Amisulpride 100mg tablets
Prescription only
Requires a prescription from a doctor or prescriber
Tablet
100mg
Oral
Amisulpride is a benzamide derivative and a dopamine receptor antagonist that selectively works on dopamine D2 and D3 receptors.
Active ingredients:
Amisulpride
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Updated 3 months ago(16 Jan 2026)Safety monitoring data
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Solian 100 tablets
Amisulpride 100mg tablets
Amisulpride 100mg tablets
Amisulpride 100mg tablets
Amisulpride 100mg tablets
Amisulpride 100mg tablets
Amisulpride 100mg tablets
Amisulpride 100mg tablets
Amisulpride 100mg tablets
Amisulpride 100mg tablets
Amisulpride 100mg tablets
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£5.20indicative price
This is the NHS Drug Tariff indicative price used for reimbursement purposes. It may not reflect the price paid by patients or pharmacies.
View full Drug TariffSource: NHS Drug Tariff via NHSBSA. Derived from dm+d VMPP (Virtual Medicinal Product Pack) pricing data. Contains public sector information licensed under the Open Government Licence v3.0.
WHO defined daily dose (DDD)
400 mg
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via NHS dm+d BNF mapping files. Contains public sector information licensed under the Open Government Licence v3.0.
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400mg/5ml
Same therapeutic group
Similarity based on WHO Anatomical Therapeutic Chemical (ATC) classification and NHS BNF section grouping. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
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Clinical guidelines and formulary information
British National Formulary
Amisulpride
BNF
Drug monograph — bnf.nice.org.ukSource: British National Formulary, NICE. Joint Formulary Committee. Contains public sector information licensed under the Open Government Licence v3.0.
NICE clinical guidance(4)
Aripiprazole for the treatment of schizophrenia in people aged 15 to 17 years (TA213)
TA213
Technology appraisal
Updated Jan 2011Rehabilitation for adults with complex psychosis (NG181)
NG181
NICE guideline
Updated Aug 2020Schizophrenia: lurasidone (ESNM48)
ESNM48
Evidence summary
Updated Sept 2014Depression in adults: treatment and management (NG222)
NG222
NICE guideline
Updated Jun 2022Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
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Codes for healthcare professionals and prescribing systems
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SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. BNF codes from NHS Business Services Authority (NHSBSA). ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
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Searching UK clinical trials...
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
1 found
Half-life
12 hours
Mechanism
Dopamine is an essential and critical neurotransmitter produced in the substanti…
Food interactions
2 warnings
Human targets
7 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
48%
Following oral administration, amisulpride is rapidly absorbed with absolute bioavailability of 48%.
[A6751]…
[A6751]…
Half-life
12 hours
Elimination is biphasic.
[A232269]
The elimination half-life of amisulpride is approximately 12 hours after an oral dose.
[L32764]…
[A232269]
The elimination half-life of amisulpride is approximately 12 hours after an oral dose.
[L32764]…
Protein binding
25%
Plasma protein binding ranges from 25% to 30% in the concentration range from 37 to 1850 ng/mL. Amisulpride distributes into erythrocytes.
[L32759]
[L32759]
Volume of distribution
5.8 L/kg
Following oral administration, the volume of distribution is 5.8…
Metabolism
4%
Amisulpride undergoes minimal metabolism [A6751] and its metabolites in plasma are largely undetectable.…
Elimination
74%
Following intravenous administration, about 74% of amisulpride is excreted in urine, where 58% of the recovered dose was excreted as unchanged amisulpride.…
Clearance
20.6 L/h
The plasma clearance of amisulpride is 20.6 L/h in surgical patients and 24.1…
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Status:
Approved
Investigational
Small molecule
About this compound
Amisulpride is a benzamide derivative and a dopamine receptor antagonist that selectively works on dopamine D2 and D3 receptors. As an antipsychotic agent, amisulpride alleviates both positive and negative symptoms of schizophrenia, and it exhibits antidepressant properties in patients with psychiatric disorders, dysthymia, and major depression.[A6755] Amisulpride predominantly works in the limbic system, which explains its relatively lower risk of extrapyramidal adverse effects compared to other atypical antipsychotic agents.[A6752][L32764] Oral tablets of amisulpride is used in European countries as a treatment for acute and chronic schizophrenic disorders, as well as secondary negative symptoms in mental health disorders such as affective disorders, depressive mood, and mental retardation.[L32764]
Amisulpride is also used as an antiemetic agent. In the US, the intravenous formulation of amisulpride is used to treat and prevent postoperative nausea and vomiting in adults, either as monotherapy or in combination with another antiemetic agent of a different drug class.[L32759] It is marketed under the brand name Barhemsys.
