amisulpride

Although according to other studies it appears to have comparable efficacy to olanzapine in the treatment of schizophrenia,{{cite journal | vauthors = Komossa K, Rummel-Kluge C, Hunger H, Schmid F, Schwarz S, Silveira da Mota Neto JI, Kissling W, Leucht S | title = Amisulpride versus other atypical antipsychotics for schizophrenia | journal = The Cochrane Database of Systematic Reviews | issue = 1 | pages = CD006624 | date = January 2010 | volume = 2013 | pmid = 20091599 | pmc = 4164462 | doi = 10.1002/14651858.CD006624.pub2 }} amisulpride augmentation, similarly to sulpiride augmentation, has been considered a viable treatment option (although this is based on low-quality evidence) in clozapine-resistant cases of schizophrenia.{{cite journal | vauthors = Solanki RK, Singh P, Munshi D | title = Current perspectives in the treatment of resistant schizophrenia | journal = Indian Journal of Psychiatry | volume = 51 | issue = 4 | pages = 254–260 | date = Oct–Dec 2009 | pmid = 20048449 | pmc = 2802371 | doi = 10.4103/0019-5545.58289 | doi-access = free }}{{cite journal | vauthors = Mouaffak F, Tranulis C, Gourevitch R, Poirier MF, Douki S, Olié JP, Lôo H, Gourion D | title = Augmentation strategies of clozapine with antipsychotics in the treatment of ultraresistant schizophrenia | journal = Clinical Neuropharmacology | volume = 29 | issue = 1 | pages = 28–33 | year = 2006 | pmid = 16518132 | doi = 10.1097/00002826-200601000-00009 | s2cid = 29682562 }} Another recent study concluded that amisulpride is an appropriate first-line treatment for the management of acute psychosis.{{cite journal | vauthors = Nuss P, Hummer M, Tessier C | title = The use of amisulpride in the treatment of acute psychosis | journal = Therapeutics and Clinical Risk Management | volume = 3 | issue = 1 | pages = 3–11 | date = March 2007 | pmid = 18360610 | pmc = 1936283 | doi = 10.2147/tcrm.2007.3.1.3 | doi-access = free }}

Amisulpride is approved and used at low doses in the treatment of dysthymia and major depressive disorder.{{cite journal | vauthors = Zangani C, Giordano B, Stein HC, Bonora S, D'Agostino A, Ostinelli EG | title = Efficacy of amisulpride for depressive symptoms in individuals with mental disorders: A systematic review and meta-analysis | journal = Hum Psychopharmacol | volume = 36 | issue = 6 | pages = e2801 | date = November 2021 | pmid = 34727399 | pmc = 8596405 | doi = 10.1002/hup.2801 | url = }}{{cite journal | vauthors = Pani L, Gessa GL | title = The substituted benzamides and their clinical potential on dysthymia and on the negative symptoms of schizophrenia | journal = Mol Psychiatry | volume = 7 | issue = 3 | pages = 247–253 | date = 2002 | pmid = 11920152 | doi = 10.1038/sj.mp.4001040 | url = }}{{cite journal | vauthors = Green B | title = Focus on amisulpride | journal = Curr Med Res Opin | volume = 18 | issue = 3 | pages = 113–117 | date = 2002 | pmid = 12094819 | doi = 10.1185/030079902125000363 | url = }}{{cite journal | vauthors = Montgomery SA | title = Dopaminergic deficit and the role of amisulpride in the treatment of mood disorders | journal = Int Clin Psychopharmacol | volume = 17 Suppl 4 | issue = | pages = S9–15; discussion S16–7 | date = December 2002 | pmid = 12685917 | doi = | url = }}{{cite journal | vauthors = Rittmannsberger H | title = Amisulpride as an Augmentation Agent in Treatment Resistant Depression: A Case Series and Review of the Literature | journal = Psychiatr Danub | volume = 31 | issue = 2 | pages = 148–156 | date = June 2019 | pmid = 31291218 | doi = 10.24869/psyd.2019.148 | url = | doi-access = free }} Whereas typical doses used in schizophrenia block postsynaptic dopamine D₂-like receptors and reduce dopaminergic neurotransmission, low doses of amisulpride preferentially block presynaptic dopamine D₂ and D₃ autoreceptors and thereby disinhibit dopamine release and enhance dopaminergic neurotransmission.{{cite journal | vauthors = Curran MP, Perry CM | title = Spotlight on amisulpride in schizophrenia | journal = CNS Drugs | volume = 16 | issue = 3 | pages = 207–211 | date = 2002 | pmid = 11888341 | doi = 10.2165/00023210-200216030-00007 | url = }}{{cite journal | vauthors = McKeage K, Plosker GL | title = Amisulpride: a review of its use in the management of schizophrenia | journal = CNS Drugs | volume = 18 | issue = 13 | pages = 933–956 | date = 2004 | pmid = 15521794 | doi = 10.2165/00023210-200418130-00007 | url = }} A 2010 Cochrane review found that low-dose amisulpride was effective in the treatment of dysthymia.{{cite journal | vauthors = Komossa K, Depping AM, Gaudchau A, Kissling W, Leucht S | title = Second-generation antipsychotics for major depressive disorder and dysthymia | journal = Cochrane Database Syst Rev | volume = | issue = 12 | pages = CD008121 | date = December 2010 | pmid = 21154393 | doi = 10.1002/14651858.CD008121.pub2 | url = }} Likewise, a 2024 literature review found that low-dose amisulpride was effective for dysthymia.{{cite journal | vauthors = Mathias L, Quagliato LA, Carta MG, Nardi AE, Cheniaux E | title = Challenges in the treatment of dysthymia: a narrative review | journal = Expert Rev Neurother | volume = 24 | issue = 7 | pages = 633–642 | date = July 2024 | pmid = 38805342 | doi = 10.1080/14737175.2024.2360671 | url = }} The drug is approved for depression specifically in Italy, Greece, and certain other European countries.

