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Clocapramine (Clofekton), also known as 3-chloroc​arpiprami​ne, is an atypical antipsychotic of the imidobenzyl class which was introduced in Japan in 1974 by Yoshitomi for the treatment of schizophrenia. In addition to psychosis, clocapramine has also been used to augment antidepressants in the treatment of anxiety and panic.

Clocapramine has been reported to act as an antagonist of the D2, 5-HT2A, α1-adrenergic, and α2-adrenergic receptors, and does not inhibit the reuptake of either serotonin or norepinephrine. It has also been shown to have affinity for the σ receptors. Clocapramine's affinity for the 5-HT2A receptor is greater than that for the D2 receptor and it has a lower propensity for inducing extrapyramidal symptoms compared to typical antipsychotics, thus underlying its atypical nature.

In several clinical trials, clocapramine has been compared to other neuroleptic agents. Against haloperidol, though there was no significant difference in efficacy at the end of the study, clocapramine tended to be superior in alleviating motor retardation, alogia, and thought disorder, and also produced fewer side effects. Against sulpiride, clocapramine demonstrated more favorable effects in the treatment of both positive and negative symptoms, including motor retardation, delusions, hallucinations, and social isolation, though it produced more side effects. Against timiperone, clocapramine showed lower efficacy against both positive and negative symptoms and produced more side effects such as dyskinesia, insomnia, constipation, and nausea.

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This page contains text from Wikipedia, the Free Encyclopedia - http://en.wikipedia.org/wiki/Clocapramine

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