Disease relevance of Aminosultopride

• Finally, we compared olanzapine with amisulpride, an SGA clinically not associated with the induction of diabetes mellitus [1].
• Both treatments were well tolerated and had a similar low incidence of extrapyramidal symptoms; however, amisulpride was associated with less weight gain and endocrine/sexual symptoms [2].
• Comparative efficacy of SSRIs and amisulpride in burning mouth syndrome: a single-blind study [3].
• Transient hyperglycemia and decreased glucose tolerance during antipsychotic monotherapy with amisulpride [4].
• Rhabdomyolysis and coma associated with amisulpride: a probable atypical presentation of neuroleptic malignant syndrome [5].

Psychiatry related information on Aminosultopride

• Moreover, in the studies where depressive symptoms were measured, a significant improvement was also shown in favor of amisulpride [6].
• Dose-related effects of amisulpride on five dimensions of psychopathology in patients with acute exacerbation of schizophrenia [7].
• Amisulpride showed a shorter response latency than the SSRIs [3].
• Moreover, its effective alleviation of negative and affective symptoms, its lower association with extrapyramidal symptoms and loss of cognitive function than conventional antipsychotics and its long-term efficacy justifies consideration of the use of higher dosages of amisulpride in this group of patients [8].
• ). Considering the involvement of delta-opioid receptors in mood regulation, the interaction between amisulpride and RB101 could lead to a new therapeutic approach in the treatment of some mood disorders [9].

High impact information on Aminosultopride

• RESULTS: Eight amisulpride-treated patients (mean dose=406 mg/day) showed moderate levels of D(2)/D(3) receptor occupancy in the striatum (56%), and significantly higher levels were seen in the thalamus (78%) and temporal cortex (82%) [10].
• No significant binding of amisulpride to 5-HT2A receptors was detected [11].
• Low basal prolactin levels predicted improvement of negative symptoms in patients treated with amisulpride [12].
• While basal TSH secretion was significantly increased by both compounds, TRH-stimulated TSH secretion was elevated only in patients treated with amisulpride [12].
• D2 receptor occupancy during high- and low-dose therapy with the atypical antipsychotic amisulpride: a 123I-iodobenzamide SPECT study [13].

Chemical compound and disease context of Aminosultopride

• In short-term studies, a definite rank order of weight-gain potential among atypical antipsychotics has been demonstrated: clozapine is related to the highest risk of weight gain, followed in decreasing order of magnitude by olanzapine, quetiapine, risperidone, amisulpride, aripiprazole and ziprasidone [14].
• METHODS: Various components of maternal behavior (pup retrieval, pup licking, nest building and pup nursing) were examined repeatedly over a period of 24 h after a single injection of three doses of amisulpiride (10, 30, and 100 mg/kg s.c.) and aripiprazole (3, 10, and 30 mg/kg) [15].
• Improvement in mean Brief Psychiatric Rating Scale total score was significantly greater for amisulpride than haloperidol (17.0 versus 12.8, P = 0.01) [16].
• These results suggested that a peripheral dopamine D(2) receptor agonists could be a useful tool in alleviating amisulpride-induced hyperprolactinemia without possibly affecting its central effect [17].
• Carmoxirole is able to reduce amisulpride-induced hyperprolactinemia without affecting its central effect [17].

Biological context of Aminosultopride

• Liver impairment has little or no effect on the pharmacokinetics of olanzapine, quetiapine, risperidone (and 9-hydroxy-risperidone) and ziprasidone, but information is lacking for amisulpride [18].
• In naive mice, apomorphine (1 mg/kg s.c.) or LY 171555 (0.4 mg/kg s.c.) induced hypothermia which was antagonized by amisulpride (12.5 mg/kg i.p.); a transiently increased body temperature was even measured 30 min after apomorphine injection in amisulpride-treated mice [19].
• When the daily dose of amisulpride was reduced from 800 mg/d to 600 mg/d, the patient's ECG quickly normalized (including blood pressure and pulse rate) within a few days [20].
• It includes concepts of human neurobiology and neuropharmacology and their application to clinical medicine, as well as the presentation of the clinical evidence on the therapeutic efficacy and safety of amisulpride in schizophrenia, highlighting dosage issues [21].
• RESULTS: Individual antipsychotic medications are associated with different degrees of treatment-induced increases in body weight and adiposity, ranging from modest effects (<2 kg) with amisulpride, ziprasidone, and aripiprazole to clinically significant increases with olanzapine (4-10 kg) [22].

