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. Author manuscript; available in PMC: 2017 Mar 20.
Published in final edited form as: ACS Chem Neurosci. 2016 Apr 25;7(6):776–798. doi: 10.1021/acschemneuro.6b00041

Table 4.

cAMP Inhibition in the Presence of GAT100, Org27569, and PSNCBAM-1a

HEK-CREb
2-AG
AEA
CP55,940
IC50 (nM) Emax IC50 (nM) Emax IC50 (nM) Emax
agonist alone 338 (203–516) 93.6 ± 5.47 508 (358–719) 87.2 ± 7.36 587 (474–678) 106.3 ± 11.4
GAT100 644 (575–761)ˆ 19.2 ± 0.95ˆˆˆ 774 (735–805)ˆ 10.4 ± 1.05ˆˆˆ 834 (786-952) ˆ 19.2 ± 1.62ˆˆˆ
Org27569 970 (836–1180)*ˆ 39.0 ± 1.40***ˆˆˆ 882 (825–961)* ˆ 28.4 ± 2.07***ˆˆˆ 969 (829–998)* ˆ 25.7 ± 1.64*ˆˆˆ
PSNCBAM-1 978 (916–1223)*ˆ 40.0 ± 2.13*** ˆˆˆ 870 (849–919)* ˆ 40.7 ± 2.45***ˆˆˆ 962 (842–997)*ˆ 45.7 ± 3.93***ˆˆˆ
a

IC50 (nM) determined using nonlinear regression analysis; Emax (% cAMP inhibition) determined using nonlinear regression analysis. Data are mean with 95% CI (IC50) and mean ± SEM (Emax).

b*

P < 0.05,

**

P < 0.01,

***

P < 0.001compared to GAT100 within orthosteric agonist treatment;

P < 0.05, compared to 2-AG within NAM treatment,

ˆ

P < 0.05,

ˆˆ

P < 0.01,

ˆˆˆ

P < 0.001 compared to agonist alone, as determined by one-way ANOVA followed by Dunnett’s multiple comparison (Emax) or nonoverlapping 95% CI (IC50). Data are from Figures 8 (Emax) and 9, orthosteric agonist + allosteric modulator (IC50). N = 4.

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