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Drug-Target Interaction

Drug

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PubChem ID:359
Structure:
Synonyms:
1,3,5-Benzenetriol
1,3,5-Benzenetriol, dihydrate
1,3,5-THB
1,3,5-Trihydroxybenzene
1,3,5-Trihydroxybenzene anhydrous
1,3,5-Trihydroxybenzene dihydrate
1,3,5-Trihydroxycyclohexatriene
1,3,5-Triol
108-73-6
3,5-Dihydroxyphenol
4-06-00-07361 (Beilstein Handbook Reference)
5-Benzenetriol
5-Hydroxyresorcinol
5-Oxyresorcinol
5-Oxyresorcinolphloroglucin
6099-90-7
626-71-1
79330_ALDRICH
79330_FLUKA
AB1004109
AC1L192D
AC1Q1GOU
AG-D-25303
AI3-08848
AIDS-017800
AIDS017800
AKOS000119851
AR-1B6233
BB_NC-2225
Benzene, 1,3,5-trihydroxy-
Benzene, trihydroxy
Benzene-1,3,5-triol
Benzene-s-triol
BRN 1341907
c0026
C02183
C6H6O3
CCRIS 4147
CHEBI:16204
CHEMBL473159
CPD-16
D00152
Dilospan S
Dilospan S (TN)
EINECS 203-611-2
Floroglucin
Floroglucin [Czech]
Floroglucinol
Floroglucinol [Czech]
I04-0078
KST-1B6373
LS-105905
MolPort-000-871-966
NCGC00166270-01
NSC 1572
NSC1572
P0249
P1178_SIGMA
P1376
P3502_SIAL
P38005_ALDRICH
Phloroglucin
Phloroglucine
Phloroglucinol
Phloroglucinol (JAN)
Phloroglucinol dihydrate
s-Trihydroxybenzene
Spasfon-Lyoc
ST5214381
sym-Trihydroxybenzene
TL8000285
WLN: QR CQ EQ
ZINC00391883
ATC-Codes:

Target

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Uniprot ID:NOS3_HUMAN
Synonyms:
cNOS
Constitutive NOS
EC-NOS
Endothelial NOS
eNOS
Nitric oxide synthase, endothelial
NOS type III
NOSIII
EC-Numbers:1.14.13.39
Organism:Homo sapiens
Human
PDB IDs:1M9J 1M9K 1M9M 1M9Q 1M9R 3EAH 3NOS
Structure:
3NOS

Binding Affinities:

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

References:

16424868
Pro-apoptotic properties of hyperforin in leukemic cells from patients with B-cell chronic lymphocytic leukemia.. C Quiney; C Billard; A M Faussat; C Salanoubat; A Ensaf; Y Nat-Si; J D Fourneron; J-P Kolb (2006) Leukemia : official journal of the Leukemia Society of America, Leukemia Research Fund, U.K display abstract
The effects of the hyperforin (HF), a natural phloroglucinol purified from Hypericum perforatum, were investigated ex vivo on leukemic cells from patients with B-cell chronic lymphocytic leukemia (B-CLL). HF was found to promote apoptosis of B-CLL cells, as shown by time- and dose-dependent stimulation of phosphatidylserine externalization and DNA fragmentation, by disruption of the mitochondrial transmembrane potential, caspase-3 activation and cleavage of the caspase substrate PARP-1. Moreover, HF-induced downregulation of Bcl-2 and Mcl-1, two antiapoptotic proteins that control mitochondrial permeability. HF also downregulated two proteins which are overexpressed by B-CLL patients' cells, the cell cycle inhibitor p27kip1 through caspase-dependent cleavage into a p23 form, and the nitric oxid (NO) synthase of type 2 (inducible NO synthase). This latter was accompanied by reduction in the production of NO known to be antiapoptotic in B-CLL cells. Preventing effects of the general caspase inhibitor z-VAD-fmk indicated that HF-promoted apoptosis of B-CLL cells was mostly caspase dependent. Furthermore, normal B lymphocytes purified from healthy donors appeared less sensitive to HF-induced apoptosis than B-CLL cells. These results indicate that HF may be of interest in the development of new therapies for B-CLL based on the induction of apoptosis and combination with cell cycle-dependent antitumor drugs.
18226577
Protective effects of St. John's wort extract and its component hyperforin against cytokine-induced cytotoxicity in a pancreatic beta-cell line.. Marta Menegazzi; Michela Novelli; Pascale Beffy; Valentina D'Aleo; Elisa Tedeschi; Roberto Lupi; Elisa Zoratti; Piero Marchetti; Hisanori Suzuki; Pellegrino Masiello (2008) The international journal of biochemistry & cell biology display abstract
In both type 1 and type 2 diabetes, increased production of cytokines on autoimmune or metabolic basis is supposed to trigger an inflammatory process leading to dysfunction and death of pancreatic beta-cells. Therefore, anti-inflammatory pharmacological approaches aimed at blocking cytokine signalling pathways and consequent cytotoxicity in beta-cells are highly advisable. Based on previous evidence of cytokine antagonistic effects in other cell types, we explored the protective action of Hypericum perforatum (St-John's-wort) extract and its component hyperforin against cytokine-induced functional impairment and apoptosis in the INS-1E beta-cell line, searching for the underlying mechanisms. The results showed that either St-John's-wort extract or hyperforin (at 1-3 microM) prevented cytokine-induced impairment in glucose-stimulated insulin secretion and protected cells against apoptosis in a dose-dependent fashion. Inducible-NO-synthase expression was also potently hindered by the vegetal compounds. Interestingly, cytokine-induced activations of the signal-transducer-and-activator-of-transcription-1 (STAT-1) and the nuclear-factor-kappaB (NF-kappaB) were both down-regulated by SJW extract or HPF (range 0.5-5 microM) when evaluated by electrophoretic-mobility-shift-assay. Other transcription factors (CBF-1, SP-1) were unaffected. Components of SJW extract other than HPF were much less effective in down-regulating cytokine signalling. Significantly, inhibition of cytokine-elicited STAT-1 and NF-kappaB activation was confirmed in isolated rat and human islets incubated in the presence of these vegetal compounds. In conclusion, St-John's-wort extract and hyperforin are non-peptidyl compounds which, at low concentrations, target key mechanisms of cytokine-induced beta-cell injury, thereby improving beta-cell function and survival. Thus, they are potentially valuable for the prevention or limitation of beta-cell loss in diabetes.