ArticleBritish journal of pharmacology2014
Prostamide F(2) α receptor antagonism combined with inhibition of FAAH may block the pro-inflammatory mediators formed following selective FAAH inhibition.
Article in British journal of pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 44 citations in OpenAlex.
- The Inhibition of Fatty Acid Amide Hydrolase-4 Affords Neuroprotection in a Toxic Model Induced by 6-Hydroxydopamine in Caenorhabditis elegans Nematodes.Molecular neurobiology · 2025Article
- Preclinical investigation in FAAH inhibition as a neuroprotective therapy for frontotemporal dementia using TDP-43 transgenic male mice.Journal of neuroinflammation · 2023Article
- Design, synthesis andJournal of enzyme inhibition and medicinal chemistry · 2021Article
- The endocannabinoid system - current implications for drug development.Journal of internal medicine · 2021Review
- Article
- New approaches and challenges to targeting the endocannabinoid system.Nature reviews. Drug discovery · 2018Review
- Activity-based protein profiling reveals off-target proteins of the FAAH inhibitor BIA 10-2474.Science (New York, N.Y.) · 2017Article
- Article
- 4'-O-methylhonokiol increases levels of 2-arachidonoyl glycerol in mouse brain via selective inhibition of its COX-2-mediated oxygenation.Journal of neuroinflammation · 2015Article
- Tapping into the endocannabinoid system to ameliorate acute inflammatory flares and associated pain in mouse knee joints.Arthritis research & therapy · 2014Article
- Combined inhibition of FAAH and COX produces enhanced anti-allodynic effects in mouse neuropathic and inflammatory pain models.Pharmacology, biochemistry, and behavior · 2014Article
- Cannabinoids: clearing the smoke on pain, inflammation and neurodegeneration.British journal of pharmacology · 2014Article
- Alterations in the anandamide metabolism in the development of neuropathic pain.BioMed research international · 2014Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeProstamides are lipid mediators formed by COX-2-catalysed oxidation of the endocannabinoid anandamide and eliciting effects often opposed to those caused by anandamide. Prostamides may be formed when hydrolysis of anandamide by fatty acid amide hydrolase (FAAH) is physiologically, pathologically or pharmacologically decreased. Thus, therapeutic benefits of FAAH inhibitors might be attenuated by concomitant production of prostamide F2 α . This loss of benefit might be minimized by compounds designed to selectively antagonize prostamide receptors and also inhibiting FAAH. EXPERIMENTAL APPROACH: Inhibition of FAAH by a series of selective antagonists of prostamide receptors, including AGN 204396, AGN 211335 and AGN 211336, was assessed using rat, mouse and human FAAH in vitro, together with affinity for human recombinant CB1 and CB2 receptors. Effects in vivo were measured in a model of formalin-induced inflammatory pain in mice. KEY
resultsThe prostamide F2 α receptor antagonists were active against mouse and rat FAAH in the low μM range and behaved as non-competitive and plasma membrane-permeant inhibitors. AGN 211335, the most potent inhibitor of rat FAAH (IC50 = 1.2 μM), raised exogenous anandamide levels in intact cells and also bound to cannabinoid CB1 receptors. Both AGN 211335 and AGN 211336 (0.25-1 mg·kg(-1) , i.p.) inhibited the formalin-induced nociceptive response in mice. CONCLUSIONS AND IMPLICATIONS: Synthetic compounds with indirect agonist activity at cannabinoid receptors and antagonist activity at prostamide receptors can be developed. Such compounds could be used as alternatives to selective FAAH inhibitors to prevent the possibility of prostamide F2 α -induced inflammation and pain. LINKED ARTICLES: This article is part of a themed section on Cannabinoids 2013. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2014.171.issue-6.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.