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Drug-Target Interaction

Drug

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PubChem ID:5281969
Structure:
Synonyms:
"anandamide; anandamide(20:4, n-6); n-arachidonoyl ethanolamine"
(5Z,8Z,11Z,14Z)- N-(2-Hydroxyethyl)- 5,8,11,14-eicosatetraenamide
(5Z,8Z,11Z,14Z)-N-(2-hydroxyethyl)-5,8,11,14-eicosatetraenamide
(5Z,8Z,11Z,14Z)-N-(2-hydroxyethyl)icosa-5,8,11,14-tetraenamide
(all-Z)-N-(2-hydroxyethyl)-5,8,11,14-eicosatetraenamide
5,8,11,14-eicosatetraenamide, N-(2-hydroxyethyl)-
5,8,11,14-Eicosatetraenamide, N-(2-hydroxyethyl)-, (5Z,8Z,11Z,14Z)-
5,8,11,14-Eicosatetraenamide, N-(2-hydroxyethyl)-, (all-Z)-
5,8,11,14-Eicosatetraenoylethanolamide
94421-68-8
A0580_SIGMA
AE
AEA
AIDS-342672
AIDS342672
Anandamide
Anandamide (20.4, n-6)
anandamide (20.4,n-6)
Anandamide(20:4, n-6)
Anandamide; Anandamide(20:4, n-6); N-arachidonoyl ethanolamine
AnNH
Arachidonic acid N-(hydroxyethyl)amide
Arachidonoyl ethanolamide
arachidonoyl-EA
arachidonoylethanolamide
Arachidonyl ethanolamide
Arachidonylethanolamide
BSPBio_001533
C078814
C11695
C22H37NO2
CHEBI:2700
CPD-7598
IDI1_034003
LMFA08040001
LS-63781
N-(2-Hydroxyethyl)-5,8,11,14-eicosatetraenamide (all-Z)-
N-(2-Hydroxyethyl)anachidonamide
N-(2-hydroxyethyl)arachidonamide
N-(5Z,8Z,11Z,14Z-icosatetraenoyl)-ethanolamide
N-arachidonoyl ethanolamine
N-arachidonoyl ethanolamine;
N-Arachidonoyl-2-hydroxyethylamide
n-arachidonoylethanolamide
N-Arachidonoylethanolamine
NCGC00161195-03
NCGC00161195-04
NCGC00161195-05
NCGC00161195-06
NCGC00161195-07
nchembio.129-comp2
nchembio.86-comp2
SMP2_000328
ZINC03809850
[14C]Anandamide
[3H]Anandamide

Target

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Uniprot ID:ICE_DROME
Synonyms:
Caspase
drICE
EC-Numbers:3.4.22.-
Organism:Drosophila melanogaster
Fruit fly
PDB IDs:-

Binding Affinities:

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

References:

15375383
Anandamide-induced cell death in primary neuronal cultures: role of calpain and caspase pathways.. V A Movsesyan; B A Stoica; A G Yakovlev; S M Knoblach; P M Lea4th; I Cernak; R Vink; A I Faden (2004) Cell death and differentiation display abstract
Anandamide (arachidonoylethanolamide or AEA) is an endocannabinoid that acts at vanilloid (VR1) as well as at cannabinoid (CB1/CB2) and NMDA receptors. Here, we show that AEA, in a dose-dependent manner, causes cell death in cultured rat cortical neurons and cerebellar granule cells. Inhibition of CB1, CB2, VR1 or NMDA receptors by selective antagonists did not reduce AEA neurotoxicity. Anandamide-induced neuronal cell loss was associated with increased intracellular Ca(2+), nuclear condensation and fragmentation, decreases in mitochondrial membrane potential, translocation of cytochrome c, and upregulation of caspase-3-like activity. However, caspase-3, caspase-8 or caspase-9 inhibitors, or blockade of protein synthesis by cycloheximide did not alter anandamide-related cell death. Moreover, AEA caused cell death in caspase-3-deficient MCF-7 cell line and showed similar cytotoxic effects in caspase-9 dominant-negative, caspase-8 dominant-negative or mock-transfected SH-SY5Y neuroblastoma cells. Anandamide upregulated calpain activity in cortical neurons, as revealed by alpha-spectrin cleavage, which was attenuated by the calpain inhibitor calpastatin. Calpain inhibition significantly limited anandamide-induced neuronal loss and associated cytochrome c release. These data indicate that AEA neurotoxicity appears not to be mediated by CB1, CB2, VR1 or NMDA receptors and suggest that calpain activation, rather than intrinsic or extrinsic caspase pathways, may play a critical role in anandamide-induced cell death.