Amisulpride is also used as an antiemetic agent. In the US, the intravenous formulation of amisulpride is used to treat and prevent postoperative nausea and vomiting in adults, either as monotherapy or in combination with another antiemetic agent of a different drug class.[L32759] It is marketed under the brand name Barhemsys.
Properties:
solid
Avg. mass: 369.48 Da
DrugBank indication
Intravenous amisulpride is indicated in adults for the prevention of postoperative nausea and vomiting, either alone or in combination with an antiemetic of a different class. It is also indicated for the treatment of postoperative nausea and vomiting in patients who have received anti-emetic prophylaxis with an agent of a different class or have not received prophylaxis.
[L32759]
Oral amisulpride is indicated for the treatment of acute and chronic schizophrenic disorders, characterized by positive symptoms with delusions, hallucinations, thought disorders, hostility and suspicious behavior; or primarily negative symptoms (deficit syndrome) with blunted affect, emotional and social withdrawal. Amisulpride also controls secondary negative symptoms in productive conditions as well as affective disorders such as depressive mood or retardation.
[L32764]
[L32759]
Oral amisulpride is indicated for the treatment of acute and chronic schizophrenic disorders, characterized by positive symptoms with delusions, hallucinations, thought disorders, hostility and suspicious behavior; or primarily negative symptoms (deficit syndrome) with blunted affect, emotional and social withdrawal. Amisulpride also controls secondary negative symptoms in productive conditions as well as affective disorders such as depressive mood or retardation.
[L32764]
Also known as(58)
4-Amino-N-((1-ethyl-2-pyrrolidinyl)methyl)-5-(ethylsulfonyl)-2-methoxybenzamide
4-Amino-N-((1-ethyl-2-pyrrolidinyl)methyl)-5-(ethylsulfonyl)-O-anisamide
Aminosultopride
Amisulprida
Amisulpride
Amisulpridum
5-HT-7
5-HT-X
Dosage forms(16)
Tablet (Oral) — 100 MG
Tablet, film coated (Oral) — 400 MG
Tablet (Oral)
Tablet, film coated (Oral)
Tablet, coated (Oral)
Injection, solution (Intravenous) — 2.5 mg/1mL
Tablet (Oral) — 400 MG
Solution (Oral) — 100 MG/ML
Molecular properties(19)
Drug interactions(1057)
Known interactions with other medications. Always consult a healthcare professional.
Buprenorphine
Moderate
Amisulpride may increase the central nervous system depressant (CNS depressant) activities of Buprenorphine.
Doxylamine
Moderate
Doxylamine may increase the central nervous system depressant (CNS depressant) activities of Amisulpride.
Dronabinol
Moderate
Dronabinol may increase the central nervous system depressant (CNS depressant) activities of Amisulpride.
Hydrocodone
Moderate
Amisulpride may increase the central nervous system depressant (CNS depressant) activities of Hydrocodone.
Magnesium sulfate
Moderate
The therapeutic efficacy of Amisulpride can be increased when used in combination with Magnesium sulfate.
Metyrosine
Moderate
Amisulpride may increase the sedative activities of Metyrosine.
Minocycline
Moderate
Minocycline may increase the central nervous system depressant (CNS depressant) activities of Amisulpride.
Mirtazapine
Moderate
Amisulpride may increase the central nervous system depressant (CNS depressant) activities of Mirtazapine.
Nabilone may increase the central nervous system depressant (CNS depressant) activities of Amisulpride.
Orphenadrine
Moderate
Amisulpride may increase the central nervous system depressant (CNS depressant) activities of Orphenadrine.
