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Amisulpride

A Review of its Pharmacodynamic and Pharmacokinetic Properties and Therapeutic Efficacy in the Management of Schizophrenia

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Abstract

Synopsis

Amisulpride is a substituted benzamide. It is a dopamine antagonist with high selectivity for dopamine D2 and D3 receptors. In high doses, amisulpride exhibits dopaminergic blocking activity similar to that induced by classical antipsychotic agents, whereas in low doses it appears to facilitate dopaminergic transmission.

In well controlled studies of patients with primary negative symptoms of schizophrenia who had high negative and low positive symptoms scores, amisulpride 50 to 300 mg/day was more effective than placebo. The drug was at least as effective as low-dose fluphenazine (2 to 12 mg/day) in less rigorous trials which included patients with negative symptoms of schizophrenia.

At higher dosages (600 to 1200 mg/day), amisulpride exhibits efficacy similar to that of haloperidol 5 to 40 mg/day or flupenthixol 25 mg/day in patients with positive symptoms of schizophrenia.

In low and high dosages, amisulpride is generally well tolerated. Extrapyramidal symptoms (EPS) induced by amisulpride can occur at both low and high dosages and are dose-dependent. Symptoms are generally mild or moderate. In comparative trials, amisulpride caused an incidence of EPS similar to that with placebo and lower than that caused by haloperidol, flupenthixol or fluphenazine. Neuroendocrine adverse events were reported rarely with low-dose amisulpride and at similar incidences with amisulpride ≥600 mg/day and haloperidol 16 mg/day. Insomnia and excitation occurred rarely.

As classical antipsychotic drugs are not generally effective in reducing negative symptoms of schizophrenia, amisulpride should be considered a promising agent in the management of patients with schizophrenia who have predominantly negative symptoms. While amisulpride does not offer superior efficacy over classical antipsychotics in the management of patients with positive symptoms of schizophrenia, its lower potential for causing EPS justifies consideration of its use, especially in patients intolerant of classical antipsychotics.

Pharmacodynamic Properties

Like classical antipsychotic drugs, amisulpride is an antagonist of dopamine D2 and D3 receptors; however, the D3 to D2 receptor selectivity of amisulpride is greater than that of classical antipsychotic drugs. Amisulpride has little affinity for other neurotransmitter receptors or dopamine receptor subtypes. Low doses of amisulpride in animals facilitate presynaptic dopamine receptormediated behaviours, whereas higher doses decrease behaviours associated with postsynaptic receptor activation.

No deleterious effects on psychometrics or memory performance were observed after single oral doses up to 200mg in healthy volunteers. Like classical antipsychotic drugs, amisulpride affects dopaminergic control of plasma hormone levels. Amisulpride produced a significant increase in daytime and nocturnal prolactin levels in healthy volunteers. Daytime, but not nocturnal, thyroid-stimulating hormone levels were increased significantly and a significant decrease in the sleep-onset growth hormone peak was recorded. Other endocrine effects were minor.

Pharmacokinetic Properties

Observed peak plasma concentrations after single oral doses of ami sui pride 50 and 200mg, respectively, are approximately 54 and 443 μg/L at 3 hours. An earlier, lower peak concentration is detectable 1 hour after drug administration. The drug distributes widely and rapidly to the tissues and is minimally bound to plasma protein. Clearance is principally through renal elimination of unchanged drug, although 10 to 15% of a dose is metabolised to inactive metabolites. Elimination is biphasic with a terminal elimination half-life of approximately 12 hours.

Therapeutic Efficacy

Amisulpride has demonstrated efficacy against both positive and negative symptoms of schizophrenia. At low dosages (≤300 mg/day) in randomised, double-blind trials which included patients with high negative symptom scores and low positive symptom scores, amisulpride reduced negative symptoms as measured by the Scale for Assessment of Negative Symptoms (SANS). Scores were reduced by 32 to 46% from baseline compared with 8 to 23% in placebo-treated patients. In 2 double-blind trials with less rigorous inclusion and exclusion criteria, low-dose amisulpride (≤300 mg/day) and fluphenazine 2 to 12 mg/day reduced Brief Psychiatric Ratings Scale (BPRS) scores and SANS scores to a similar extent (BPRS 40 and 29% and SANS 18 and 22%, respectively).

In patients with positive symptoms of schizophrenia, amisulpride 400 to 1200 mg/day reduced BPRS scores by approximately 50%, a response rate not significantly different from that produced by haloperidol or flupenthixol in doubleblind, randomised trials.

Tolerability

In low and high dosages, amisulpride is generally well tolerated. At low dosages (50 to 300 mg/day), amisulpride was as well tolerated as placebo. Adverse events reported in comparative trials included extrapyramidal symptoms (EPS), endocrine adverse events, insomnia, agitation and dryness of the mouth.

EPS can occur at both low and high dosages of amisulpride, but the incidence is dose-related, with increases at dosages greater than 800 mg/day. Symptoms are usually mild or moderate and occur less frequently in amisulpride-treated patients than in comparable patients receiving haloperidol, flupenthixol or fluphenazine.

The incidence of neuroendocrinological adverse events associated with low dosages of amisulpride is similar to that associated with placebo, and with high dosages the incidence is similar to that observed in haloperidol-treated patients.

Dosage and Administration

Amisulpride is administered orally twice daily. The recommended dosages of amisulpride are 50 to 300 mg/day for the treatment of patients with predominantly negative symptoms of schizophrenia and 400 to 800 mg/day for those with positive symptoms. Dosages as high as 1200 mg/day have been studied, but were not clearly superior to amisulpride 800 mg/day. Dosage reduction may be necessary in patients with creatinine clearance below 30 ml/min.

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    Allan J. Coukell, Caroline M. Spencer & Paul Benfield

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Various sections of the manuscript reviewed by: W.T. Carpenter Jr, Maryland Psychiatric Research...

W.T. Carpenter Jr, Maryland Psychiatric Research Center, University of Maryland, Baltimore, Maryland, USA; Y. Lecrubier, Psychopathologie et Pharmacologie des Comportements, Institute National de la Santé et de la Recherche Médicale, Hôpital La Salpêtrière, Paris, France; J.-L. Martinot, Service Hospitalier Frédéric Joliot, Institute National de la Santé et de la Recherche Médicale, Orsay, France; H.-J. Möller, Psychiatrische Klinik und Poliklinik mit Konsiliardienst Grosshadem, Friedrich-Willhelms-Universität, Bonn, Germany; L.A. Opler, New York State Psychiatric Institute, New York, New York, USA; P. Protais, U.F.R. de Médecine et de Pharmacie, Université de Rouen—Haute Normandie, Saint Etienne Rouvray, France; P. Sokoloff, Unité de Neurobiologie et Pharmacologie, Centre Paul Broca, Institute National de la Santé et de la Recherche Médicale, Paris, France.

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Coukell, A.J., Spencer, C.M. & Benfield, P. Amisulpride. CNS Drugs 6, 237–256 (1996). https://doi.org/10.2165/00023210-199606030-00006

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