Home
Drugs
Targets
Pathways
Ontologies
Cyp450s
Adv.search
Help/FAQ

Drug-Target Interaction

Drug

show drug details
PubChem ID:110634
Structure:
Synonyms:
1-((3-(3,4-Dihydro-5-methyl-4-oxo-7-propylimidazo(5,1-f)-as-triazin-2-yl)-4-ethoxyphenyl)sulfonyl)-4-ethylpiperazine
2-(2-Ethoxy-5-(4-ethylpiperazin-1-yl-1-sulfonyl)phenyl)-5-methyl-7-propyl-
2-(2-Ethoxy-5-(4-ethylpiperazin-1-yl-1-sulfonyl)phenyl)-5-methyl-7-propyl-3H-imidazo(5,1-f)(1,2,4)triazin-4-one
2-[2-ethoxy-5-(4-ethylpiperazin-1-yl)sulfonylphenyl]-5-methyl-7-propyl-1H-imidazo[5,1-f][1,2,4]triazin-4-one
2-{2-ETHOXY-5-[(4-ETHYLPIPERAZIN-1-YL)SULFONYL]PHENYL}-5-METHYL-7-PROPYLIMIDAZO[5,1-F][1,2,4]TRIAZIN-4(1H)-ONE
224785-90-4
BAY 38-9456
BSPBio_002392
DB00862
HSDB 7304
Levitra
Levitra (TN)
LS-111467
NCGC00167533-01
Piperazine, 1-((3-(1,4-dihydro-5-methyl-4-oxo-7-propylimidazo(5,1-f)(1,2,4)triazin-2-yl)-4-ethoxyphenyl)sulfonyl)-4-ethyl-
STK642629
STOCK6S-20068
Vardenafil
VARDENAFIL, LEVITRA
Vardenafil, Vivanza,
VDN
ATC-Codes:
Side-Effects:
Side-EffectFrequency
headache0.095
rhinitis0.060000002
flushing0.06
dyspepsia0.024999999
flu syndrome0.024999999
sinusitis0.02
nausea0.015
dizziness0.014999999
visual field defect0.0010
seizure0.0010
anxiety0.0010
decreased vision0.0010
neuropathy0.0010
vision loss0.0010
loss of hearing0.0010
amnesia0.0010
arrhythmia0.0010
coronary artery disease0.0010
diabetes0.0010
hematemesis0.0010
hematuria0.0010
hemorrhage0.0010
hyperlipidemia0.0010
hypertension0.0010
burning sensation0
palpitations0
dyspnea0
pain0
sinus congestion0
dysphagia0
somnolence0
sweating0
myocardial ischemia0
gastroesophageal reflux0
tinnitus0
diarrhea0
vertigo0
asthenia0
anaphylaxis0
syncope0
transient global amnesia0
photophobia0
blurred vision0
hypotension0
hot flashes0
paresthesia0
eye redness0
myalgia0
arthralgia0
priapism0
photosensitivity0
global amnesia0
ejaculation premature0
feeling abnormal0
liver function tests abnormal0
vomiting0
epistaxis0
esophagitis0
neck pain0
myocardial infarction0
insomnia0
nasal congestion0
erythema0
glaucoma0
conjunctivitis0
back pain0
rash0
edema0
eye pain0
hyperhidrosis0
tachycardia0
angina pectoris0
abdominal pain upper0
postural hypotension0
pharyngitis0
dry mouth0
abdominal pain0
reflux esophagitis0
chest pain0
watery eyes0
hypersensitivity0
pruritus0
sgot increased0
gastritis0

Target

show target details
Uniprot ID:PDE10_RAT
Synonyms:
cAMP and cAMP-inhibited cGMP 3',5'-cyclic phosphodiesterase 10A
EC-Numbers:3.1.4.17
3.1.4.35
Organism:Rat
Rattus norvegicus
PDB IDs:2O8H 2OVV 2OVY 3HQW 3HQY 3HQZ 3HR1
Structure:
3HR1

Binding Affinities:

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

References:

19187094
Phosphodiesterase 5 inhibitors prevent 3,4-methylenedioxymethamphetamine-induced 5-HT deficits in the rat.. Elena Puerta; Isabel Hervias; Beatriz Goi-Allo; Berta Lasheras; Joaquin Jordan; Norberto Aguirre (2009) Journal of neurochemistry display abstract
Phosphodiesterase 5 (PDE5) inhibitors are often used in combination with club drugs such as 3,4-methylenedioxymethamphetamine (MDMA or ecstasy). We investigated the consequences of such combination in the serotonergic system of the rat. Oral administration of sildenafil citrate (1.5 or 8 mg/kg) increased brain cGMP levels and protected in a dose-dependent manner against 5-hydroxytryptamine depletions caused by MDMA (3 x 5 mg/kg, i.p., every 2 h) in the striatum, frontal cortex and hippocampus without altering the acute hyperthermic response to MDMA. Intrastriatal administration of the protein kinase G (PKG) inhibitor, KT5823 [(9S, 10R, 12R)-2,3,9,10,11,12-Hexahydro-10-methoxy-2,9-dimethyl-1-oxo-9,12-epoxy-1H-diindolo[1,2,3-fg:3',2',1'-kl]pyrrolo[3,4-i][1,6]benzodiazocine-10-carboxylic acid, methyl ester)], suppressed sildenafil-mediated protection. By contrast, the cell permeable cGMP analogue, 8-bromoguanosine cyclic 3',5'-monophosphate, mimicked sildenafil effects further suggesting the involvement of the PKG pathway in mediating sildenafil protection. Because mitochondrial ATP-sensitive K(+) channels are a target for PKG, we next administered the specific mitochondrial ATP-sensitive K(+) channel blocker, 5-hydroxydecanoic acid, 30 min before sildenafil. 5-hydroxydecanoic acid completely reversed the protection afforded by sildenafil, thereby implicating the involvement of mitochondrial ATP-sensitive K(+) channels. Sildenafil also increased Akt phosphorylation, and so the possible involvement of the Akt/endothelial nitric oxide synthase (eNOS)/sGC signalling pathway was analysed. Neither the phosphatidylinositol 3-kinase inhibitor, wortmannin, nor the selective eNOS inhibitor, L-N5-(1-iminoethyl)-L-ornithine dihydrochloride, reversed the protection afforded by sildenafil, suggesting that Akt/eNOS/sGC cascade does not participate in the protective mechanisms. Our data also show that the protective effect of sildenafil can be extended to vardenafil, another PDE5 inhibitor. In conclusion, sildenafil protects against MDMA-induced long-term reduction of indoles by a mechanism involving increased production of cGMP and subsequent activation of PKG and mitochondrial ATP-sensitive K(+) channel opening.