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. Author manuscript; available in PMC: 2014 Jun 1.
Published in final edited form as: Toxicol Appl Pharmacol. 2013 Mar 26;269(2):100–108. doi: 10.1016/j.taap.2013.03.012

Figure 5. Monohydroxylated metabolites of JWH-018 and JWH-073 inhibit forskolin-stimulated adenylyl cyclase (AC)-activity via CB2Rs in intact cells.

Figure 5

A measure of maximal efficacy (EMAX) for CB2R-mediated inhibition of forskolin-stimulated AC-activity produced by JWH-018 [A] and [B], JWH-073 [C] and [D] and respective metabolites, was obtained by evaluating the level of intracellular cAMP levels in response to vehicle or a receptor saturating concentration (10 µM) of each test compound in intact CHO-hCB2 [A] and [C] or CHO-hMOR [B] and [D] cells. AC-inhibition produced by the MOR agonists DAMGO (10 µM) and morphine (10 µM) was evaluated as positive controls in CHO-hMOR cells. The mean ± SEM of AC-inhibition produced by test compounds is presented. EMAX values (mean ± SEM) are provided in Table 2.

*Significantly different from percent of AC-inhibition produced by CP-55,940 (P<0.05; ANOVA + Dunnett’s post-hoc comparison).

**Significantly different from basal cAMP levels (P<0.05; One sample t-test).