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Drug-Target Interaction

Drug

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PubChem ID:2162
Structure:
Synonyms:
3,5-Pyridinedicarboxylic acid,
3,5-Pyridinedicarboxylic acid, 2-((2-aminoethoxy)methyl)-4-(2-chlorophenyl)-1,4-dihydro-6-methyl-, 3-ethyl 5-methyl ester
3-ethyl 5-methyl 2-{[(2-aminoethyl)oxy]methyl}-4-(2-chlorophenyl)-6-methyl-1,4-dihydropyridine-3,5-dicarboxylate
3-Ethyl-5-methyl ( -)-2-((2-aminoethoxy)methyl)-4-(2-chlorphenyl)-1,4-dihydro-6-methyl-3,5-pyridindicarboxylat
3-Ethyl-5-methyl ( -)-2-((2-aminoethoxymethyl)-4-(o-chlorophenyl)-1,4-dihydro-6-methyl-3,5-pyridinedicarboxylate
3-Ethyl-5-methyl (.+/-.)-2-[(2-aminoethoxy)methyl]-4-(o-chlorophenyl)-1,4-dihydro-6-methyl-3,5-pyridinedicarboxylate
88150-42-9
88150-47-4
Ambap6294
Amlocard
Amlodipine
Amlodipine (INN)
AMLODIPINE BASE
Amlodipine Benzenesulfonate
Amlodipine Besilate
Amlodipine Besylate
Amlodipine Free Base
Amlodipine [INN:BAN]
Amlodipine, Istin, Norvasc, Caduet
Amlodipino
Amlodipino [Spanish]
Amlodipinum
Amlodipinum [Latin]
Amlodis
Amlopres
BSPBio_002727
C06825
CHEBI:2668
Coroval
CPD000469198
D07450
DB00381
Exforge
Intervask
KBio3_001947
KBioGR_001643
Lipinox
Lotrel
LS-131183
Mixture Name
MLS001401409
NCGC00165957-01
NCGC00165957-02
NCGC00165957-03
Norvasc
Norvasc (TN)
O3-ethyl O5-methyl 2-(2-aminoethoxymethyl)-4-(2-chlorophenyl)-6-methyl-1,4-dihydropyridine-3,5-dicarboxylate
Racemic Amlodipine
SAM001246705
SMR000469198
SPBio_000351
Spectrum2_000486
Spectrum3_001004
Spectrum4_001132
Spectrum5_001550
UK-4834011
ATC-Codes:
Side-Effects:
Side-EffectFrequency
edema0.100999996
flushing0.030000001
palpitations0.0235
somnolence0.014500001
coronary artery disease0.0010
peripheral vascular disease0.0010
chronic obstructive pulmonary disease0.0010
congestive heart failure0.0010
hepatitis0.0010
diabetes mellitus0.0010
jaundice0.0010
gynecomastia0.0010
syncope0
tachycardia0
thrombocytopenia0
tinnitus0
tremor0
stevens - johnson syndrome0
pancreatitis0
paresthesia0
peripheral neuropathy0
polyuria0
pruritus0
sexual dysfunction0
purpura0
rhinitis0
pain0
erythema0
urticaria0
muscle weakness0
eye pain0
dry skin0
malaise0
myalgia0
bradycardia0
urinary frequency0
increased sweating0
insomnia0
migraine0
peripheral edema0
apathy0
vasculitis0
ventricular tachycardia0
vertigo0
abnormal vision0
vomiting0
weight gain0
weight loss0
dry mouth0
agitation0
allergic reaction0
nocturia0
abdominal pain0
back pain0
chest pain0
conjunctivitis0
constipation0
cough0
dysphagia0
depersonalization0
dermatitis0
atrial fibrillation0
ataxia0
alopecia0
amnesia0
angioedema0
anorexia0
anxiety0
arrhythmia0
arthralgia0
asthenia0
diarrhea0
diplopia0
dizziness0
postural hypotension0
ischemia0
arthrosis0
leukopenia0
gastritis0
muscle cramps0
myocardial infarction0
nausea0
hyperglycemia0
headache0
dyspepsia0
dyspnea0
dysuria0
epistaxis0
erythema multiforme0
rash0
fatigue0
flatulence0
nervousness0

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:

14553824
Amlodipine activates the endothelial nitric oxide synthase by altering phosphorylation on Ser1177 and Thr495.. Helena Lenasi; Karin Kohlstedt; Birgit Fichtlscherer; Alexander Mülsch; Rudi Busse; Ingrid Fleming (2003) Cardiovascular research display abstract
OBJECTIVE: The Ca2+ antagonist amlodipine increases the generation of nitric oxide (NO) from native and cultured endothelial cells. The aim of this investigation was to determine whether or not the activation of the endothelial NO synthase (eNOS) by this Ca2+ antagonist is related to alterations in eNOS phosphorylation. METHODS AND RESULTS: In isolated, pre-contracted, endothelium-intact porcine coronary arteries, amlodipine elicited an NO-mediated relaxation and a leftward shift in the concentration-relaxation curve to bradykinin. Moreover, the Ca2+ antagonist increased the generation of NO from native endothelial cells, as detected by electron spin resonance spectroscopy and stimulated an 8-fold increase in cyclic GMP levels in cultured endothelial cells. In unstimulated endothelial cells, eNOS was not phosphorylated on Ser1177 but was phosphorylated on Thr495. Amlodipine elicited the phosphorylation of Ser1177 and attenuated Thr495 phosphorylation, with a time course similar to that of eNOS activation. The amlodipine-induced relaxation of porcine coronary arteries was attenuated by the B2 kinin receptor antagonist, icatibant, but this antagonist did not affect amlodipine-induced changes in eNOS phosphorylation in cultured endothelial cells. Moreover, amlodipine elicited the NO-mediated relaxation of rat aortic rings which do not express the B2 receptor. Amlodipine time-dependently attenuated the phosphorylation of protein kinase C (PKC) in endothelial cells, with a time course similar to the changes in eNOS phosphorylation, and prevented the phorbol-12-myristate-13-acetate-induced activation of PKC. The PKC inhibitor, Ro 31-8220, also elicited the phosphorylation of Ser1177 and the dephosphorylation of Thr495 in cultured cells and induced a leftward shift in the concentration-relaxation curve to bradykinin in rings of porcine coronary artery. CONCLUSION: The Ca2+ antagonist, amlodipine, enhances endothelial NO generation by inducing changes in the phosphorylation of eNOS. Although the activation of eNOS was related to the activation of the B2 kinin receptor in the porcine coronary artery, a B2 receptor-independent mechanism involving the inhibition of PKC appears to account for the effects observed in the rat aorta as well as in cultured endothelial cells.