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Drug-Target Interaction

Drug

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PubChem ID:5280443
Structure:
Synonyms:
"4′,5,7-trihydroxyflavone"
"apigenin; 4',5,7-trihydroxyflavone"
10798_FLUKA
10798_SIGMA
2-(p-Hydroxyphenyl)-5,7-dihydroxychromone
3cf9
4′,5,7-Trihydroxyflavone
4',5,7-Trihydroxyflavone
461015-54-3
4H-1-Benzopyran-4-one, 5,7-dihydroxy-2-(4-hydroxyphenyl)-
4H-1-Benzopyran-4-one, 5,7-dihydroxy-2-(4-hydroxyphenyl)- (9CI)
5,7,4'-Trihydroxyflavone
5,7-Dihydroxy-2-(4-hydroxyphenyl)-4-benzopyrone
5,7-Dihydroxy-2-(4-hydroxyphenyl)-4H-1-benzopyran-4-one
5,7-dihydroxy-2-(4-hydroxyphenyl)-4H-chromen-4-one
5,7-dihydroxy-2-(4-hydroxyphenyl)chromen-4-one
5-18-04-00574 (Beilstein Handbook Reference)
520-36-5
A 3145
A3145_SIGMA
AC-11665
AC1NQX15
ACon1_002450
AG-F-76922
AGI
AIDS-001401
AIDS001401
AKOS002140699
Apigenin
Apigenin-Supplied by Selleck Chemicals
Apigenin; 4',5,7-Trihydroxyflavone
Apigenine
Apigenol
BB_NC-1751
BIDD:ER0135
Bio1_000376
Bio1_000865
Bio1_001354
Biochem Biophys Res Comm 212: 767 (1997)
BiomolKI2_000082
BiomolKI_000078
BPBio1_000406
BRD-K01493881-001-10-4
BRN 0262620
BSPBio_000368
BSPBio_003384
C.I. Natural Yellow 1
C01477
C15H10O5
CAS-520-36-5
CCG-40061
CCRIS 3789
Chamomile
CHEBI:18388
CHEMBL28
D50A2D8A-6D8B-4708-B21E-2DE9580D033F
DB07352
DivK1c_000798
EINECS 208-292-3
EU-0100065
Flavone, 4',5,7-trihydroxy-
ghl.PD_Mitscher_leg0.1194
HMS1569C10
HMS1922P22
HMS2096C10
HMS2230D17
HMS3260M11
HMS502H20
HSCI1_000221
HSDB 7573
I06-0221
IDI1_000798
K00045
KBio1_000798
KBio3_002887
KBioGR_002565
LMPK12110005
Lopac-A-3145
Lopac0_000065
LS-2209
MEGxp0_000176
MLS000697626
MLS000859991
MLS001074874
MolPort-001-740-354
NCGC00015049-01
NCGC00015049-02
NCGC00015049-03
NCGC00015049-04
NCGC00015049-05
NCGC00015049-06
NCGC00015049-07
NCGC00015049-08
NCGC00015049-09
NCGC00015049-10
NCGC00015049-11
NCGC00015049-12
NCGC00015049-13
NCGC00015049-14
NCGC00015049-15
NCGC00015049-16
NCGC00025057-01
NCGC00025057-02
NCGC00025057-03
NCGC00025057-04
NCGC00025057-05
NCGC00025057-06
NCGC00025057-07
NCGC00025057-08
NCGC00025057-09
NCGC00169835-01
NCGC00169835-02
NCGC00169835-03
nchembio790-comp26
NCI60_041830
ND-9076
NINDS_000798
NSC 83244
NSC-83244
NSC83244
Oprea1_622293
Pelargidenon 1449
Prestwick0_000414
Prestwick1_000414
Prestwick2_000414
Prestwick3_000414
Prestwick_719
S2262_Selleck
SDCCGMLS-0066379.P001
SMP2_000338
SMR000326850
SPBio_000416
SPBio_002307
SPECTRUM200846
Spectrum2_000428
Spectrum3_001882
Spectrum4_001999
Spigenin
ST056301
STK801630
Tocris-1227
UCCF 031
Versulin
ZINC03871576

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:
----
----
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References:

14602723
Apigenin induces apoptosis through proteasomal degradation of HER2/neu in HER2/neu-overexpressing breast cancer cells via the phosphatidylinositol 3-kinase/Akt-dependent pathway.. Tzong-Der Way; Ming-Ching Kao; Jen-Kun Lin (2004) The Journal of biological chemistry display abstract
Apigenin is a low toxicity and non-mutagenic phytopolyphenol and protein kinase inhibitor. It exhibits anti-proliferating effects on human breast cancer cells. Here we examined several human breast cancer cell lines having different levels of HER2/neu expression and found that apigenin exhibited potent growth-inhibitory activity in HER2/neu-overexpressing breast cancer cells but was much less effective for those cells expressing basal levels of HER2/neu. Induction of apoptosis was also observed in HER2/neu-overexpressing breast cancer cells in a dose- and time-dependent manner. However, the one or more molecular mechanisms of apigenin-induced apoptosis in HER2/neu-overexpressing breast cancer cells remained to be elucidated. A cell survival pathway involving phosphatidylinositol 3-kinase (PI3K), and Akt is known to play an important role in inhibiting apoptosis in response to HER2/neu-overexpressing breast cancer cells, which prompted us to investigate whether this pathway plays a role in apigenin-induced apoptosis in HER2/neu-overexpressing breast cancer cells. Our results showed that apigenin inhibits Akt function in tumor cells in a complex manner. First, apigenin directly inhibited the PI3K activity while indirectly inhibiting the Akt kinase activity. Second, inhibition of HER2/neu autophosphorylation and transphosphorylation resulting from depleting HER2/neu protein in vivo was also observed. In addition, apigenin inhibited Akt kinase activity by preventing the docking of PI3K to HER2/HER3 heterodimers. Therefore, we proposed that apigenin-induced cellular effects result from loss of HER2/neu and HER3 expression with subsequent inactivation of PI3K and AKT in cells that are dependent on this pathway for cell proliferation and inhibition of apoptosis. This implies that the inhibition of the HER2/HER3 heterodimer function provided an especially effective strategy for blocking the HER2/neu-mediated transformation of breast cancer cells. Our results also demonstrated that apigenin dissociated the complex of HER2/neu and GRP94 that preceded the depletion of HER2/neu. Apigenin-induced degradation of mature HER2/neu involves polyubiquitination of HER2/neu and subsequent hydrolysis by the proteasome.
15746177
Apigenin inhibits VEGF and HIF-1 expression via PI3K/AKT/p70S6K1 and HDM2/p53 pathways.. Jing Fang; Chang Xia; Zongxian Cao; Jenny Z Zheng; Eddie Reed; Bing-Hua Jiang (2005) The FASEB journal : official publication of the Federation of American Societies for Experimental Biology display abstract
Apigenin is a nontoxic dietary flavonoid that has been shown to possess anti-tumor properties and therefore poses special interest for the development of a novel chemopreventive and/or chemotherapeutic agent for cancer. Ovarian cancer is one of the most common causes of cancer death among women. Here we demonstrate that apigenin inhibits expression of vascular endothelial growth factor (VEGF) in human ovarian cancer cells. VEGF plays an important role in tumor angiogenesis and growth. We found that apigenin inhibited VEGF expression at the transcriptional level through expression of hypoxia-inducible factor 1alpha (HIF-1alpha). Apigenin inhibited expression of HIF-1alpha and VEGF via the PI3K/AKT/p70S6K1 and HDM2/p53 pathways. Apigenin inhibited tube formation in vitro by endothelial cells. These findings reveal a novel role of apigenin in inhibiting HIF-1 and VEGF expression that is important for tumor angiogenesis and growth, identifying new signaling molecules that mediate this regulation.
16722316
Effect of three flavones on enzyme activity of recombinant human phosphoinositide 3-kinase p110beta catalytic subunit. Wen Liu; Nian-Ci Liang; Ren-Bin Huang (2006) Zhong yao cai display abstract
OBJECTIVE: To study the effect of three flavones-luteolin, apigenin and genistein on activity of recombinant human phosphoinositide 3-kinase (PI3-K) p110beta catalytic subunit. METHODS: Recombinant human P13-K p110beta catalytic subunit was expressed by gene engineering. PI3-K activity was assayed by incubation recombinant PI3-K p110beta with phosphatidylinostiol-4,5-bisphosphate and [gamma-32P] ATP; the 32P-radiolabeled lipids were extracted with cholroform and methanol, and assessed by scintillation counter. RESULTS: Luteolin and apigenin showed inhibition on the recombinant p110beta catalytic subunit with IC50 8. 65 micromol/L and 11.56 micromol/L, but genistein had no inhibition. CONCLUSION: Luteolin and apigenin are inhibitors of P13-K. The recombinant P13-K p1100 catalytic subunit may be used as a molecular target for simpler screening and development of more effective inhibitors of P13-K.