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Drug-Target Interaction

Drug

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PubChem ID:5318569
Structure:
Synonyms:
3''',8-Biflavone, 5,5'',7,7''-tetrahydroxy-4',4'''-dimethoxy-
4',4'''-Dimethylamentoflavone
548-19-6
8-[5-(5,7-dihydroxy-4-oxochromen-2-yl)-2-methoxyphenyl]-5,7-dihydroxy-2-(4
AC1NSX10
BRD-K72661036-001-02-1
BSPBio_002844
CCG-38579
CHEBI:782701
CHEMBL1208903
DivK1c_006529
Isoginkgetin
KBio1_001473
KBio2_000886
KBio2_003454
KBio2_006022
KBio3_002064
KBioGR_002352
KBioSS_000886
NCGC00094722-01
NCGC00094722-02
NCGC00178438-01
SDCCGMLS-0066448.P001
SPBio_000264
SpecPlus_000433
Spectrum2_000302
Spectrum3_001112
Spectrum4_001945
Spectrum5_000819
Spectrum_000406

Target

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Uniprot ID:Q9Y354_HUMAN
Synonyms:
Matrix metalloproteinase 9
EC-Numbers:3.4.24.35
Organism:Homo sapiens
Human
PDB IDs:-

Binding Affinities:

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

References:

17121913
Isoginkgetin inhibits tumor cell invasion by regulating phosphatidylinositol 3-kinase/Akt-dependent matrix metalloproteinase-9 expression.. Sang-Oh Yoon; Sejeong Shin; Ho-Jae Lee; Hyo-Kon Chun; An-Sik Chung (2006) Molecular cancer therapeutics display abstract
Matrix metalloproteinase (MMP)-9 plays a key role in tumor invasion. Inhibitors of MMP-9 were screened from Metasequoia glyptostroboides (Dawn redwood) and one potent inhibitor, isoginkgetin, a biflavonoid, was identified. Noncytotoxic levels of isoginkgetin decreased MMP-9 production profoundly, but up-regulated the level of tissue inhibitor of metalloproteinase (TIMP)-1, an inhibitor of MMP-9, in HT1080 human fibrosarcoma cells. The major mechanism of Ras-dependent MMP-9 production in HT1080 cells was phosphatidylinositol 3-kinase (PI3K)/Akt/nuclear factor-kappaB (NF-kappaB) activation. Expression of dominant-active H-Ras and p85 (a subunit of PI3K) increased MMP-9 activity, whereas dominant-negative forms of these molecules decreased the level of MMP-9. H-Ras did not increase MMP-9 in the presence of a PI3K inhibitor, LY294002, and a NF-kappaB inhibitor, SN50. Further studies showed that isoginkgetin regulated MMP-9 production via PI3K/Akt/NF-kappaB pathway, as evidenced by the findings that isoginkgetin inhibited activities of both Akt and NF-kappaB. PI3K/Akt is a well-known key pathway for cell invasion, and isoginkgetin inhibited HT1080 tumor cell invasion substantially. Isoginkgetin was also quite effective in inhibiting the activities of Akt and MMP-9 in MDA-MB-231 breast carcinomas and B16F10 melanoma. Moreover, isoginkgetin treatment resulted in marked decrease in invasion of these cells. In summary, PI3K/Akt is a major pathway for MMP-9 expression and isoginkgetin markedly decreased MMP-9 expression and invasion through inhibition of this pathway. This suggests that isoginkgetin could be a potential candidate as a therapeutic agent against tumor invasion.