Amisulpride is indicated for use in the United States in adults for the prevention of postoperative nausea and vomiting (PONV), either alone or in combination with an antiemetic of a different class; and to treat PONV in those who have received antiemetic prophylaxis with an agent of a different class or have not received prophylaxis.

Amisulpride is available in the form of 100, 200, and 400{{nbsp}}mg oral tablets.{{cite book | vauthors = Lindsay Murray M, Little M, Ovidiu Pascu M, Hoggett K | title=Toxicology Handbook - Epub3 | publisher=Elsevier Health Sciences | year=2015 | isbn=978-0-7295-8496-8 | url=https://books.google.com/books?id=pbYfEQAAQBAJ&pg=PA159 | access-date=24 October 2024 | page=159}} In the United States, it is available in the form of a 5{{nbsp}}mg/2{{nbsp}}mL (2.5{{nbsp}}mg/mL) solution for intravenous administration.{{cite web | title=Drugs@FDA: FDA-Approved Drugs | website=accessdata.fda.gov | url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm | access-date=24 October 2024}}

Amisulpride's use is contraindicated in the following disease states and populations

• Pheochromocytoma
• Concomitant prolactin-dependent tumours e.g. prolactinoma, breast cancer
• Movement disorders (e.g. Parkinson's disease and dementia with Lewy bodies)
• Lactation
• Children before the onset of puberty

Neither is it recommended to use amisulpride in patients with hypersensitivities to amisulpride or the excipients found in its dosage form.

;Very Common (≥10% incidence)

• Extrapyramidal side effects (EPS; including dystonia, tremor, akathisia, parkinsonism).

;Common (≥1%, <10% incidence)Truven Health Analytics, Inc. DRUGDEX System (Internet) [cited 2013 Sep 19]. Greenwood Village, CO: Thomsen Healthcare; 2013.{{cite book | isbn = 978-0-85711-084-8 | title = British National Formulary (BNF) | vauthors = ((Joint Formulary Committee)) | year = 2013 | publisher = Pharmaceutical Press | location = London, UK | edition = 65 | url-access = registration | url = https://archive.org/details/bnf65britishnati0000unse }}{{cite book | veditors = Rossi S | isbn = 978-0-9805790-9-3 | title = Australian Medicines Handbook | place = Adelaide | publisher = The Australian Medicines Handbook Unit Trust | year = 2013 | edition = 2013 }}

{{div col|colwidth=22em}}

• Insomnia
• Somnolence
• Hypersalivation
• Nausea
• Headache
• Hyperactivity
• Vomiting

