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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:PGH2_HUMAN
Synonyms:
COX-2
Cyclooxygenase-2
PGH synthase 2
PGHS-2
PHS II
Prostaglandin G/H synthase 2
Prostaglandin H2 synthase 2
Prostaglandin-endoperoxide synthase 2
EC-Numbers:1.14.99.1
Organism:Homo sapiens
Human
PDB IDs:1V0X
Structure:
1V0X

Binding Affinities:

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

References:

16099783
The endogenous cannabinoid, anandamide, induces cell death in colorectal carcinoma cells: a possible role for cyclooxygenase 2.. H A Patsos; D J Hicks; R R H Dobson; A Greenhough; N Woodman; J D Lane; A C Williams; C Paraskeva (2005) Gut display abstract
BACKGROUND AND AIMS: Cyclooxygenase 2 (COX-2) is upregulated in most colorectal cancers and is responsible for metabolism of the endogenous cannabinoid, anandamide, into prostaglandin-ethanolamides (PG-EAs). The aims of this study were to determine whether anandamide and PG-EAs induce cell death in colorectal carcinoma (CRC) cells, and whether high levels of COX-2 in CRC cells could be utilised for their specific targeting for cell death by anandamide. METHODS: We determined the effect of anandamide on human CRC cell growth by measuring cell growth and cell death, whether this was dependent on COX-2 protein expression or enzyme activity, and the potential involvement of PG-EAs in induction of cell death. RESULTS: Anandamide inhibited the growth of CRC cell lines HT29 and HCA7/C29 (moderate and high COX-2 expressors, respectively) but had little effect on the very low COX-2 expressing CRC cell line, SW480. Induction of cell death in HT29 and HCA7/C29 cell lines was partially rescued by the COX-2 selective inhibitor NS398. Cell death induced by anandamide was neither apoptosis nor necrosis. Furthermore, inhibition of fatty acid amide hydrolase potentiated the non-apoptotic cell death, indicating that anandamide induced cell death was mediated via metabolism of anandamide by COX-2, rather than its degradation into arachidonic acid and ethanolamine. Interestingly, both PGE2-EA and PGD2-EA induced classical apoptosis. CONCLUSIONS: These findings suggest anandamide may be a useful chemopreventive/therapeutic agent for colorectal cancer as it targets cells that are high expressors of COX-2, and may also be used in the eradication of tumour cells that have become resistant to apoptosis.