD1839), is a leading example of a molecular targeted agent, and has an anti-proliferative effect on various cancer cells. But the details of the anti-cancer effect and mechanism have not been elucidated. We studied the anti-cancer effect of gefitinib in breast cancer cell lines and the intracellular pathway downstream of EGFR associated with cell migration. METHODS: In this study, we analysed the anti-proliferative and anti-migratory effect of gefitinib in EGFR (+) breast cancer cell lines by WST-1 analysis and chemotaxis chamber analysis. We analyzed several intracellular phosphorylated pathways which are activated by mitogen activated kinases (extracellular signal-regulated protein kinase 1 and 2: MEK), phosphatidylinositol 3'-kinase (PI3K) and phpspholipase C (PLC), by blocking those pathways using inhibitors of each kinase, and also investigated the effects on the phosphorylation of myosin light chain (MLC). RESULTS: Gefitinib inhibited proliferation in most of these cell lines. MDA-MB231 was shown to be resistant. Furthermore, proliferation of MDA-MB231 cells was not affected by EGF stimulation, but migration of MDA-MB231 cells was significantly inhibited. PI3K and PLC inhibitors blocked EGF-stimulated cell migration and MLC phosphorylation, but the MEK inhibitor did not influence cell migration. CONCLUSIONS: Gefitinib has an anti-migratory effect on MDA-MB231 that results in an anti-proliferative effect. PI3K and PLC are important for the migration of MDA-MB231 cells, and gefitinib may inhibit migration by blocking these signalling pathways.