Fluphenazine decanoate ep monograph

The mechanism of action of all first-generation antipsychotics (FGAs) appears to be postsynaptic blockade of brain dopamine D2 receptors. Evidence supporting this mechanism includes strong antagonism of D2 receptors in both cortical and striatal areas [ 1 ], a high correlation between D2 receptor binding and clinical potency [ 2 ], and a consistent requirement of 65 percent D2 receptor occupancy for antipsychotic efficacy in functional imaging studies [ 3 ]. The nonspecific localization of FGA dopamine binding throughout the central nervous system is consistent with their risk of movement disorders and prolactinemia. Aside from their common activity as D2 antagonists, each FGA has distinct effects on neuronal 5-HT2a, alpha-1, histaminic, and muscarinic receptors, which generally correspond to their individual side effect profiles, as shown in the table ( table 1 ).

Fluphenazine decanoate ep monograph

fluphenazine decanoate ep monograph

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