Anatomical context of Aminosultopride

• RESULTS: D2/D3 receptor occupancy was 42% in caudate and 31% in putamen for risperidone (t=5.9, df=11, p=0.0001) and 51% in caudate and 37% in putamen for amisulpride (t=11.1, df=15, p<0.0001) [23].
• Higher D2/D3 receptor occupancy at the pituitary gland than at central regions is a possible explanation for amisulpride PRL elevation with low EPS [24].
• Amisulpride has poor blood-brain barrier penetration and reaches much higher concentration at the pituitary, which is outside the blood-brain barrier [24].
• It was predicted therefore that amisulpride would alleviate both the under-activity in the frontal cortex and the over-activity in the limbic system [25].
• Amisulpride is readily absorbed from the gastrointestinal tract, distributed to all body systems with little binding to plasma proteins [26].

Associations of Aminosultopride with other chemical compounds

• Binding of antipsychotic drugs to cortical 5-HT2A receptors: a PET study of chlorpromazine, clozapine, and amisulpride in schizophrenic patients [11].
• METHOD: PET scans were performed on 6 controls and 18 patients with schizophrenia treated with haloperidol or with risperidone, clozapine, amisulpride or olanzapine [27].
• The purpose of this study was to investigate the binding of amisulpride to extrastriatal (i.e., thalamus and temporal cortex) and striatal D2 dopamine receptors with respect to plasma amisulpride determinations [28].
• RESULTS: We found 5 blind placebo-controlled clinical trials (105 patients), 24 open-label clinical trials (387 patients), and 33 case series (115 patients) describing the use of the atypical neuroleptics clozapine, risperidone, olanzapine, sulpiride, tiapride, amisulpride, remoxipride, and clothiapine in children and adolescents [29].
• The relationship between the daily oral dose of the benzamide amisulpride and the striatal D2-dopamine receptors occupancy was investigated in 11 schizophrenic patients using positron emission tomography with 76Br-bromolisuride [30].

Gene context of Aminosultopride

• The SGA amisulpride, however, only binds to D2/D3 receptors, which makes it an interesting tool to test this assumption [31].
• Both amisulpride doses were significantly more effective than placebo on the primary evaluation criterion (SANS total score, MANOVA P < 0.02) [32].
• BACKGROUND: Amisulpride is a selective D(2)-D(3) antagonist that has been reported to be effective in the treatment of schizophrenia and major depressive disorder [33].
• RESULTS: The mean PRL was 1166 (range 499-1892 mIU/l) for a mean amisulpride dose of 406 mg/day (range 150-600 mg/day) [24].
• To investigate this hypothesis, we tested four atypical antipsychotics, two that are commonly associated with prolactin elevation (amisulpride and risperidone) and two that are less frequently associated (quetiapine and olanzapine) [34].

Analytical, diagnostic and therapeutic context of Aminosultopride

• The mean effect sizes found for amisulpride were compared with those of an updated meta-analysis of the 5-HT(2)/D(2) antagonists [35].
• RESULTS: Eighteen randomized controlled trials of amisulpride (N=2,214) were found [35].
• This finding may indicate that amisulpride is especially useful at the beginning of drug therapy of BMS [3].
• CONCLUSIONS: This first prospective study on amisulpride in the treatment of mania suggests that, despite the limitations of the open, observational design and small sample size, amisulpride may be effective and reasonably safe in the treatment of bipolar mania [33].
• EEG abnormalities under treatment with atypical antipsychotics: effects of olanzapine and amisulpride as compared to haloperidol [36].

References