Paraldehyde
Moderate
Amisulpride may increase the central nervous system depressant (CNS depressant) activities of Paraldehyde.
Perampanel
Moderate
Perampanel may increase the central nervous system depressant (CNS depressant) activities of Amisulpride.
Rotigotine
Moderate
Amisulpride may increase the sedative activities of Rotigotine.
Rufinamide
Unknown severity
The risk or severity of adverse effects can be increased when Rufinamide is combined with Amisulpride.
Sodium oxybate
Moderate
Amisulpride may increase the central nervous system depressant (CNS depressant) activities of Sodium oxybate.
Suvorexant
Moderate
Amisulpride may increase the central nervous system depressant (CNS depressant) activities of Suvorexant.
Tapentadol
Moderate
Tapentadol may increase the central nervous system depressant (CNS depressant) activities of Amisulpride.
Thalidomide
Moderate
Amisulpride may increase the central nervous system depressant (CNS depressant) activities of Thalidomide.
Amisulpride may increase the central nervous system depressant (CNS depressant) activities of Zolpidem.
Reserpine may increase the antipsychotic activities of Amisulpride.
Ziprasidone
Moderate
Ziprasidone may increase the antipsychotic activities of Amisulpride.
Olanzapine
Moderate
Olanzapine may increase the antipsychotic activities of Amisulpride.
Clozapine may increase the antipsychotic activities of Amisulpride.
Thiethylperazine
Moderate
Thiethylperazine may increase the antipsychotic activities of Amisulpride.
Sulpiride may increase the antipsychotic activities of Amisulpride.
Loxapine may increase the antipsychotic activities of Amisulpride.
Remoxipride
Moderate
Remoxipride may increase the antipsychotic activities of Amisulpride.
Promazine may increase the antipsychotic activities of Amisulpride.
Prochlorperazine
Moderate
Prochlorperazine may increase the antipsychotic activities of Amisulpride.
Chlorpromazine
Moderate
Chlorpromazine may increase the antipsychotic activities of Amisulpride.
Haloperidol
Moderate
Haloperidol may increase the antipsychotic activities of Amisulpride.
Triflupromazine
Moderate
Triflupromazine may increase the antipsychotic activities of Amisulpride.
Amoxapine may increase the antipsychotic activities of Amisulpride.
Fluphenazine
Moderate
Fluphenazine may increase the antipsychotic activities of Amisulpride.
Thioridazine
Moderate
Thioridazine may increase the antipsychotic activities of Amisulpride.
Moricizine
Moderate
Moricizine may increase the antipsychotic activities of Amisulpride.
Risperidone
Moderate
Risperidone may increase the antipsychotic activities of Amisulpride.
Trifluoperazine
Moderate
Trifluoperazine may increase the antipsychotic activities of Amisulpride.
Perphenazine
Moderate
Perphenazine may increase the antipsychotic activities of Amisulpride.
Flupentixol
Moderate
Flupentixol may increase the antipsychotic activities of Amisulpride.
Mesoridazine
Moderate
Mesoridazine may increase the antipsychotic activities of Amisulpride.
Acetophenazine
Moderate
Acetophenazine may increase the antipsychotic activities of Amisulpride.
Promethazine
Moderate
Promethazine may increase the antipsychotic activities of Amisulpride.
Pimozide may increase the antipsychotic activities of Amisulpride.
Quetiapine
Moderate
Quetiapine may increase the antipsychotic activities of Amisulpride.
Aripiprazole
Moderate
Aripiprazole may increase the antipsychotic activities of Amisulpride.
Chlorprothixene
Moderate
Chlorprothixene may increase the antipsychotic activities of Amisulpride.
Alimemazine
Moderate
Alimemazine may increase the antipsychotic activities of Amisulpride.
Paliperidone
Moderate
Paliperidone may increase the antipsychotic activities of Amisulpride.
Lithium cation
Moderate
Lithium cation may increase the antipsychotic activities of Amisulpride.
Showing 50 of 1057 interactions
Food & lifestyle interactions
Avoid Alcohol
Avoid alcohol. Amisulpride may enhance the effects of alcohol.
