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PMID: 7935333 Published · ppublish English Journal Article Research Support, U.S. Gov't, P.H.S.

Cannabinoid receptor binding and agonist activity of amides and esters of arachidonic acid.

Molecular pharmacology ·Vol. 46 ·No. 3 ·1994-09-00 ·Pages 516-22

Pinto JC, Potié F, Rice KC, Boring D, Johnson MR, Evans DM, Wilken GH, Cantrell CH, Howlett AC

Abstract

The cannabinoid receptor in brain (CB1) specifically binds delta 9-tetrahydrocannabinol, the predominant central nervous system-active component of marijuana. An eicosanoid found in brain, N-(2-hydroxyethyl)arachidonylamide (anandamide), binds to CB1 with similar affinity. This report considers structure-activity requirements for a series of novel amides and rigid hairpin conformations typified by N-(2-hydroxyethyl)prostaglandin amides, assayed with phenylmethylsulfonyl fluoride inactivation of esterases/amidases. Arachidonyl esters were 30-fold less potent than N-(2-hydroxyethyl)arachidonylamide, showing a rank order of potency of methyl = ethyl > propyl = isopropyl. Within the N-(hydroxyalkyl)arachidonylamide series, a one-carbon increase in chain length increased the potency 2-fold, but continued extension decreased affinity. Substituting the amide for the N-(2-hydroxyethyl)amide function produced a 4-fold loss of affinity. The N-(propyl)-, N-(butyl)-, and N-(benzyl)arachidonylamide derivatives exhibited a 3-fold increase, no change, and a 5-fold decrease, respectively, in affinity, compared with N-(2-hydroxyethyl)arachidonylamide. Both the methoxy ether and the formamide derivatives suffered > 20-fold loss of potency, compared with N-(2-hydroxyethyl)arachidonylamide. N-(2-Aminoethyl)arachidonylamide interacted poorly with CB1. At 100 microM, N-(2-hydroxyethyl)amide analogs of prostaglandin E2, A2, B2, and B1 failed to alter [3H]CP55940 binding to CB1. N-(2-Hydroxyethyl)arachidonylamide inhibited adenylate cyclase with lesser potency but with similar efficacy, compared with desacetyllevonantradol. Extending the length of the hydroxyalkyl moiety by one carbon increased the apparent potency by 1 order of magnitude. The N-(propyl) derivative exhibited a 5-fold greater potency than did the N-(2-hydroxyethyl) analog. It appears that the bulk and length of the moiety appended to arachidonic acid are more important determinants of affinity for CB1 than is hydrogen-bonding capability.

MeSH Terms
Adenylyl Cyclase Inhibitors Adenylyl Cyclases/metabolism Amides/metabolism Animals Arachidonic Acids/metabolism,pharmacology Binding Sites Brain/drug effects,metabolism Dose-Response Relationship, Drug Esters/metabolism In Vitro Techniques Rats Receptors, Cannabinoid Receptors, Drug/agonists,drug effects,metabolism Structure-Activity Relationship
Chemicals
Adenylyl Cyclase Inhibitors Amides Arachidonic Acids Esters Receptors, Cannabinoid Receptors, Drug Adenylyl Cyclases
Authors & Affiliations
9 authors, click to expand affiliations / ORCID
Pinto J C
Laboratory of Medicinal Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892.
Potié F
Rice K C
Boring D
Johnson M R
Evans D M
Wilken G H
Cantrell C H
Howlett A C
Article Info
Journal
Molecular pharmacology
Abbr.
Mol Pharmacol
ISSN
0026-895X
Published
1994-09-00
Pages
516-22
Language
English
Region
United States
NLM ID
0035623
Subset
IM
Grants
NIDA NIH HHS · K05-DA00182 · United States
NIDA NIH HHS · R01-DA03690 · United States
NIDA NIH HHS · R01-DA06912 · United States
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