{{div col end}}

• Hyperprolactinaemia (which can lead to galactorrhoea, breast enlargement and tenderness, sexual dysfunction, etc.)
• Weight gain (produces less weight gain than chlorpromazine, clozapine, iloperidone, olanzapine, paliperidone, quetiapine, risperidone, sertindole, zotepine and more (although not statistically significantly) weight gain than haloperidol, lurasidone, ziprasidone and approximately as much weight gain as aripiprazole and asenapine)
• Anticholinergic side effects (although it does not bind to the muscarinic acetylcholine receptors and hence these side effects are usually quite mild) such as

:- constipation

:- dry mouth

:- disorder of accommodation

:- Blurred vision

;Rare (<1% incidence)

{{div col|colwidth=22em}}

• Hyponatraemia
• Bradycardia
• Hypotension
• Palpitations
• Urticaria
• Seizures
• Mania
• Oculogyric crisis
• Tardive dyskinesia

{{div col end}}

• Blood dyscrasias such as leucopenia, neutropenia and agranulocytosis
• QT interval prolongation (in a recent meta-analysis of the safety and efficacy of 15 antipsychotic drugs amisulpride was found to have the 2nd highest effect size for causing QT interval prolongation{{cite journal | vauthors = Leucht S, Cipriani A, Spineli L, Mavridis D, Orey D, Richter F, Samara M, Barbui C, Engel RR, Geddes JR, Kissling W, Stapf MP, Lässig B, Salanti G, Davis JM | title = Comparative efficacy and tolerability of 15 antipsychotic drugs in schizophrenia: a multiple-treatments meta-analysis | journal = Lancet | volume = 382 | issue = 9896 | pages = 951–962 | date = September 2013 | pmid = 23810019 | doi = 10.1016/S0140-6736(13)60733-3 | s2cid = 32085212 }})

Hyperprolactinaemia results from antagonism of the D₂ receptors located on the lactotrophic cells found in the anterior pituitary gland. Amisulpride has a high propensity for elevating plasma prolactin levels as a result of its poor blood–brain barrier penetrability and hence the resulting greater ratio of peripheral D₂ occupancy to central D₂ occupancy. This means that to achieve the sufficient occupancy (~60–80%{{cite book | isbn = 978-0-07-162442-8 | title = Goodman and Gilman's The Pharmacological Basis of Therapeutics | edition = 12th | vauthors = Brunton L, Chabner B, Knollman B | year = 2010 | publisher = McGraw-Hill Professional | location = New York | title-link = Goodman and Gilman's The Pharmacological Basis of Therapeutics }}) of the central D₂ receptors in order to elicit its therapeutic effects a dose must be given that is enough to saturate peripheral D₂ receptors including those in the anterior pituitary.{{cite journal | vauthors = McKeage K, Plosker GL | title = Amisulpride: a review of its use in the management of schizophrenia | journal = CNS Drugs | volume = 18 | issue = 13 | pages = 933–956 | year = 2004 | pmid = 15521794 | doi = 10.2165/00023210-200418130-00007 | s2cid = 9054960 }}{{cite journal | vauthors = Natesan S, Reckless GE, Barlow KB, Nobrega JN, Kapur S | title = Amisulpride the 'atypical' atypical antipsychotic--comparison to haloperidol, risperidone and clozapine | journal = Schizophrenia Research | volume = 105 | issue = 1–3 | pages = 224–235 | date = October 2008 | pmid = 18710798 | doi = 10.1016/j.schres.2008.07.005 | s2cid = 11315672 }}

The British National Formulary recommends a gradual withdrawal when discontinuing antipsychotics to avoid acute withdrawal syndrome or rapid relapse.{{cite book | editor = Joint Formulary Committee | title = British National Formulary | edition = 57 | date = March 2009 |publisher=Royal Pharmaceutical Society of Great Britain |location=United Kingdom |isbn=978-0-85369-845-6 |page=192 |chapter=4.2.1 |quote=Withdrawal of antipsychotic drugs after long-term therapy should always be gradual and closely monitored to avoid the risk of acute withdrawal syndromes or rapid relapse.}} Symptoms of withdrawal commonly include nausea, vomiting, and loss of appetite.{{cite book | vauthors = Haddad PM, Dursun S, Deakin B |title=Adverse Syndromes and Psychiatric Drugs: A Clinical Guide |date=2004 |publisher=OUP Oxford |isbn=978-0-19-852748-0 |pages=207–216 |url=https://books.google.com/books?id=CWR7DwAAQBAJ&pg=PA207 |language=en}} Other symptoms may include restlessness, increased sweating, and trouble sleeping. Less commonly there may be a feeling of the world spinning, numbness, or muscle pains. Symptoms generally resolve after a short period of time.

