Amoxapine - CAS 14028-44-5
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Not Intended for Therapeutic Use. For research use only.
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Amoxapine is a tricyclic dibenzoxazepine (an N-aryl piperazine) which acts similarly to several other tricyclic antidepressants, amoxapine inhibits GLYT2a transport activity with IC50 of 92 μM.
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1. Prolactin Stimulating Effects of Amoxapine and Loxapine in Psychiatric Patients*
Alan G. Robertson, Robert Berry, and Herbert Y. Meltzer. Psychopharmacology (7982) 78:287- 292
Amoxapine is a tricyclic dibenzoxazepine, the demethylated derivativeof loxapine, a neuroleptic. Numerous clinical trials have confirmed the antidepressant action of amoxapine in man (Ayd 1980; Ban et al. 1980; Smith and Ayd I981). Animal experiments using behavioral paradigms have shown that amoxapine possesses the profile characteristic of both antidepressant and neuroleptic drugs (Greenblatt et al. 1978; Chermat et al.n1979). Amoxapine produces biochemical effects characteristic of both antidepressant and neuroleptic drugs. Coupet et al. (1979) reported that amoxapine is as potent as imipramine in blocking norepinephrine uptake, and that amoxapine and its major metabolite in man, 8-OH-amoxapine, are weak inhibitors of ser otonin (5-HT) uptake in rat brain synaptosomes. However, we have found amoxapine is a fairly potent inhibitor of 5-HT uptake by human platelets in vitro and that platelet 5-HT uptake is significantly inhibited during clinical treatment with amoxapine (Arora and Meltzer, in preparation). Amoxapine is inactive in preventing the stimulation of adenylate cyclase by dopamine in the rat striatum, but it is moderately active in displacing 3H-spiroperidol from its binding sites (Coupet et at. 1979), suggesting it is a D2 dopamine receptor blocker. We have found it is as potent as thioridazine in displacing 3H-spiroperidol from rat striatal membranes in vitro (Meltzer and So, unpublished data). Amoxapine can also stimulate tyrosine hydroxylase activity in the rat striatum and nucleus accumbens (unpublished data of Pelham and Thibault cited by Greenblatt et al. 1978). These biochemical findings are in accord with the behavioral data indicating that amoxapine has a neuroleptic-like action in addition to its antidepressant action.
2. Amoxapine and amitriptyline
Douglas M. McNair, Richard J. Kahn, Laura M. Frankenthaler, and Linda L. Faldetta. Psyehopharmacology (t 984) 83:134-139
Impaired cognitive function is recognized in depression (Miller 1975). Both cognitive improvement and impairment are known to result from antidepressant treatment (Sternberg and Jarvik 1976; Glass et al. 1981). Impaired cognitive function also can be produced by centrally active anticholinergic agents (Granacher and Baldessarini 1975), such as the tricyclic antidepressants (Snyder and Yamamura 1977). How then is cognitive function related to degree of depression, to relief of depression by antidepressants, to the degree of anticholinergic activity of antidepressant agents, and to such critical influences as age of the patient? Are there general effects of the various treatments across cognitive functions? Or, are specific patterns of cognitive impairment and facilitation associated with specific medications? This study compared speed of onset of antidepressant activity of a tricyclic antidepressant, amitriptyline (Elavil), with a dibenzoxazepine, amoxapine (Asendin). It provided an opportunity to compare the effects of these agents on several cognitive functions and on peripheral autonomic activity especially relevant to anticholinergic action. Speed of action and efficacy data are reported in the preceding paper (McNair et al. /984); this paper focuses upon the cognitive and peripheral autonomic activity comparisons.
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CAS 14028-44-5 Amoxapine

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