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Drug-Target Interaction

Drug

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PubChem ID:60823
Structure:
Synonyms:
(3R,5R)-7-[2-(4-fluorophenyl)-3-phenyl-4-(phenylcarbamoyl)-5-propan-2-ylpyrrol-1-yl]-3,5-dihydroxyheptanoic acid
(3R,5R)-7-[3-(anilinocarbonyl)-5-(4-fluorophenyl)-2-isopropyl-4-phenyl-1H-pyrrol-1-yl]-3,5-dihydroxyheptanoic acid
(3R,5R)-7-[3-(anilinocarbonyl)-5-(4-fluorophenyl)-4-phenyl-2-(propan-2-yl)-1H-pyrrol-1-yl]-3,5-dihydroxyheptanoic acid
(betaR,deltaR)-2-(p-Fluorophenyl)-beta,delta-dihydroxy-5-isopropyl-3-pheny
(betaR,deltaR)-2-(p-Fluorophenyl)-beta,delta-dihydroxy-5-isopropyl-3-phenyl-4-(phenylcarbamoyl)pyrrole-1-heptanoic acid
(R-(R*,R*))-2-(4-Fluorophenyl)-beta,delta-dihydroxy-5-(1-methylethyl)-3-phenyl-4-((phenylamino)carbonyl)-1H-pyrrole-1-heptanoic acid
134523-00-5
134523-03-8
1H-Pyrrole-1-heptanoic acid, 2-(4-fluorophenyl)-beta,delta-dihydroxy-5-(1-methylethyl)-3-phenyl-4-((phenylamino)carbonyl)-, (R-(R*,R*))-
7-[2-(4-FLUORO-PHENYL)-5-ISOPROPYL-3-PHENYL-4-PHENYLCARBAMOYL-PYRROL-1-YL]- 3,5-DIHYDROXY-HEPTANOIC ACID
7-[2-(4-FLUORO-PHENYL)-5-ISOPROPYL-3-PHENYL-4-PHENYLCARBAMOYL-PYRROL-1-YL]-3,5-DIHYDROXY-HEPTANOIC ACID
Atorvastatin
Atorvastatin (INN)
Atorvastatin (R-(R*,R*))
Atorvastatin calcium
Atorvastatin [INN:BAN]
atrovastin
C06834
C33H35FN2O5
Cardyl
CCRIS 7159
CHEBI:39548
CI 981
D07474
DB01076
HSDB 7039
Lipitor
Lipitor (TN)
Liprimar
LS-136975
NCGC00159458-02
Sortis
Sortis (TN)
Sotis
Torvast
Totalip
Tozalip
Tulip
Xavator
ATC-Codes:

Target

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Uniprot ID:NOS2_HUMAN
Synonyms:
HEP-NOS
Hepatocyte NOS
Inducible NO synthase
Inducible NOS
iNOS
Nitric oxide synthase, inducible
NOS type II
EC-Numbers:1.14.13.39
Organism:Homo sapiens
Human
PDB IDs:1NSI 2NSI 3E7G 3EJ8 3HR4 4NOS
Structure:
4NOS

Binding Affinities:

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

References:

11735125
Inhibition of LOX-1 by statins may relate to upregulation of eNOS.. J L Mehta; D Y Li; H J Chen; J Joseph; F Romeo (2001) Biochemical and biophysical research communications display abstract
LOX-1, a receptor for oxidized low-density lipoprotein (ox-LDL), plays a critical role in endothelial dysfunction and atherosclerosis; both of these conditions are associated with diminished expression of constitutive endothelial nitric oxide synthase (eNOS). Recent studies show that HMG CoA reductase inhibitors (statins) exert cardioprotective effect. We examined the role of LOX-1 in eNOS expression and modulation of this relationship by two different statins, simvastatin and atorvastatin in human coronary artery endothelial cells (HCAECs). Ox-LDL (40 microg/ml) upregulated the expression of LOX-1; simultaneously, there was a reduction in eNOS expression. Pretreatment of HCAECs with simvastatin or atorvastatin (1 and 10 microM) reduced ox-LDL-induced upregulation of LOX-1 and downregulation of eNOS (both P < 0.05). High concentration of statins (10 microM) was more potent than the low concentration (1 microM) (P < 0.05). Both statins also attenuated ox-LDL-mediated activation of MAP kinase. These observations indicate that statins attenuate the effect of ox-LDL on eNOS expression. Inhibitory effect on LOX-1 and subsequently MAP kinase activity provides a potential mechanism of beneficial effects of statins beyond lowering cholesterol.