Advice
Take with or without food. A high fat meal does not significantly affect drug pharmacokinetics, although a carbohydrate rich meal decreases drug absorption and levels.
Toxicity & overdose
In mice, oral LD50 is 1024 mg/kg, intraperitoneal LD50 is 175 mg/kg, and subcutaneous LD50 is 224 mg/kg. The Lowest published toxic dose (TDLo) following subcutaneous administration is 0.24 mg/kg in rats. The oral TDLo in men is 4.3 mg/kg.
[L32769]
Oral doses of amisulpride above 1200 mg/day are associated with adverse effects related to dopamine-2 (D2) antagonism.
Cardiovascular adverse reactions include prolongation of the QT interval, torsades de pointes, bradycardia, and hypotension. Neuropsychiatric adverse reactions include sedation, coma, seizures, and dystonic and extrapyramidal reactions. As there is no specific antidote for amisulpride overdosage, management includes cardiac monitoring and treatment of severe extrapyramidal symptoms.
Drug elimination with the use of hemodialysis is effective.
[L32759]
Severe extrapyramidal effects may be managed with anticholinergic drugs.
[L32764]
[L32769]
Oral doses of amisulpride above 1200 mg/day are associated with adverse effects related to dopamine-2 (D2) antagonism.
Cardiovascular adverse reactions include prolongation of the QT interval, torsades de pointes, bradycardia, and hypotension. Neuropsychiatric adverse reactions include sedation, coma, seizures, and dystonic and extrapyramidal reactions. As there is no specific antidote for amisulpride overdosage, management includes cardiac monitoring and treatment of severe extrapyramidal symptoms.
Drug elimination with the use of hemodialysis is effective.
[L32759]
Severe extrapyramidal effects may be managed with anticholinergic drugs.
[L32764]
How it works
Mechanism of action
Dopamine is an essential and critical neurotransmitter produced in the substantia nigra and ventral tegmental regions of the brain. Dopaminergic projection function in the nigrostriatal, mesolimbic, and mesocortical systems. Hyperactive dopamine transmission in the mesolimbic areas, or dopamine dysregulation in various major brain regions, is understood as the key driver of positive and negative symptoms of schizophrenia.[A189156] Many antipsychotic agents act as D2 receptor antagonists, as with amisulpride.[A6752] Amisulpride is a selective dopamine D2 and D3 receptor antagonist.[L32759] It has high preferential activity towards dopamine receptors in the limbic system rather than the striatum, leading to a lower risk of extrapyramidal side effects than other atypical antipsychotic agents.[A6754][A232269] At low doses, amisulpride reduces negative symptoms of schizophrenia by blocking pre-synaptic dopamine D2 and D3 receptors, increasing the levels of dopamine in the synaptic cleft and facilitating dopaminergic transmission.[A6754] At higher doses, amisulpride blocks postsynaptic receptors, inhibiting dopaminergic hyperactivity: this explains the drug improving positive symptoms.[A6751] Amisulpride also works as an antagonist at 5-HT7A receptors [A16931] and 5-HT2A receptors,[A6754] which may be related to its antidepressant effects.[A6755]
The chemoreceptor trigger zone (CTZ), also commonly known as the area postrema (AP), is an important brain region located within the dorsal surface of the medulla oblongata. CTZ is involved in emesis: it contains receptors, such as dopamine receptors, that are activated in response to emetic agents in the blood and relay information to the vomiting center, which is responsible for inducing the vomiting reflex.[A232374] Amisulpride is an antiemetic agent that works to limit signals that promote nausea and vomiting. Amisulpride binds to D2 and D3 receptors in the CTZ, leading to reduced dopaminergic signalling into the vomiting center.[L32759]
The chemoreceptor trigger zone (CTZ), also commonly known as the area postrema (AP), is an important brain region located within the dorsal surface of the medulla oblongata. CTZ is involved in emesis: it contains receptors, such as dopamine receptors, that are activated in response to emetic agents in the blood and relay information to the vomiting center, which is responsible for inducing the vomiting reflex.[A232374] Amisulpride is an antiemetic agent that works to limit signals that promote nausea and vomiting. Amisulpride binds to D2 and D3 receptors in the CTZ, leading to reduced dopaminergic signalling into the vomiting center.[L32759]
