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Drug-Target Interaction

Drug

show drug details
PubChem ID:54454
Structure:
Synonyms:
(1S,3R,7S,8S,8aR)-8-{2-[(2R,4R)-4-hydroxy-6-oxotetrahydro-2H-pyran-2-yl]et
(1S,3R,7S,8S,8aR)-8-{2-[(2R,4R)-4-hydroxy-6-oxotetrahydro-2H-pyran-2-yl]ethyl}-3,7-dimethyl-1,2,3,7,8,8a-hexahydronaphthalen-1-yl 2,2-dimethylbutanoate
2,2-Dimethylbutanoic acid (1S,3R,7S,8S,8aR)-1,2,3,7,8,8a-hexahydro-3,7-dimethyl-8-[2-[(2R,4R)-tetrahydro-4-hydroxy-6-oxo-2H-pyran-2-yl]ethyl]-1-naphthalenyl ester
2,2-Dimethylbutyric acid, 8-ester with (4R,6R)-6-(2-((1S,2S,6R,8S,8aR)-1,2,6,7,8,8a-hexahydro-8-hydroxy-2,6-dimethyl-1-naphthyl)ethyl)tetrahydro-4-hydroxy-2H-pyran-2-one
79902-63-9
AIDS-111666
AIDS111666
BB_NC-1255
BCBcMAP01_000007
BPBio1_001001
BRN 4768037
BSPBio_000909
BSPBio_002337
Butanoic acid, 2,2-dimethyl-, (1S,3R,7S,8S,*aR)-1,2,3,7,8,8a-hexahydro-3,7-dimethyl-8-(2-((2R,4R)-tetrahydro-4-hydroxy-6-oxo-2H-pyran-2-yl)ethyl)-1-naphthalenyl ester
Butanoic acid, 2,2-dimethyl-, (1S,3R,7S,8S,8aR)-1,2,3,7,8,8a-hexahydro-3,7-dimethyl-8-(2-((2R,4R)-tetrahydro-4-hydroxy-6-oxo-2H-pyran-2-yl)ethyl)-1-naphthalenyl ester
Butanoic acid, 2,2-dimethyl-, (1S,3R,7S,8S,8aR)-1,2,3,7,8,8a-hexahydro-3,7-dimethyl-8-[2-[(2R,4R)-tetrahydro-4-hydroxy-6-oxo-2H-pyran-2-yl]ethyl]-1-naphthalenyl ester
Butanoic acid, 2,2-dimethyl-, 1,2,3,7,8,8a-hexahydro-3,7-dimethyl-8-(2-(tetrahydro-4-hydroxy-6-oxo-2H-pyran-2-yl)ethyl)-1-naphthalenyl ester, (1S-(1alpha,3alpha,7beta,8beta(2S*,4S*),8abeta))-
butanoic acid, 2,2-dimethyl-,1,2,3,7,8,8a-hexahydro-3,7-dimethyl-8-[2-(tetrahydro-4-hydroxy-6-oxo-2H-pyran-2-yl)-ethyl]-1-naphthalenyl ester, [1S-[1 alpha,3 alpha,7 beta,8 beta(2S*,4S*),-8a beta
C25H38O5
CCRIS 7558
CHEBI:9150
Cholestat
Coledis
Colemin
Corolin
D00434
DB00641
Denan
DivK1c_006991
DRG-0320
HSDB 7208
KBio1_001935
KBio2_002197
KBio2_004765
KBio2_007333
KBio3_001557
KBioGR_001244
KBioSS_002197
KS-1113
L 644128-000U
Labistatin
Lipex
Lipovas
Lodal s
Lodales
LS-46264
Medipo
Mixture Name
MK 0733
MK-0733
MK-733
MLS001304029
MLS001333077
MLS001333078
MLS002154038
NCGC00017324-01
NCGC00017324-02
NCGC00017324-03
nchembio790-comp16
Nivelipol
Pantok
Prestwick0_000865
Prestwick1_000865
Prestwick2_000865
Prestwick3_000865
Prestwick_171
Rendapid
S6196_SIGMA
Simovil
SIMVASTATIN
Simvastatin (JAN/USP/INN)
Simvastatin [USAN:BAN:INN]
Simvastatin [USAN:INN:BAN]
Simvastatin, Compactin
Simvastatina
Simvastatina [Spanish]
Simvastatine
Simvastatine [French]
Simvastatinum
Simvastatinum [Latin]
Sinvacor
Sivastin
SMR000718785
SPBio_001881
SPBio_002830
SpecPlus_000895
SPECTRUM1504236
Spectrum2_001671
Spectrum3_000669
Spectrum4_000632
Spectrum5_001428
Spectrum_001717
Synvinolin
TNP00259
Vasotenal
Vytorin
ZINC03780893
Zocor
Zocor (TN)
Zocord
[(1S,3R,7S,8S,8aR)-8-[2-[(2R,4R)-4-hydroxy-6-oxooxan-2-yl]ethyl]-3,7-dimethyl-1,2,3,7,8,8a-hexahydronaphthalen-1-yl] 2,2-dimethylbutanoate
ATC-Codes:
Side-Effects:
Side-EffectFrequency
constipation0.13426316
atrial fibrillation0.057
flatulence0.050999995
abdominal pain0.044826083
endocrine disorders0.042
diabetes mellitus0.042
headache0.041736852
nausea0.03603572
infection0.032
diarrhea0.03185714
upper respiratory infection0.026157895
dyspepsia0.020000003
asthenia0.014600003
eczema0.012625001
cataract0.005666666
myalgia0.0038536591
rash0.0014054052
pruritus0.0014
gynecomastia0.0010
hepatic failure0.0010
chills0.0010
toxic epidermal necrolysis0.0010
anaphylaxis0.0010
hemolytic anemia0.0010
positive ana0.0010
erythema multiforme0.00068
vasculitis0.00054
urticaria0.00054
thrombocytopenia0.00054
lupus0.00054
malaise0.00054
photosensitivity0.00054
arthralgia0.00054
polymyalgia rheumatica0.00054
arthritis0.00054
angioedema0.00054
dermatomyositis0.00054
flushing0.00054
fever0.00054
dyspnea0.00054
eosinophilia0.00054
esr increased0.0005
vomiting0.00035
stevens - johnson syndrome0.00035
rhabdomyolysis0.00035
purpura0.00035
anemia0.00035
dizziness0.00035
hepatitis0.00035
jaundice0.00035
leukopenia0.00035
muscle cramps0.00035
pancreatitis0.00035
paresthesia0.00035
alopecia0.00035
hypersensitivity0.00035
peripheral neuropathy0.00034
anorexia0.00033
sensory disturbance0.00033
elevated alkaline phosphatase0.00033
muscle weakness0.00033
anxiety0.00033
skin erythema0.0
bronchitis0
decreased libido0
myopathy0
memory loss0
hepatic necrosis0
tremor0
nerve palsy0
chronic active hepatitis0
ophthalmoplegia0
sinusitis0
vertigo0
gastritis0
weakness0
regurgitation0
hepatoma0
cirrhosis0
swelling0
edema0
insomnia0
memory impairment0

