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Drug-Target Interaction

Drug

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PubChem ID:289
Structure:
Synonyms:
1,2-benzenediol
1,2-dihydroxybenzene
1,3-dihydroxybenzene
120-80-9
12385-08-9
135011_SIAL
16474-89-8
16474-90-1
2-(5,8-Dihydroxy-1-methoxy-3-methyl(2-naphthyl))-5-methoxy-7-methylnaphthalene-1,4-diol
2-hydroxyphenol
20244-21-7
20244-21-7 (unspecified hydrochloride salt)
37349-32-9
4-06-00-05557 (Beilstein Handbook Reference)
430749_ALDRICH
430749_SIAL
AB-131/40235236
AB1002105
AC1L18WM
AC1Q78GA
AG-D-45381
AI3-03995
AIDS-108194
AIDS108194
AKOS000119002
alpha-hydroxyphenol
BBL002408
BB_NC-2239
Benzcatechin
Benzene, o-dihydroxy-
benzene-1,2-diol
benzenediol
BIDD:ER0327
bmse000385
Brenzcatechin
BRN 0471401
C 9510
C.I. 76500
C.I. Oxidation Base 26
C00090
c0097
C01785
C034221
C15571
C3561_SIAL
C9510_SIAL
C9593_SIGMA
CAQ
Catechin
Catechin (phenol)
CATECHOL
Catechol (phenol)
catechol dipotassium salt
catechol sodium salt
catechol, 14C-labeled cpd
Catechol-pyrocatechol
Catechol-UL-14C
CCG-204375
CCRIS 741
CHEBI:18135
CHEMBL280998
CI 76500
CI Oxidation Base 26
DB02232
Dihydroxybenzene
Durafur developer C
Durafur Developer CFouramine PCH
EINECS 204-427-5
EU-0100280
Fouramine PCH
Fourrine 68
HMS2233A17
HMS3260H22
HSDB 1436
I01-2906
Katechol
Katechol [Czech]
Lopac-C-9510
Lopac0_000280
LS-637
MLS002153385
MLS002303022
MolPort-000-871-939
NCGC00015283-01
NCGC00015283-02
NCGC00015283-03
NCGC00015283-04
NCGC00015283-05
NCGC00015283-06
NCGC00015283-07
NCGC00015283-08
NCGC00091262-01
NCGC00091262-02
NCGC00091262-03
nchembio801-comp10
NCI-C55856
NSC 1573
NSC1573
o Dihydroxybenzene
o-Benzenediol
o-Dihydroxybenzene
o-Dioxybenzene
o-Diphenol
o-Hydroquinone
o-Hydroxyphenol
o-Phenylenediol
ortho-Benzenediol
ortho-Dihydroxybenzene
ortho-Dioxybenzene
ortho-Hydroquinone
ortho-Hydroxyphenol
ortho-Phenylenediol
Oxyphenic acid
P0317
P0567
Pelagol Grey C
phenol derivative, 2
Phthalhydroquinone
pyrocatechin
Pyrocatechine
Pyrocatechinic acid
Pyrocatechinic acidPyrocatechol
pyrocatechol
pyrocatechol-ul-14C
Pyrocatechuic acid
Pyrokatechin
Pyrokatechin [Czech]
Pyrokatechol
Pyrokatechol [Czech]
SMR000326660
ST5214346
STK398651
WLN: QR BQ
ZINC13512214

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:

17539658
Tea polyphenol (-)-epigallocatechin 3-gallate suppresses heregulin-beta1-induced fatty acid synthase expression in human breast cancer cells by inhibiting phosphatidylinositol 3-kinase/Akt and mitogen-activated protein kinase cascade signaling.. Min-Hsiung Pan; Cheng-Chan Lin; Jen-Kun Lin; Wei-Jen Chen (2007) Journal of agricultural and food chemistry display abstract
Tumor-associated fatty acid synthase (FAS) is implicated in tumorigenesis and connected to HER2 (human epidermal growth factor receptor 2) by systemic analyses. Suppression of FAS in cancer cells may lead to growth inhibition and cell apoptosis. Our previous study demonstrated that (-)-epigallocatechin 3-gallate (EGCG), the green tea catechin, could down-regulate FAS expression by suppressing EGFR (epidermal growth factor receptor) signaling and downstream phosphatidylinositol 3-kinase (PI3K)/Akt activation in the MCF-7 breast cancer cell line. Herein, we examined the effects of EGCG on FAS expression modulated by another member of the erbB family, that is, HER2 or HER3. We identified that heregulin-beta1 (HRG-beta1), a HER3 ligand, stimulated dose-dependent FAS expression in breast cancer cell lines MCF-7 and AU565, but not MDA-MB-453. The time-dependent increase in FAS expression after HRG-beta1 stimulation was also observed in MCF-7 cells, and this up-regulation was de novo RNA synthesis dependent. Treatment of MCF-7 cells with EGCG markedly inhibited HRG-beta1-dependent induction of mRNA and protein of FAS. EGCG also decreased the phosphorylation of Akt and extracellular signal-regulated kinase 1/2 that were demonstrated as selected downstream HRG-beta1-responsive kinases required for FAS expression using dominant-negative Akt, PI3K inhibitors (LY294002 and wortmannin), or MEK inhibitor (PD98059). FAS induction by HRG-beta1 was also blocked by AG825, a selective HER2 inhibitor, and by genistein, a selective tyrosine kinase inhibitor, indicating the formation of a heterodimer between HER2 and HER3, and their tyrosine kinase activities are essential for HRG-beta1-mediated elevation of FAS. Additionally, growth inhibition of HRG-beta1-treated cells was parallel to suppression of FAS by EGCG. Taken together, these findings extend our previous study to indicate that EGCG may be useful in the chemoprevention of breast carcinoma in which FAS overexpression results from HER2 or/and HER3 signaling.