Pharmacodynamics
Amisulpride is a selective dopamine D2 and D3 receptor antagonist with no affinity towards other dopamine receptor subtypes. Amisulpride is an atypical antipsychotic agent that works as an antagonist at dopamine receptors in the limbic system. Since it works preferentially in the limbic system, amisulpride is less likely to be associated with extrapyramidal adverse effects than other atypical antipsychotic agents. Amisulpride has no affinity for serotonin, alpha-adrenergic, H1-histamine, cholinergic, and sigma receptors. In clinical trials, amisulpride improved reduced secondary negative symptoms, affective symptoms, and psychomotor retardation in patients with acute exacerbation of schizophrenia. Notably, amisulpride has a differential target binding profile at different doses: at low doses, amisulpride selectively binds to presynaptic dopamine autoreceptors. At high doses, it preferentially binds to post-synaptic dopamine receptors.[A6753] This explains how amisulpride reduces negative symptoms at low doses and mediates antipsychotic effects at high doses.[L32764] One study alluded that the antinociceptive effects of amisulpride are mediated through opioid receptor acvitation and D2 receptor antagonism. [A6753][A6755] The actions of amisulpride at opioid receptors may explain its pro-convulsant properties.[A6755]
Amisulpride is also an antiemetic agent that prevents and alleviates postoperative nausea and vomiting. It primarily works by blocking dopamine signalling in the chemoreceptor trigger zone, which is a brain area that relays stimuli to the vomiting center.[L32764]
In clinical trials comprising Caucasian and Japanese subjects, amisulpride caused dose- and concentration-dependent prolongation of the QT interval; thus, intravenous infusion under a strict dosing regimen and close monitoring of patients with pre-existing cardiovascular conditions are recommended.[L32759] Amisulpride increases plasma prolactin levels, leading to an association with benign pituitary tumours such as prolactinoma.[L32764]
Amisulpride is also an antiemetic agent that prevents and alleviates postoperative nausea and vomiting. It primarily works by blocking dopamine signalling in the chemoreceptor trigger zone, which is a brain area that relays stimuli to the vomiting center.[L32764]
In clinical trials comprising Caucasian and Japanese subjects, amisulpride caused dose- and concentration-dependent prolongation of the QT interval; thus, intravenous infusion under a strict dosing regimen and close monitoring of patients with pre-existing cardiovascular conditions are recommended.[L32759] Amisulpride increases plasma prolactin levels, leading to an association with benign pituitary tumours such as prolactinoma.[L32764]
Pharmacokinetics
How the body processes this drug — absorption, distribution, metabolism, and elimination
Absorption
Following oral administration, amisulpride is rapidly absorbed with absolute bioavailability of 48%.
[A6751]
Amisulpride has two absorption peaks, with one rapidly achieved within one hour post-dose and a second peak occurring between three to four hours post-dose. Following oral administration of a 50 mg dose, two peak plasma concentrations were 39 ± 3 and 54 ± 4 ng/mL.
[L32764]
Following intravenous administration, the peak plasma concentration of amisulpride is achieved at the end of the infusion period and the plasma concentration decreases by 50% within approximately 15 minutes. The AUC(0-∞) increases dose-proportionally in the dose range from 5 mg to 40 mg, which is about four times the maximum recommended dose.
In healthy patients receiving intravenous amisulpride, the mean (SD) Cmax was 200 (139) ng/mL at the dose of 5 mg and 451 (230) ng/mL at the dose of 10 mg. The AUC ranged from 136 to 154 ng x h/mL in the dose range of 5 mg to 10 mg. In patients undergoing surgery, the mean (SD) Cmax ranged from 127 (62) to 161 (58) ng/mL at the dose of 5 mg.
At the dose of 10 mg, it was 285 (446) ng/mL. The AUC ranged from 204 to 401 ng x h/mL.
