Table 1. The pharmacology of the endocannabinoid system–selected compounds.

Compound	Mechanism of action	Effect in pain
THC	Primarily activation of CB receptors, although has off-target actions (e.g. Barann et al., 2002)	Inflammatory: + Neuropathic: +
AM1241	CB₂-receptor selective ligand; acts as a “protean” agonist in vitro (Yao et al., 2006) and CB2 agonist in vivo	Inflammatory: + Neuropathic: +
GW405833	CB₂-receptor selective ligand (efficacy dependent upon assay used, see Yao et al., 2008)	Inflammatory: + Neuropathic: +
LY2318912	Blocks the accumulation and metabolism of AEA (Moore et al., 2005). Acts primarily as a potent FAAH inhibitor, but with many off-target actions (Alexander and Cravatt, 2006)	Inflammatory: +
URB597	Selective FAAH inhibitor (Kathuria et al., 2003). Some off-target actions have been reported, but their importance is unclear	Inflammatory: + Visceral: + Neuropathic: +/−
ibu-am5	Dual COX- and FAAH-inhibitory compound (Holt et al., 2007).	Visceral: +
N-arachidonoylserotonin	Dual TRPV1 antagonist/FAAH-inhibitory compound (Maione et al., 2007).	Inflammatory: + Neuropathic: +
Pravadoline	Dual CB agonist/COX-inhibitory compound (D’Ambra et al., 1992).	Inflammatory: + Visceral: +

The compounds shown in this table have been selected since they are those principally discussed in this review.“+” indicates efficacy in a preclinical model of this pain type (for details, see text). For a more complete list, see Fowler (2008).