ABT-107, a selective α7 neuronal nicotinic receptor agonist, demonstrates neuroprotective effects against nigrostriatal damage in rats with unilateral 6-hydroxydopamine lesions.

ABT-107 exhibits good bioavailability in mouse (orally, 51.1%; intraperitoneally,100%), rat (orally, 81.2%; intraperitoneally, 100.0%), and monkey (orally, 40.6%; intramuscularly,

100%), and good CNS penetration in rodents with a brain/plasma ratio of 1[1]. ABT-107 (0.01-1 μmol/kg i.p., 15 min before sacrifice) produces a dose-dependent increase in ERK1/2 and CREB[1]. ABT-107 (0.01, 0.1, and 1.0 mg/kg i.p.) increases S 9 -GSK3 and decreases p-tau in mouse cortex and hippocampus in mice[1]. ABT-107 (5 mg/kg/day i.p.) infusion attenuates tau hyperphosphorylation in AD transgenic APP-tau mice[1]. Animal Model: Rats (male Sprague-Dawley; 350-380 g b.wt.)[1]. Dosage: 1, 3 μmol/kg. Administration: I.P. daily for 3 consecutive days. Result: Induced a significant, dose-dependent increase in ACh release by day 3 of repeated administration. Higher doses may be required to evoke ACh release in naive rats not engaged in stimulated, i.e., cognitive-related behavior. Animal Model: Female TAPP (and wild-type littermates) mice[1]. Dosage: 1 mg/kg. Administration: Continuous subcutaneous infusion for 2 weeks. Result: Produced a dose-dependent increase in Ser9 phosphorylation in the cingulate cortex 15 min after acute administration in mice.