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Drug-Target Interaction

Drug

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PubChem ID:5280445
Structure:
Synonyms:
"3′,4′,5,7-tetrahydroxyflavone"
2-(3,4-Dihydroxyphenyl)-5,7-dihydroxy-4-benzopyrone
2-(3,4-dihydroxyphenyl)-5,7-dihydroxy-4H-1-benzopyran-4-one
2-(3,4-dihydroxyphenyl)-5,7-dihydroxy-4H-chromen-4-one
2-(3,4-dihydroxyphenyl)-5,7-dihydroxychromen-4-one
23A002A4-B47B-46CD-848C-65042EACF3FF
3′,4′,5,7-Tetrahydroxyflavone
3',4',5,7-Tetrahydroxy-Flavone
3',4',5,7-Tetrahydroxyflavone
491-70-3
4H-1-Benzopyran-4-one, 2-(3,4-dihydroxyphenyl)-5,7-dihydroxy-
4H-1-Benzopyran-4-one, 2-(3,4-dihydroxyphenyl)-5,7-dihydroxy- (9CI)
4H-Benzopyran-4-one, 2-(3,4-dihydroxyphenyl)-5,7-dihydroxy-
4H-Benzopyran-4-one, 2-(3,4-dihydroxyphenyl)-5,7-dihydroxy-;
5,7,3',4'-Tetrahydroxyflavone
5-18-05-00296 (Beilstein Handbook Reference)
AC-1125
AC1NQX1A
ACon1_000223
AIDS-001406
AIDS001406
AKOS002140588
BB_NC-1244
BIDD:ER0122
BIDD:PXR0059
BPBio1_001011
BRD-K05236810-001-05-9
BRN 0292084
BSPBio_000919
C.I. 75590
C.I. Natural Yellow 2
C01514
C15H10O6
CAS-491-70-3
CCRIS 3790
CHEBI:15864
CHEMBL151
Cyanidenon 1470
D047311
Digitoflavone
EINECS 207-741-0
Flacitran
FLAVONE, 3',4',5,7-TETRAHYDROXY-
HMS1570N21
HMS2097N21
HMS2220C06
I06-0436
IN1269
L 9283
L9283_SIGMA
LMPK12110006
Lopac0_000660
LS-69039
Luteolin
Luteolin, 3',4',5,7-Tetrahydroxyflavone, Luteoline, Luteolol
Luteolin-Supplied by Selleck Chemicals
Luteoline
Luteolol
MEGxp0_000143
MLS000697655
MLS000860038
MLS002154043
MolPort-000-706-683
NCGC00016467-01
NCGC00016467-02
NCGC00016467-03
NCGC00016467-04
NCGC00016467-05
NCGC00016467-06
NCGC00016467-07
NCGC00142375-01
NCGC00142375-02
NCGC00142375-03
NCGC00179375-01
NCGC00179375-02
Oprea1_849964
Prestwick0_000870
Prestwick1_000870
Prestwick2_000870
Prestwick3_000870
Prestwick_122
S00110
S2320_Selleck
Salifazide
SMP2_000042
SMR000326896
SPBio_002840
ST024703
STK801923
TNP00073
Weld Lake
Yama kariyasu
ZINC18185774

Target

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Uniprot ID:Q8CHM5_MOUSE
Synonyms:
Ribosomal protein S6 kinase
EC-Numbers:-
Organism:Mouse
Mus musculus
PDB IDs:-

Binding Affinities:

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

15520200
Luteolin inhibits vascular endothelial growth factor-induced angiogenesis; inhibition of endothelial cell survival and proliferation by targeting phosphatidylinositol 3'-kinase activity.. Eleni Bagli; Maria Stefaniotou; Lucia Morbidelli; Marina Ziche; Konstantinos Psillas; Carol Murphy; Theodore Fotsis (2004) Cancer research display abstract
In an attempt to identify phytochemicals contributing to the well-documented preventive effect of plant-based diets on cancer incidence and mortality, we have previously shown that certain flavonoids inhibit in vitro angiogenesis. Here, we show that the flavonoid luteolin inhibited tumor growth and angiogenesis in a murine xenograft model. Furthermore, luteolin inhibited vascular endothelial growth factor (VEGF)-induced in vivo angiogenesis in the rabbit corneal assay. In agreement, luteolin inhibited both VEGF-induced survival and proliferation of human umbilical vein endothelial cells (HUVECs) with an IC(50) of about 5 mumol/L. Luteolin inhibited VEGF-induced phosphatidylinositol 3'-kinase (PI3K) activity in HUVECs, and this inhibition was critical for both the antisurvival and antimitotic affects of the compound. Indeed, luteolin abolished VEGF-induced activation of Akt, a downstream target of PI3K conveying both survival and mitotic downstream signals. Because overexpression of a constitutively active form of Akt rescued HUVECs only from the antisurvival effects of luteolin, the result indicated that luteolin targeted mainly the survival signals of the PI3K/Akt pathway. With regard to its antimitotic activity, luteolin inhibited VEGF-induced phosphorylation of p70 S6 kinase (S6K), a downstream effector of PI3K responsible for G(1) progression. Indeed, VEGF-induced proliferation of HUVECs was sensitive to rapamycin, an inhibitor of p70 S6K activation. Surprisingly, luteolin did not affect VEGF-induced phosphorylation of extracellular signal-regulated kinase 1/2 mitogen-activated protein kinases, a pathway that is considered important for the mitotic effects of VEGF. Thus, blockade of PI3K by luteolin was responsible for the inhibitory effects of the compound on VEGF-induced survival and proliferation of HUVECs. The antisurvival effects of luteolin were mediated via blockage of PI3K/Akt-dependent pathways, whereas inhibition of the PI3K/p70 S6K pathway mediated the antimitotic effects of the compound.