[L32759]
[A6751]
Amisulpride has two absorption peaks, with one rapidly achieved within one hour post-dose and a second peak occurring between three to four hours post-dose. Following oral administration of a 50 mg dose, two peak plasma concentrations were 39 ± 3 and 54 ± 4 ng/mL.
[L32764]
Following intravenous administration, the peak plasma concentration of amisulpride is achieved at the end of the infusion period and the plasma concentration decreases by 50% within approximately 15 minutes. The AUC(0-∞) increases dose-proportionally in the dose range from 5 mg to 40 mg, which is about four times the maximum recommended dose.
In healthy patients receiving intravenous amisulpride, the mean (SD) Cmax was 200 (139) ng/mL at the dose of 5 mg and 451 (230) ng/mL at the dose of 10 mg. The AUC ranged from 136 to 154 ng x h/mL in the dose range of 5 mg to 10 mg. In patients undergoing surgery, the mean (SD) Cmax ranged from 127 (62) to 161 (58) ng/mL at the dose of 5 mg.
At the dose of 10 mg, it was 285 (446) ng/mL. The AUC ranged from 204 to 401 ng x h/mL.
[L32759]
Half-life
Elimination is biphasic.
[A232269]
The elimination half-life of amisulpride is approximately 12 hours after an oral dose.
[L32764]
The mean elimination half-life is approximately four to five hours in both healthy subjects and patients undergoing surgery receiving intravenous amisulpride.
[L32759]
[A232269]
The elimination half-life of amisulpride is approximately 12 hours after an oral dose.
[L32764]
The mean elimination half-life is approximately four to five hours in both healthy subjects and patients undergoing surgery receiving intravenous amisulpride.
[L32759]
Protein binding
Plasma protein binding ranges from 25% to 30% in the concentration range from 37 to 1850 ng/mL. Amisulpride distributes into erythrocytes.
[L32759]
[L32759]
Volume of distribution
Following oral administration, the volume of distribution is 5.8 L/kg.
[L32764]
Following intravenous infusion, the mean volume of distribution of amisulpride is estimated to be 127 to 144 L in surgical patients and 171 L in healthy subjects.
[L32759]
[L32764]
Following intravenous infusion, the mean volume of distribution of amisulpride is estimated to be 127 to 144 L in surgical patients and 171 L in healthy subjects.
[L32759]
Metabolism
Amisulpride undergoes minimal metabolism [A6751] and its metabolites in plasma are largely undetectable. Two identified metabolites, formed by de-ethylation
and oxidation, are pharmacologically inactive [A232269] and account for approximately 4% of the dose.
[L32764]
Metabolites remain largely uncharacterized. Metabolism of amisulpride does not involve cytochrome P450 enzymes.
[L32759]
and oxidation, are pharmacologically inactive [A232269] and account for approximately 4% of the dose.
[L32764]
Metabolites remain largely uncharacterized. Metabolism of amisulpride does not involve cytochrome P450 enzymes.
[L32759]
Route of elimination
Following intravenous administration, about 74% of amisulpride is excreted in urine, where 58% of the recovered dose was excreted as unchanged amisulpride. About 23% of the dose is excreted in feces, with 20% of the excreted dose as unchanged parent drug. Following intravenous administration, about four metabolites were identified in urine and feces, accounting for less than 7% of the total dose administered.
[L32759]
About 22 to 25% of orally administered amisulpride is excreted in urine, mostly as the unchanged parent drug.
[A6751]
[L32759]
About 22 to 25% of orally administered amisulpride is excreted in urine, mostly as the unchanged parent drug.
[A6751]
Clearance
The plasma clearance of amisulpride is 20.6 L/h in surgical patients and 24.1 L/h in healthy subjects following intravenous administration. Renal clearance was estimated to be 20.5 L/hr (342 mL/min) in healthy subjects.
[L32759]
[L32759]
Drug targets(7)
Proteins and enzymes this drug interacts with in the body
5-hydroxytryptamine receptor 7
HTR7
antagonist
Specific functionG protein-coupled serotonin receptor activity
Cellular location
Cell membrane
General function & pharmacology
G-protein coupled receptor for 5-hydroxytryptamine (serotonin), a biogenic hormone that functions as a neurotransmitter, a hormone and a mitogen .
