Table 4. Full allosteric quantification of selected analogues.
Comp. # | [3H]-NMS binding | CAMYEL activation | β-arrestin 2 recruitment | |||||
---|---|---|---|---|---|---|---|---|
pKB | Log α(ACh)a | Log τBc | Log α βc | Log τBd | Log α βd | |||
le | 6.22 ± 0.08a | 2.12 ± 0.12 | − 0.45 ± 0.03 | 2.34 ± 0.15 | 0.99 ± 0.10 | 1.94 ± 0.26 | ||
6c | 5.84 ± 0.04a | 1.95 ± 0.10 | − 0.54 ± 0.03 | 2.22 ± 0.12 | 0.64 ± 0.11 | 1.29 ± 0.25 | ||
6f | 6.11 ± 0.04a | 1.92 ± 0.10 | − 0.88 ± 0.06* | 2.01 ± 0.15 | 0.56 ± 0.06 | 1.10 ± 0.24 | ||
6j | 4.68 ± 0.11b* | 1.98 ± 0.13 | 0.04 ± 0.05* | 2.46 ± 0.18 | 0.87 ± 0.10 | 1.87 ± 0.18 | ||
6k | 4.53 ± 0.13b* | 2.04 ± 0.14 | − 0.07 ± 0.05* | 2.65 ± 0.19 | 0.31 ± 0.13 | 1.55 ± 0.16 | ||
6l | 4.75 ± 0.30a* | 1.87 ± 0.14 | − 1.29 ± 0.17* | 1.91 ± 0.17 | 0.39 ± 0.12 | 1.18 ± 0.23 | ||
6o | 4.49 ± 0.10b* | 1.47 ± 0.14* | − 0.58 ± 0.09 | 2.03 ± 0.17 | - 0.83 ± 0.53* | 1.06 ± 0.19 | ||
12a | 5.33 ± 0.18a* | 2.18 ± 0.18 | − 0.81 ± 0.07* | 2.47 ± 0.21 | 0.51 ± 0.12 | 2.09 ± 0.15 | ||
12e | 4.55 ± 0.56b* | 1.41 ± 0.14* | − 0.74 ± 0.09 | 1.81 ± 0.16 | 0.07 ± 0.26* | 0.94 ± 0.40* |
Data are the mean ± SEM of 4 independent experiments with repeats in duplicate. Data were analysed by one-way ANOVA followed by a Dunnett’s post-hoc test
where *p < 0.05 was considered to be significantly different to the parent ligand 1e.
Data were fitted with the allosteric ternary complex model (equation (2)), with the affinity of [3H]-NMS (LogKA = –9.6) and the actual concentration of [3H]-NMS (LogHot = –9.3).
Affinity (pKB) determined by the global allosteric pKI model (Supp. Fig. 6; equation (4)) which was then used to fix the pKB value in the allosteric ternary complex model (equation (2)) to derive logα(ACh).
Data fitted with the complete model of allosterism and agonism (equation (6)) where LogKA was fixed to the LogKI (ACh, –5.17) determined from competition binding between [3H]-NMS and ACh. LogKB was fixed to the pKB determined from the allosteric interaction binding assays. The slope was fixed to 0.7073 which was determined by fitting the iperoxo, ACh, xanomeline and oxotremorine concentration-response curves to a four parameter logistic equation and sharing the slopes. The system Emax was fixed to 450.9 which was the Emax determined for iperoxo, by fitting concentration-response curves with the operational model of agonism (equation (5)).
Data were fitted to the simplified operational model of allosterism (equation 7) with LogKB fixed to the affinity of the allosteric modulator determined from allosteric interaction binding assays. The slope was fixed to 1.