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Drug-Target Interaction

Drug

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PubChem ID:5712
Structure:
Synonyms:
"3-(5′-hydroxymethyl-2′-furyl)-1-benzylindazole"
154453-18-6
170632-47-0
17351-10-9
2-Furanmethanol, 5-[1-(phenylmethyl)-1H-indazol-3-yl]-
3-(5′-Hydroxymethyl-2′-furyl)-1-benzylindazole
3-(5'-Hydroxymethyl-2'-furyl)-1-benzyl indazole
3-(5'-Hydroxymethyl-2'-furyl)-1-benzylindazole
AC1L1KYW
AC1Q4YM3
AR-1A9100
Bio2_000324
Bio2_000804
BRD-K60476892-001-02-1
BSPBio_000987
C090937
C19H16N2O2
CCG-205304
CHEBI:302965
CHEMBL333985
EU-0101230
HMS1362A09
HMS1792A09
HMS1990A09
HMS2235B17
HMS3263F22
IDI1_002079
KBio2_000327
KBio2_002895
KBio2_005463
KBio3_000653
KBio3_000654
KBioGR_000327
KBioSS_000327
KST-1A2012
Lificiguat
Lopac-Y-102
Lopac0_001230
LS-173463
MLS001333257
MLS001333258
MLS002172480
NCGC00016103-01
NCGC00016103-02
NCGC00016103-03
NCGC00016103-04
NCGC00016103-05
NCGC00016103-06
NCGC00016103-07
NCGC00094472-01
NCGC00094472-02
NCGC00094472-03
NCGC00094472-04
NSC728165
QTL1_000091
SMR000857214
UNII-515CC1WPTE
Y-102
Y102_SIGMA
YC 1
YC-1
ZINC01492386
[5-(1-benzyl-1h-indazol-3-yl)-2-furyl]methanol
[5-(1-benzylindazol-3-yl)furan-2-yl]methanol

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:

17213816
YC-1 inhibits HIF-1 expression in prostate cancer cells: contribution of Akt/NF-kappaB signaling to HIF-1alpha accumulation during hypoxia.. H-L Sun; Y-N Liu; Y-T Huang; S-L Pan; D-Y Huang; J-H Guh; F-Y Lee; S-C Kuo; C-M Teng (2007) Oncogene display abstract
Hypoxia-inducible factor 1 (HIF-1), a transcription factor that is critical for tumor adaptation to microenvironmental stimuli, represents an attractive chemotherapeutic target. YC-1 is a novel antitumor agent that inhibits HIF-1 through previously unexplained mechanisms. In the present study, YC-1 was found to prevent HIF-1alpha and HIF-1beta accumulation in response to hypoxia or mitogen treatment in PC-3 prostate cancer cells. Neither HIF-1alpha protein half-life nor mRNA level was affected by YC-1. However, YC-1 was found to suppress the PI3K/Akt/mTOR/4E-BP pathway, which serves to regulate HIF-1alpha expression at the translational step. We demonstrated that YC-1 also inhibited hypoxia-induced activation of nuclear factor (NF)-kappaB, a downstream target of Akt. Two modulators of the Akt/NF-kappaB pathway, caffeic acid phenethyl ester and evodiamine, were observed to decrease HIF-1alpha expression. Additionally, overexpression of NF-kappaB partly reversed the ability of wortmannin to inhibit HIF-1alpha-dependent transcriptional activity, suggesting that NF-kappaB contributes to Akt-mediated HIF-1alpha accumulation during hypoxia. Overall, we identify a potential molecular mechanism whereby YC-1 serves to reduce HIF-1 expression.