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. 2020 Nov 23;10:20405. doi: 10.1038/s41598-020-77175-y

Table 2.

hCB1R- or hCB2R-dependent inhibition of FSK-stimulated cAMP accumulation.

Compound hCB1R hCB2R
EC50 (nM) Emax (%) EC50 (nM) Emax (%)
CP55,940 7.7 (0.13–14) 100 ± 6.2 4.0 (0.86–12) 100 ± 8.2
9-THC 240 (100–320)* 56 ± 9.6* 18.0 (5.0–102) 76 ± 8.6*
9-THCa > 10,000 35 ± 11 1800 (360–3800)*^ 95 ± 1.5^
THCV 260 (46–1200)* 59 ± 3.9* 280 (49–610)*^ 79 ± 1.3*
CBD > 10,000 26 ± 1.6* > 10,000 61 ± 2.3*
CBDa 30 (2.8–200) 22 ± 1.1* 140 (29–310)* 32 ± 4.2*
CBDV > 10,000 68 ± 5.7* 5.0 (0.46–33) 51 ± 12*
CBG 120 (7.4–700) 68 ± 2.4* 130 (30–550)* 39 ± 11*^
CBC 190 (23–1700)* 68 ± 9.7* 7.1 (2.0–24) 76 ± 5.4*

hCB1R- or hCB2R-dependent inhibition of FSK-stimulated cAMP accumulation was quantified in HitHunter CHO cells stably expressing hCB1R or hCB2R and treated with compounds for 90 min. Data were fit to a variable slope (4 parameter) non-linear regression in GraphPad (v. 8). n ≥ 6 independent experiments performed in triplicate. EMax refers to the top of the concentration–response curve. Data are expressed as nM with 95% CI or %CP55,940 response, mean ± SEM. *p < 0.05 compared to CP55,940 within receptor; ^p < 0.05 compared to ∆9-THC within receptor; p < 0.05 compared to hCB1R within compound; as determined via non-overlapping 95% CI or one-way ANOVA followed by Tukey's post-hoc test. Corresponding graphs are presented in Figs. 3 and 6.