Target

show target details
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:

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.
12860247
Influence of 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase inhibitors on endothelial nitric oxide synthase and the formation of oxidants in the vasculature.. Rex A Parker; Qi Huang; Belay Tesfamariam (2003) Atherosclerosis display abstract
HMGCoA reductase inhibitors (statins) can have effects outside the target tissue, liver, including serious side-effects such as rhabdomyolysis as well as beneficial pleiotrophic effects. One such effect is upregulation of endothelial nitric oxide synthase (e-NOS) which generally leads to vasorelaxation. However, changing the balance between localized NO and O(2-) fluxes can also lead to oxidant stress and cellular injury through formation of reactive secondary oxidants such as peroxynitrite. We compared different statins for e-NOS subcellular localization, formation of pro-oxidants, and endothelial-dependent vascular function. Vascular relaxation in aortas of statin-dosed rats was inhibited with simvastatin (sevenfold higher EC50 for acetyl-choline induced relaxation) and atorvastatin (twofold increase) but not pravastatin. Ex vivo oxidation of the fluorescent redox probe dihydrorhodamine-123 (DHR-123) was increased in aortas from simvastatin treated rats, indicating increased reactive nitrogen and oxygen species. Human aortic endothelial cells incubated with simvastatin exhibited up to threefold higher intracellular oxidation of DHR-123 along with a twofold increase in total e-NOS protein. The elevated e-NOS was found in the Golgi/mitochondrial fraction and not in the plasma membrane, and using immunofluorescence greater e-NOS was observed proximal to Golgi and cytoskeletal structures and away from plasma membrane in simvastatin-treated cells. The data suggest that the action of lipophilic statins in endothelium can shift e-NOS localization towards intracellular domains, thereby increasing the encounter with metabolically generated O(2-) to produce peroxynitrite and related oxidants. Thus, under some conditions the direct action of lipophilic HMGCoA reductase inhibitors may unbalance NO and O(2-) fluxes and promote oxidant stress, compromising potentially beneficial vascular effects of e-NOS upregulation and increasing the potential for damage to muscle and other tissues.