There is tentative evidence that discontinuation of antipsychotics can result in psychosis.{{cite journal | vauthors = Moncrieff J | title = Does antipsychotic withdrawal provoke psychosis? Review of the literature on rapid onset psychosis (supersensitivity psychosis) and withdrawal-related relapse | journal = Acta Psychiatrica Scandinavica | volume = 114 | issue = 1 | pages = 3–13 | date = July 2006 | pmid = 16774655 | doi = 10.1111/j.1600-0447.2006.00787.x | s2cid = 6267180 }} It may also result in reoccurrence of the condition that is being treated.{{cite book | vauthors = Sacchetti E, Vita A, Siracusano A, Fleischhacker W |title=Adherence to Antipsychotics in Schizophrenia |date=2013 |publisher=Springer Science & Business Media |isbn=978-8-84-702679-7 |page=85 |url=https://books.google.com/books?id=odE-AgAAQBAJ&pg=PA85 |language=en}} Rarely tardive dyskinesia can occur when the medication is stopped.

Torsades de pointes is common in overdose.{{cite journal | vauthors = Isbister GK, Balit CR, Macleod D, Duffull SB | title = Amisulpride overdose is frequently associated with QT prolongation and torsades de pointes | journal = Journal of Clinical Psychopharmacology | volume = 30 | issue = 4 | pages = 391–395 | date = August 2010 | pmid = 20531221 | doi = 10.1097/JCP.0b013e3181e5c14c | s2cid = 205710487 }}{{cite journal | vauthors = Joy JP, Coulter CV, Duffull SB, Isbister GK | title = Prediction of torsade de pointes from the QT interval: analysis of a case series of amisulpride overdoses | journal = Clinical Pharmacology and Therapeutics | volume = 90 | issue = 2 | pages = 243–245 | date = August 2011 | pmid = 21716272 | doi = 10.1038/clpt.2011.107 | s2cid = 26412012 }} Amisulpride is moderately dangerous in overdose (with the TCAs being very dangerous and the SSRIs being modestly dangerous).{{cite book |title=Maudsley Prescribing Guidelines in Psychiatry |vauthors=Taylor D, Paton C, Shitij K |date=2012 |publisher=Wiley-Blackwell |isbn=978-0-47-097948-8 |edition=11th |location=West Sussex}}{{cite journal | vauthors = Levine M, Ruha AM | title = Overdose of atypical antipsychotics: clinical presentation, mechanisms of toxicity and management | journal = CNS Drugs | volume = 26 | issue = 7 | pages = 601–611 | date = July 2012 | pmid = 22668123 | doi = 10.2165/11631640-000000000-00000 | s2cid = 24628641 }}

Amisulpride should not be used in conjunction with drugs that prolong the QT interval (such as citalopram, bupropion, clozapine, tricyclic antidepressants, sertindole, ziprasidone, etc.), as this can cause potential life threatening arrhythmias (Torsades de pointes, Ventricular tachycardia, and Ventricular fibrillation)

{{See also|Atypical antipsychotic#Pharmacodynamics|Antipsychotic#Comparison of medications}}

Amisulpride functions primarily as a dopamine D₂ and D₃ receptor antagonist. It has high affinity for these receptors with dissociation constants of 3.0 and 3.5 nM, respectively. Although standard doses used to treat psychosis inhibit dopaminergic neurotransmission, low doses preferentially block inhibitory presynaptic autoreceptors. This results in a facilitation of dopamine activity, and for this reason, low-dose amisulpride has also been used to treat dysthymia.

