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A plain-language summary of the cited sources below. Informational only — not medical advice.
Amisulpride works by blocking specific receptors in the brain called dopamine D2 and D3 receptors. This action can help reduce symptoms of schizophrenia, including hallucinations, delusions, and disorganised thinking, as well as symptoms like emotional withdrawal and reduced motivation. The medication stays in the body for about 12 hours after each dose, and studies show the liver doesn't break it down much through the usual pathways, which means fewer interactions with other medications that are processed by liver enzymes.
The medication is prescribed for acute and chronic schizophrenia, particularly when symptoms include delusions, hallucinations, thought disorders, reduced emotional expression, or social withdrawal. Some people taking amisulpride experience weight gain, difficulty sleeping, anxiety, or agitation. Movement-related side effects can also occur, such as stiffness, tremor, or restlessness.
More serious effects are possible and need urgent medical attention if they occur. These include neuroleptic malignant syndrome, a rare but potentially life-threatening reaction involving high fever, muscle rigidity, and confusion. After long-term use, some people develop tardive dyskinesia, which causes involuntary rhythmic movements, usually of the tongue or face. Heart rhythm disturbances, including potentially fatal irregular heartbeats, have been reported. Blood clots in the legs or lungs and a severe drop in white blood cells (agranulocytosis) are also serious risks.
Amisulpride cannot be used by people with prolactin-dependent tumours such as certain pituitary or breast cancers, phaeochromocytoma, or known allergy to the medication. It must not be given to children who have not yet reached puberty or to people who are breastfeeding. The medication cannot be combined with levodopa or with a range of other medications that affect heart rhythm, including certain antibiotics, heart medications, and antipsychotics. People with liver impairment may not be able to take amisulpride safely.
“Amisulpride binds selectively to the human dopaminergic D2 (Ki 2.8 nM) and D3 (Ki 3.2 nM) receptor subtypes without any affinity for D1, D4 and D5 receptor subtypes (Ki > 1 μM).”
“The elimination half-life of amisulpride is approximately 12 hours after an oral dose.”
“In vitro studies using human liver microsomes and cryopreserved human hepatocytes did not show evidence of significant amisulpride metabolism. Based on these results, it is unlikely that drug interactions involving amisulpride would occur due to inhibition or induction of cytochrome P450 –mediated metabolism.”
A plain-language summary of the cited sources below. Informational only — not medical advice.
Amisulpride is a benzamide antipsychotic with selective high-affinity binding to dopaminergic D2 and D3 receptor subtypes (Ki 2.8 nM and 3.2 nM respectively), without affinity for D1, D4, or D5 receptors. It is approved for the treatment of acute and chronic schizophrenic disorders characterised by positive symptoms (delusions, hallucinations, thought disorders) and/or negative symptoms (blunted affect, emotional and social withdrawal), including patients in whom negative symptoms predominate. The elimination half-life is approximately 12 hours after an oral dose.
In vitro studies using human liver microsomes and cryopreserved hepatocytes show no evidence of significant amisulpride metabolism; drug interactions via cytochrome P450 inhibition or induction are unlikely. Amisulpride is contraindicated in combination with agents that prolong the QT interval and carry torsades de pointes risk, including class Ia antiarrhythmics (quinidine, disopyramide), class III antiarrhythmics (amiodarone, sotalol), and other medications such as thioridazine, methadone, intravenous erythromycin, and sparfloxacin. It is also contraindicated with levodopa due to reciprocal antagonism, in patients with prolactin-dependent tumours (pituitary prolactinomas, breast cancer), phaeochromocytoma, and in hepatic impairment.
Common adverse effects include extrapyramidal disorder, insomnia, anxiety, agitation, and weight increase. Serious adverse effects include neuroleptic malignant syndrome, agranulocytosis, tardive dyskinesia (typically after long-term administration), ventricular arrhythmias (torsades de pointes, ventricular tachycardia, ventricular fibrillation, cardiac arrest, sudden death), and venous thromboembolism (pulmonary embolism, deep vein thrombosis).
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Curated subset. The full adverse-effect list is in the TGA Product Information; click any citation above to open it.