PMID:35714614 PMID:8226867
Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of downstream effectors .
PMID:35714614 PMID:8226867
HTR7 is coupled to G(s) G alpha proteins and mediates activation of adenylate cyclase activity PMID:35714614
PMID:35714614 PMID:8226867
Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of downstream effectors .
PMID:35714614 PMID:8226867
HTR7 is coupled to G(s) G alpha proteins and mediates activation of adenylate cyclase activity PMID:35714614
5-hydroxytryptamine receptor 2A
HTR2A
antagonist
Specific function1-(4-iodo-2,5-dimethoxyphenyl)propan-2-amine binding
Cellular location
Cell membrane
General function & pharmacology
G-protein coupled receptor for 5-hydroxytryptamine (serotonin) .
PMID:1330647 PMID:18703043 PMID:19057895 PMID:21645528 PMID:22300836 PMID:35084960 PMID:38552625
Also functions as a receptor for various drugs and psychoactive substances, including mescaline, psilocybin, 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) and lysergic acid diethylamide (LSD) .
PMID:28129538 PMID:35084960
Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of downstream effectors .
PMID:28129538 PMID:35084960
HTR2A is coupled to G(q)/G(11) G alpha proteins and activates phospholipase C-beta, releasing diacylglycerol (DAG) and inositol 1,4,5-trisphosphate (IP3) second messengers that modulate the activity of phosphatidylinositol 3-kinase and promote the release of Ca(2+) ions from intracellular stores, respectively .
PMID:18703043 PMID:28129538 PMID:35084960
Beta-arrestin family members inhibit signaling via G proteins and mediate activation of alternative signaling pathways .
PMID:28129538 PMID:35084960
Affects neural activity, perception, cognition and mood .
PMID:18297054
Plays a role in the regulation of behavior, including responses to anxiogenic situations and psychoactive substances. Plays a role in intestinal smooth muscle contraction, and may play a role in arterial vasoconstriction (By similarity)
PMID:1330647 PMID:18703043 PMID:19057895 PMID:21645528 PMID:22300836 PMID:35084960 PMID:38552625
Also functions as a receptor for various drugs and psychoactive substances, including mescaline, psilocybin, 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) and lysergic acid diethylamide (LSD) .
PMID:28129538 PMID:35084960
Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of downstream effectors .
PMID:28129538 PMID:35084960
HTR2A is coupled to G(q)/G(11) G alpha proteins and activates phospholipase C-beta, releasing diacylglycerol (DAG) and inositol 1,4,5-trisphosphate (IP3) second messengers that modulate the activity of phosphatidylinositol 3-kinase and promote the release of Ca(2+) ions from intracellular stores, respectively .
PMID:18703043 PMID:28129538 PMID:35084960
Beta-arrestin family members inhibit signaling via G proteins and mediate activation of alternative signaling pathways .
PMID:28129538 PMID:35084960
Affects neural activity, perception, cognition and mood .
PMID:18297054
Plays a role in the regulation of behavior, including responses to anxiogenic situations and psychoactive substances. Plays a role in intestinal smooth muscle contraction, and may play a role in arterial vasoconstriction (By similarity)
D(2) dopamine receptor
DRD2
antagonist
Specific functiondopamine binding
Cellular location
Cell membrane
General function & pharmacology
Dopamine receptor whose activity is mediated by G proteins which inhibit adenylyl cyclase .
PMID:21645528
Positively regulates postnatal regression of retinal hyaloid vessels via suppression of VEGFR2/KDR activity, downstream of OPN5 (By similarity)
PMID:21645528
Positively regulates postnatal regression of retinal hyaloid vessels via suppression of VEGFR2/KDR activity, downstream of OPN5 (By similarity)
D(3) dopamine receptor
DRD3
antagonist
Specific functiondopamine neurotransmitter receptor activity, coupled via Gi/Go
Cellular location
Cell membrane
General function & pharmacology
Dopamine receptor whose activity is mediated by G proteins which inhibit adenylyl cyclase. Promotes cell proliferation
Mu-type opioid receptor
OPRM1
agonist
Specific functionbeta-endorphin receptor activity
Cellular location
Cell membrane
General function & pharmacology
Receptor for endogenous opioids such as beta-endorphin and endomorphin .
