Malan and colleagues reported effective CB2 mediated antinociception to thermal activation following systemic administration of AM1241 at 15 min postinjection. But, our results do not preclude the possibility that antinociception might happen to poisonous degrees of activation. Furthermore, AM1241 does curb mechanical hypersensitivity to von Frey activation under conditions of injury, where mechanical thresholds are (-)-MK 801 reduced in accordance with standard. Mechanical paw withdrawal thresholds were increased by coadministration of rimonabant with AM1241. This observation parallels our recent finding of antiallodynia in paclitaxel addressed animals that received rimonabant ahead of administration of the CB2 agonist AM1714. Improved efficacy of a CB2 agonist following administration of a CB1 antagonist has also been reported in a cerebral ischemic damage model. These data claim that blockade of CB1 receptors with rimonabant may increase the tone of the endogenous cannabinoid system, thus increasing the efficiency of the agonist. Antinociceptive properties of the enantiomers of AM1241 have not previously been evaluated in naive rats. Like a tool to study functional roles of CB2 receptor activation this Plastid characterization is essential because of the widespread use of AM1241. Antihyperalgesic effects of AM1241 were previously reported in a visceral and inflammatory pain model. Within our study, AM1241 presented a pharmacological profile that has been almost identical to racemic AM1241. We noticed an inverted U shaped amount Cresponse curve following administration of both AM1241 or AM1241 at the time point of maximal antinociception. Our data also illustrate that both lowest and the greatest doses of AM1241 developed greater antinociception than comparable doses of both AM1241 or AM1241. At intermediate doses, the substances made similar antinociceptive effects. Previous in vitro assist the enantiomers noted AM1241 and that are inverse agonists for rat CB2 receptors in the assay, although AM1241 can be a full agonist. Hence, it is possible that agonist activity within the assay predicts the antinociceptive efficacy of AM1241, thus reconciling the in vivo observations with results from pifithrin �� in vitro receptor binding assays. Both and AM1241 developed thermal antinociception that outlasted that of AM1241 at an identical dose. This observation might be related to the agonist properties of the racemic compound along with mixture of inverse agonist. Differences in metabolic transformation of and AM1241 could also give rise to differences in in vivo efficacy of the enantiomers. This statement could be dose dependent, while AM1241 was recommended to function as more active enantiomer in vivo in controlling acute visceral and inflammatory pain.