Amisulpride and its relatives sulpiride, levosulpiride, and sultopride have been shown to bind to the high-affinity GHB receptor at concentrations that are therapeutically relevant ({{abbrlink|IC₅₀|Half-maximal inhibitory concentration}} = 50 nM for amisulpride).{{cite journal | vauthors = Maitre M, Ratomponirina C, Gobaille S, Hodé Y, Hechler V | title = Displacement of [3H] gamma-hydroxybutyrate binding by benzamide neuroleptics and prochlorperazine but not by other antipsychotics | journal = European Journal of Pharmacology | volume = 256 | issue = 2 | pages = 211–214 | date = April 1994 | pmid = 7914168 | doi = 10.1016/0014-2999(94)90248-8 }}

Amisulpride, sultopride and sulpiride respectively present decreasing in vitro affinities for the D₂ receptor (IC₅₀ = 27, 120 and 181 nM) and the D₃ receptor (IC₅₀ = 3.6, 4.8 and 17.5 nM).{{cite book | vauthors = Blomme A, Conraux L, Poirier P, Olivier A, Koenig JJ, Sevrin M, Durant F, George P | chapter = Amisulpride, Sultopride and Sulpiride: Comparison of Conformational and Physico-Chemical Properties|date=2000| title = Molecular Modeling and Prediction of Bioactivity|pages=404–405|publisher=Springer US|language=en|doi=10.1007/978-1-4615-4141-7_97|isbn=978-1-4613-6857-1 }}

Though it was long widely assumed that dopaminergic modulation is solely responsible for the respective antidepressant and antipsychotic properties of amisulpride, it was subsequently found that the drug also acts as a potent antagonist of the serotonin 5-HT₇ receptor (K_i = 11.5 nM). 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. The study found that in two widely used rodent models of depression, the tail suspension test, and the forced swim test, those mice did not exhibit an antidepressant response upon treatment with amisulpride. These results suggest that 5-HT₇ receptor antagonism mediates the antidepressant effects of amisulpride.

Amisulpride also appears to bind with high affinity to the serotonin 5-HT_2B receptor (K_i = 13 nM), where it acts as an antagonist. The clinical implications of this, if any, are unclear. In any case, there is no evidence that this action mediates any of the therapeutic effects of amisulpride.

Amisulpride shows stereoselectivity in its actions.{{cite journal | vauthors = Hopkins SC, Wilkinson S, Corriveau TJ, Nishikawa H, Nakamichi K, Loebel A, Koblan KS | title = Discovery of Nonracemic Amisulpride to Maximize Benefit/Risk of 5-HT7 and D2 Receptor Antagonism for the Treatment of Mood Disorders | journal = Clinical Pharmacology and Therapeutics | volume = 110 | issue = 3 | pages = 808–815 | date = September 2021 | pmid = 33961287 | pmc = 8453756 | doi = 10.1002/cpt.2282 | doi-access = free }} Aramisulpride ((R)-amisulpride) has higher affinity for the 5-HT₇ receptor (K_i = 47 nM vs. 1,900 nM) while esamisulpride ((S)-amisulpride) has higher affinity for the D₂ receptor (4.0 nM vs. 140 nM).{{cite journal | vauthors = Grattan V, Vaino AR, Prensky Z, Hixon MS | title = Antipsychotic Benzamides Amisulpride and LB-102 Display Polypharmacy as Racemates, S Enantiomers Engage Receptors D₂ and D₃, while R Enantiomers Engage 5-HT₇ | journal = ACS Omega | volume = 4 | issue = 9 | pages = 14151–14154 | date = August 2019 | pmid = 31497735 | pmc = 6714530 | doi = 10.1021/acsomega.9b02144 }}

Through a high direct unmetabolized excretion, it has, despite its high usual dose, also high affinity for dopamine-D₂-D₃-receptors. Also the available literature gives us hints about also relatively high receptor dissociation kinetics (through a delayed but high occupancy at dopamine receptors after 6 hours from a 100 mg exposure).

Not just is this level of occupation (90%) enough for the normally therapeutic adwished level of the needing receptors occupated against schizophrenia, but even with this occurring after a single dose of amisulprid (compared with the receptoroccupation of about 12% in the striatalregion of the brain when taken cariprazine (which reaches an occupation between 63-69% not until several weeks and doses of administration)).https://pmc.ncbi.nlm.nih.gov/articles/PMC3210913/

So one can say that the dynamics of dopamin-receptoroccupation and how this does affect the human body are very complex, for example can the body and the brain work totally accurately even when over 90% of the dopaminreceptors are occupated, yet though does the triggering of presynaptic autoreceptors to enhance mood in cases of dysthymia depending on an insaturated occupation of postsynaptic D2 receptors.

