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Replacing this group with (4-fluorophenyl) amino moiety, along with optimal substitutions at the N-7, C-2, and C-3 positions discussed above, resulted in Compound 18 , which exhibited the most potent (IC 50 : 21 nM) and selective (over 480-fold versus PDE8) PDE1 inhibitor among the synthesized derivatives, along with good metabolic stability in rat liver microsomes (T 1/2 : 28.5 min)
The deficiency of neurotrophic support leads to neuronal atrophy, impaired axonal transport, and decreased nerve regeneration capacity
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