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Perospirone (Lullan) is an atypical antipsychotic of the azapirone family.[1] It was introduced in Japan by Dainippon Sumitomo Pharma in 2001 for the treatment of schizophrenia and acute cases of bipolar mania.[3][4]
Its primary uses are in the treatment of schizophrenia and bipolar mania.[3][4]
In a clinical trial that compared it to haloperidol in the treatment of schizophrenia it was found to produce significantly superior overall symptom control.[5] In another clinical trial perospirone was compared with mosapramine and produced a similar reduction in total PANSS score, except with respect to the blunted affect part of the PANSS negative score, in which perospirone produced a significantly greater improvement.[6] In an open-label clinical trial comparing aripiprazole with perospirone there was no significant difference between the two treatments discovered in terms of both efficacy and tolerability.[7] In 2009 a clinical trial found that perospirone produced a similar reduction of PANSS score than risperidone and the extrapyramidal side effects was similar in both frequency and severity between groups.[8]
A meta-analysis published in 2013 found that it is statistically significantly less efficacious than other second-generation antipsychotics.[9]
Has a higher incidence of extrapyramidal side effects than the other atypical antipsychotics, but still less than that seen with typical antipsychotics.[1][10] A trend was observed in a clinical trial comparing mosapramine with perospirone that favoured perospirone for producing less prominent extrapyramidal side effects than mosapramine although statistical significant was not reached.[6] It may produce less QT intervalprolongation than zotepine, as in one patient who had previously been on zotepine switching to perospirone corrected their prolonged QT interval.[11] It also tended to produce less severe extrapyramidal side effects than haloperidol in a clinical trial comparing the two (although statistical significance was not reached).[5]
Perospirone binds to the following receptors with very high affinity (as an antagonist unless otherwise specified):[12][9][13][12][14][15][16]
and the following receptor with high affinity:[9]
and the following with moderate affinity:[9]
and with low affinity for the following receptor:[9]
: PSO/PSI
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* Note that many TCAs, TeCAs, antipsychotics, ergolines, and some piperazines like buspirone and trazodone all antagonize α1-adrenergic receptors as well, which contributes to their side effects such as orthostatic hypotension.
* Note that many atypical antipsychotics and azapirones like buspirone (via metabolite 1-PP) antagonize α2-adrenergic receptors as well.
* Note that MAO-B inhibitors also influence norepinephrine/epinephrine levels since they inhibit the breakdown of their precursor dopamine.
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