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1 C-42, and a third by structural analogs of N-desmethylclozapine.
2 about its biologically active metabolite, N-desmethylclozapine.
3 azol-2-one) , and the clozapine metabolite N-desmethylclozapine.
4 perties of AC-42 and AC-260584 but not for N-desmethylclozapine and clozapine, indicating that they m
5 oro-4H-benzo[1,4]oxazin-3-one (AC-260584), N-desmethylclozapine, and clozapine with the M(1) muscarin
7 ns studied, and the docking indicated that N-desmethylclozapine bound to a site distinct from AC-42 a
8 se observations raise the possibility that N-desmethylclozapine contributes to clozapine's clinical a
9 ly, these results indicate that Clozapine, N-desmethylclozapine, DETC, and U0126 protect PC-12 cells
12 idence that the brain penetrant metabolite N-desmethylclozapine is a potent, allosteric agonist at hu
13 verse allosteric agonists AC-42, TBPB, and N-desmethylclozapine may interact with different subsets o
15 prompted us to investigate the effects of N-desmethylclozapine on cloned human M1-M5 muscarinic rece
16 r map the binding site of AC-42, TBPB, and N-desmethylclozapine, point mutations previously reported
17 irected mutagenesis studies suggested that N-desmethylclozapine preferentially activated M1 receptors
19 chotic disorders, the neuronal activity of N-desmethylclozapine was electrophysiologically investigat
23 ponses to AC-42, AC-260584, clozapine, and N-desmethylclozapine were all substantially reduced, but u
25 ssues is demonstrated, where clozapine and N-desmethylclozapine were observed from mouse and rat brai
26 omocytoma (PC-12) cell line, Clozapine and N-desmethylclozapine were tested for their ability to prot
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