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Systematic (IUPAC) name
Clinical data
Routes of
Oral, intramuscular[1]
Legal status
Legal status
  • ℞ (Prescription only)
Pharmacokinetic data
Bioavailability 48%[2]
Metabolism ?
Biological half-life 12 h[2]
Excretion Renal[2]
CAS Number 71675-85-9 [1]
ATC code N05AL05 (WHO)
PubChem CID 2159
DrugBank none
ChemSpider 2074
Chemical data
Formula C17H27N3O4S
Molar mass 369.48 g/mol[[Script error: No such module "String".]]
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Amisulpride (sold as Solian, Sulpitac or Soltus), is an atypical antipsychotic used to treat psychosis in schizophrenia and episodes of mania in bipolar disorder. In small doses it is also used to treat depression. It was introduced by Sanofi-Aventis in the 1990s.


Amisulpride functions primarily as a D2 and D3 receptor antagonist. It has high affinity for these receptors with dissociation constants of 2.8 nM and 3.2 nM, respectively. Although standard doses in the 400 to 1200 mg a day range used to treat psychosis inhibit dopaminergic neurotransmission, low doses in the 50 to 200 mg range preferentially block inhibitory pre-synaptic autoreceptors. This results in a facilitation of dopamine activity, and for this reason, low dose amisulpride has also been used to treat clinical depression.

Amisulpride and its relative sulpiride have been shown to bind to and activate the GHB receptor at doses that are used for therapeutic purposes.[3] Activation of the GHB receptor is known to inhibit the release of dopamine and even appears to have neuroleptic effects itself[citation needed]. For this reason it is believed that amisulpride and sulpiride's action at this receptor may contribute to their efficacy in treating psychosis.

Though it has long been widely assumed that dopaminergic modulation is solely responsible for the respective antidepressant and antipsychotic properties of amisulpride, it has recently been shown that it also acts as a potent antagonist at the 5-HT7 receptor.[4] Several of the other atypical antipsychotics such as risperidone and ziprasidone are potent antagonists at the 5-HT7 receptor as well, and selective antagonists of the receptor show antidepressant properties themselves. To characterize the role of the 5-HT7 receptor in the antidepressant effects of amisulpride, a study prepared 5-HT7 receptor knockout mice.[4] The study found that in two widely used rodent models of depression, the tail suspension test, and the forced swim test, the mice did not exhibit an antidepressant response upon treatment with amisulpride.[4] These results indicate that 5-HT7 receptor antagonism plays a major role in the antidepressant effects of amisulpride.[4]


Amisulpride is not approved by the Food and Drug Administration for use in the United States, but it is used in Europe (France, Germany, Italy, Switzerland, Russia, United Kingdom, ...) and Australia to treat psychoses and schizophrenia.[5][6] In Italy, in 50 mg doses, it is also used as a treatment for dysthymia (under the brand name Deniban).


In one study, anxiety measured by HAM-A total mean score decreased significantly more with amisulpride 50 mg/day (63%) than with fluoxetine 20 mg/day (54%; P = 0.021).[7] Another recent study[8] concludes that amisulpride is an appropriate first-line treatment for the management of acute psychosis.

Side effects

Prolactin induction, thereby causing amenorrhoea and galactorrhoea in women, nausea, weight gain, insomnia, Sexual Dysfunction, although much less than similar drugs in its class, and less commonly QT interval prolongation (which can lead to serious heart arrhythmias). Overdoses of amisulpride have been linked with torsades de pointes.[9]

See also


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fr:Amisulpride nl:Amisulpride pl:Amisulpryd pt:Amissulprida ru:Амисульприд

  1. 1.0 1.1 BIAM (2000) AMISULPRIDE, (HTML) Banque de Données Automatisée sur les Médicaments [online] Available from: Accessed on 25 November 2005. (French)
  2. 2.0 2.1 2.2 Rosenzweig P, Canal M, Patat A, Bergougnan L, Zieleniuk I, Bianchetti G. (2002). "A review of the pharmacokinetics, tolerability and pharmacodynamics of amisulpride in healthy volunteers". Human Psychopharmacology. 17 (1): 1–13. doi:10.1002/hup.320. PMID 12404702. 
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  4. 4.0 4.1 4.2 4.3 Abbas AI, Hedlund PB, Huang XP, Tran TB, Meltzer HY, Roth BL. (2009). "Amisulpride is a potent 5-HT(7) antagonist: relevance for antidepressant actions in vivo". Psychopharmacology (Berl). 205 (1): 119–28. doi:10.1007/s00213-009-1521-8. PMC 2821721Freely accessible. PMID 19337725. 
  5. Lecrubier Y; et al. (2001). "Consensus on the Practical Use of Amisulpride, an Atypical Antipsychotic, in the Treatment of Schizophrenia". Neuropsychobiology. 44 (1): 41–6. doi:10.1159/000054913. PMID 11408792. 
  6. Kaplan, Arline. (2004). "Psychotropic Medications Around the World". Psychiatric Times. 21 (5). 
  7. Smeraldi E (1998). "Amisulpride versus fluoxetine in patients with dysthymia or major depression in partial remission: a double-blind, comparative study". J Affect Disord. 48 (1): 47–56. doi:10.1016/S0165-0327(97)00139-0. PMID 9495601. 
  8. Nuss, Philippe; Martina Hummer and Cédric Tessier (2007). "The use of amisulpride in the treatment of acute psychosis". Therapeutics and Clinical Risk Management. 3 (1): 3–11. doi:10.2147/tcrm.2007.3.1.3. PMC 1936283Freely accessible. PMID 18360610. 
  9. Isbister G, Murray L, John S, Hackett L, Haider T, O'Mullane P, Gosselin S, Daly F (2006). "Amisulpride deliberate self-poisoning causing severe cardiac toxicity including QT prolongation and torsades de pointes". Med J Aust. 184 (7): 354–6. PMID 16584372.