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Drug-Target Interaction

Drug

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PubChem ID:441233
Structure:
Synonyms:
(1R)-2-phenylcyclopropan-1-amine
155-09-9
AC1L9ASR
C07155
D08625
DB00752
Parnate
Tranylcypromine
Tranylcypromine (INN)
ATC-Codes:
Side-Effects:
Side-EffectFrequency
insomnia0
thrombocytopenia0
tachycardia0
spasm0
scleroderma0
paresthesia0
weakness0
palpitations0
numbness0
tinnitus0
tremor0
urinary incontinence0
memory loss0
urinary frequency0
manic0
blurred vision0
chills0
urinary retention0
dry mouth0
urticaria0
nausea0
leukopenia0
constipation0
confusion0
ataxia0
anxiety0
anorexia0
anemia0
alopecia0
agranulocytosis0
cystic acne0
diarrhea0
dizziness0
siadh0
impotence0
hepatitis0
blood dyscrasia0
headache0
rash0
edema0
somnolence0
abdominal pain0

Target

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Uniprot ID:AOFA_HUMAN
Synonyms:
Amine oxidase [flavin-containing] A
MAO-A
Monoamine oxidase type A
EC-Numbers:1.4.3.4
Organism:Homo sapiens
Human
PDB IDs:1H8Q 2BXR 2BXS 2Z5X 2Z5Y
Structure:
2Z5Y

Binding Affinities:

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

References:

9194688
Pharmacologic inhibition of transglutaminase-induced cross-linking of Alzheimer's amyloid beta-peptide.. W Zhang; B R Johnson; T D Bjornsson (1997) Life sciences display abstract
The brain of Alzheimer's disease (AD) patients contains deposits of amyloid beta-peptide (A beta). Recent studies have shown that A beta is a substrate for tissue transglutaminase (TGase), which induces the formation of cross-linked dimers and polymers, and that tacrine, indomethacin and deferoxamine, which have widely different chemical structures, attenuate the progression of symptoms of AD. This report evaluated the potential of a total of ten different pharmacological agents to inhibit TGase-induced cross-linking of A beta, including known TGase inhibitors (dansylcadaverine, spermine), non-steroidal anti-inflammatory drugs (indomethacin, meclofenamic acid, diflunisal, salicylic acid), monoamine oxidase inhibitors (tranylcypromine, phenelzine), an acetylcholinesterase inhibitor (tacrine), and an iron chelating agent (deferoxamine). All but one (salicylic acid) of these ten agents had an inhibitory effect on TGase-induced A beta cross-linking. These results suggest that inhibition of TGase-induced cross-linking of A beta is a potential pharmacologic target for the treatment of AD. A method is also presented for the determination of percent inhibition of TGase-induced A beta cross-linking based on the separated monomer, dimer and polymer bands on SDS-PAGE gels.
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