However, this dopamine exposure could be slightly more "balanced" providing some little advantages over haloperidol in using it for drug exposure. Due to its lack of compensatory serotonin effects and also not having an anticholinergic profile, it may not considered as an effective alternative if akathasia is a problem.{{cite journal | vauthors = Jethwa KD| doi=10.1192/apt.bp.114.013797 | title=Pharmacological management of antipsychotic-induced akathisia: An update and treatment algorithm | year=2015 | journal=BJPsych Advances | volume=21 | issue=5 | pages=342–344 | s2cid=146670706 | doi-access=free }}

The oral bioavailability of amisulpride is 48%. Its plasma protein binding is 16%. The drug is metabolized by the liver but its metabolism is minimal. Its elimination half-life is 12{{nbsp}}hours. Amisulpride is eliminated in urine (23–46%) and feces and is excreted mostly unchanged.

Amisulpride is a benzamide derivative. It is structurally related to other benzamide dopamine receptor antagonists employed as antipsychotics and antiemetics including levosulpiride, metoclopramide, nemonapride, remoxipride, sulpiride, sultopride, tiapride, and veralipride. Chemically, it is also known as aminosultopride, differing from sultopride only in possessing an amino substituent on its benzene ring.

Amisulpride was introduced by Sanofi-Aventis in the 1990s.{{Citation needed|date=October 2024}} Its patent expired by 2008, and generic formulations became available.

The U.S. Food and Drug Administration (FDA) approved a 10 mg/4mL amisulpride IV formulation for use in post-operative nausea based on evidence from four clinical trials of 2323 subjects undergoing surgery or experiencing nausea and vomiting after the surgery. The trials were conducted at 80 sites in the United States, Canada and Europe.

Two trials (Trials 1 and 2) enrolled subjects scheduled to have surgery. Subjects were randomly assigned to receive either amisulpride or a placebo drug at the beginning of general anesthesia. In Trial 1, subjects received amisulpride or placebo alone, and in Trial 2, they received amisulpride or placebo in combination with one medication approved for prevention of nausea and vomiting. Neither the subjects nor the health care providers knew which treatment was being given until after the trial was complete.

The trials counted the number of subjects who had no vomiting and did not use additional medications for nausea or vomiting in the first day (24 hours) after the surgery. The results then compared amisulpride to placebo.

The other two trials (Trials 3 and 4) enrolled subjects who were experiencing nausea and vomiting after surgery. In Trial 3, subjects did not receive any medication to prevent nausea and vomiting before surgery and in Trial 4 they received the medication, but the treatment did not work. In both trials, subjects were randomly assigned to receive either amisulpride or placebo. Neither the subjects nor the health care providers knew which treatment was being given until after the trial was complete.

The trials counted the number of subjects who had no vomiting and did not use additional medications for nausea or vomiting in the first day (24 hours) after the treatment. The trial compared amisulpride to placebo.

The FDA has not approved amisulpride for use in any psychiatric indication. LB Pharmaceuticals is developing N-methyl amisulpride for the use in the treatment of schizophrenia; a Phase 2 first-in-patient study is planned for 2023.{{cite web | title = Investor Presentation | date = December 2022 | publisher = LB Pharmaceuticals | url = http://lbpharma.us/wp-content/uploads/2022/12/LB-Investor-Presentation-December-2022.pdf}}

Brand names include: Amazeo, Amipride (AU), Amival, Deniban, Solian (AU, IE, RU, UK, ZA), Soltus, Sulpitac (IN), Sulprix (AU), Midora (RO) and Socian (BR).{{cite web | title=Amisulpride international | website=Drugs.com | date=3 February 2020 | url=https://www.drugs.com/international/amisulpride.html | access-date=26 February 2020}}{{cite web | url=https://www.ema.europa.eu/docs/en_GB/document_library/Periodic_safety_update_single_assessment/2017/10/WC500236063.pdf | date=28 September 2017 | id=EMA/658194/2017; Procedure no.: PSUSA/00000167/201701 | title=Active substance: amisulpride | access-date=26 February 2020 | archive-date=15 June 2018 | archive-url=https://web.archive.org/web/20180615011314/http://www.ema.europa.eu/docs/en_GB/document_library/Periodic_safety_update_single_assessment/2017/10/WC500236063.pdf | url-status=dead }}

