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. Author manuscript; available in PMC: 2016 Oct 15.
Published in final edited form as: Biochem Pharmacol. 2015 Jul 29;97(4):566–575. doi: 10.1016/j.bcp.2015.07.030

Fig. 10.

Fig. 10

Baseline versus blockade studies of [18F]ASEM with mouse-equivalent doses of clinical α7-nAChR drugs in CD-1 mice. Data: %ID/g tissue ± SD (n = 4). The control mice were treated with vehicle saline. Abbreviations: CB = cerebellum, Hipp = hippocampus; Ctx = cortex. Statistics in all three graphs: *P < 0.01, blockade is significantly different from controls (ANOVA). a: DMXB-A (GTS-21), dose-escalation. Note: a mouse-equivalent dose = 25 mg/kg[81] of the clinical dose (150 mg). 90 min post [18F]ASEM injection. b: EVP-6124, a mouse-equivalent dose (0.18 mg/kg) of the clinical dose (1 mg). 60 min post [18F]ASEM injection. c: Varenicline, a mouse-equivalent dose (0.18 mg/kg) of the clinical dose (1 mg). 60 min post [18F]ASEM injection. The graph demonstrates that in vivo binding of [18F]ASEM in the mouse brain regions enriched with α7-nAChR is significantly blocked by the α7-nAChR drugs DMXB-A, EVP-6124 and varenicline. Reprinted from[68] with permission of Copyright Clearance Center's RightsLink service.