Amisulpride is not approved by the Food and Drug Administration for use in the United States in psychiatric indications, but it is approved and in use throughout Europe, Asia, Mexico, New Zealand and Australia to treat psychosis and schizophrenia.{{cite journal | vauthors = Lecrubier Y, Azorin M, Bottai T, Dalery J, Garreau G, Lempérière T, Lisoprawski A, Petitjean F, Vanelle JM | title = Consensus on the Practical Use of Amisulpride, an Atypical Antipsychotic, in the Treatment of Schizophrenia | journal = Neuropsychobiology | volume = 44 | issue = 1 | pages = 41–46 | year = 2001 | pmid = 11408792 | doi = 10.1159/000054913 | s2cid = 21103201 }}{{ cite journal | vauthors = Kaplan A | title = Psychotropic Medications Around the World | journal = Psychiatric Times | volume = 21 | issue = 5 | year = 2004 | url = http://www.psychiatrictimes.com/showArticle.jhtml?articleID=175802519 }}

{{anchor|Us2020y}}An IV formulation of Amisulpride was approved for the treatment of postoperative nausea and vomiting ("PONV") in the United States in February 2020.{{cite web | title=Barhemsys: FDA-Approved Drugs | website=U.S. Food and Drug Administration (FDA) | url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=209510 | access-date=26 February 2020}}{{cite web | title=Drug Trials Snapshots: Barhemsys | website=U.S. Food and Drug Administration (FDA) | date=26 February 2020 | url=http://www.fda.gov/drugs/development-approval-process-drugs/drug-trials-snapshots-barhemsys | access-date=27 March 2020}} {{PD-notice}}

SEP-4199 (non-racemic amisulpride), an 85:15 ratio of aramisulpride ((R)-amisulpride) to esamisulpride ((S)-amisulpride), which is theorized to provide more balanced serotonin 5-HT₇ and dopamine D₂ receptor antagonism than racemic amisulpride (a 50:50 ratio of its (R)- and (S)-enantiomers), is or was under development by Sunovion Pharmaceuticals for the treatment of bipolar depression in the United States and other countries.{{Cite web|url=https://adisinsight.springer.com/drugs/800052192|title=SEP 4199 | work = AdisInsight | publisher = Springer Nature Switzerland AG }}{{cite web | title=Delving into the Latest Updates on Aramisulpride/Esamisulpride with Synapse | website=Synapse | date=15 October 2024 | url=https://synapse.patsnap.com/drug/946c3f3c25ab44f495f0fe9a4ce9b559 | access-date=24 October 2024}}{{cite journal | vauthors = Wu J, Kwan AT, Rhee TG, Ho R, d'Andrea G, Martinotti G, Teopiz KM, Ceban F, McIntyre RS | title = A narrative review of non-racemic amisulpride (SEP-4199) for treatment of depressive symptoms in bipolar disorder and LB-102 for treatment of schizophrenia | journal = Expert Rev Clin Pharmacol | volume = 16 | issue = 11 | pages = 1085–1092 | date = 2023 | pmid = 37864424 | doi = 10.1080/17512433.2023.2274538 | url = }} However, its development may have been discontinued.

The intravenous formulation of amisulpride approved for treatment of postoperative nausea and vomiting is additionally under development for the treatment of chemotherapy-induced nausea and vomiting.{{cite web | title=Amisulpride - Acacia Pharma | website=AdisInsight | date=15 March 2023 | url=https://adisinsight.springer.com/drugs/800033690 | access-date=24 October 2024}}

A more lipophilic and centrally permeable derivative of amisulpride, N-methylamisulpride (developmental code name LB-102), is under development by LB Pharmaceuticals for the treatment of schizophrenia in the United States and other countries.{{cite web | title=N-methyl amisulpride | website=AdisInsight | date=26 December 2023 | url=https://adisinsight.springer.com/drugs/800056770 | access-date=24 October 2024}}

• ENX-104 (an analogue under development for use at low doses to treat depression)

{{Reflist}}

• {{cite web| url = https://druginfo.nlm.nih.gov/drugportal/name/amisulpride | publisher = U.S. National Library of Medicine| work = Drug Information Portal | title = Amisulpride }}

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Category:5-HT2B antagonists

Category:5-HT7 antagonists

Category:Anilines

Category:Antidepressants

Category:Antiemetics

Category:Atypical antipsychotics

Category:Benzosulfones

Category:D2 antagonists

Category:D3 antagonists

Category:GHB receptor ligands

Category:Pyrrolidines

Category:Salicylamide ethers