PMID:10529478 PMID:12589820 PMID:7891175 PMID:7905839 PMID:7957926 PMID:9689128
Receptor for natural and synthetic opioids including morphine, heroin, DAMGO, fentanyl, etorphine, buprenorphin and methadone .
PMID:10529478 PMID:10836142 PMID:12589820 PMID:19300905 PMID:7891175 PMID:7905839 PMID:7957926 PMID:9689128
Also activated by enkephalin peptides, such as Met-enkephalin or Met-enkephalin-Arg-Phe, with higher affinity for Met-enkephalin-Arg-Phe (By similarity). Agonist binding to the receptor induces coupling to an inactive GDP-bound heterotrimeric G-protein complex and subsequent exchange of GDP for GTP in the G-protein alpha subunit leading to dissociation of the G-protein complex with the free GTP-bound G-protein alpha and the G-protein beta-gamma dimer activating downstream cellular effectors .
PMID:7905839
The agonist- and cell type-specific activity is predominantly coupled to pertussis toxin-sensitive G(i) and G(o) G alpha proteins, GNAI1, GNAI2, GNAI3 and GNAO1 isoforms Alpha-1 and Alpha-2, and to a lesser extent to pertussis toxin-insensitive G alpha proteins GNAZ and GNA15 .
PMID:12068084
They mediate an array of downstream cellular responses, including inhibition of adenylate cyclase activity and both N-type and L-type calcium channels, activation of inward rectifying potassium channels, mitogen-activated protein kinase (MAPK), phospholipase C (PLC), phosphoinositide/protein kinase (PKC), phosphoinositide 3-kinase (PI3K) and regulation of NF-kappa-B (By similarity). Also couples to adenylate cyclase stimulatory G alpha proteins (By similarity).
The selective temporal coupling to G-proteins and subsequent signaling can be regulated by RGSZ proteins, such as RGS9, RGS17 and RGS4 (By similarity). Phosphorylation by members of the GPRK subfamily of Ser/Thr protein kinases and association with beta-arrestins is involved in short-term receptor desensitization (By similarity). Beta-arrestins associate with the GPRK-phosphorylated receptor and uncouple it from the G-protein thus terminating signal transduction (By similarity).
The phosphorylated receptor is internalized through endocytosis via clathrin-coated pits which involves beta-arrestins (By similarity). The activation of the ERK pathway occurs either in a G-protein-dependent or a beta-arrestin-dependent manner and is regulated by agonist-specific receptor phosphorylation (By similarity). Acts as a class A G-protein coupled receptor (GPCR) which dissociates from beta-arrestin at or near the plasma membrane and undergoes rapid recycling (By similarity).
Receptor down-regulation pathways are varying with the agonist and occur dependent or independent of G-protein coupling (By similarity). Endogenous ligands induce rapid desensitization, endocytosis and recycling (By similarity). Heterooligomerization with other GPCRs can modulate agonist binding, signaling and trafficking properties (By similarity)
PMID:10529478 PMID:12589820 PMID:7891175 PMID:7905839 PMID:7957926 PMID:9689128
Receptor for natural and synthetic opioids including morphine, heroin, DAMGO, fentanyl, etorphine, buprenorphin and methadone .
PMID:10529478 PMID:10836142 PMID:12589820 PMID:19300905 PMID:7891175 PMID:7905839 PMID:7957926 PMID:9689128
Also activated by enkephalin peptides, such as Met-enkephalin or Met-enkephalin-Arg-Phe, with higher affinity for Met-enkephalin-Arg-Phe (By similarity). Agonist binding to the receptor induces coupling to an inactive GDP-bound heterotrimeric G-protein complex and subsequent exchange of GDP for GTP in the G-protein alpha subunit leading to dissociation of the G-protein complex with the free GTP-bound G-protein alpha and the G-protein beta-gamma dimer activating downstream cellular effectors .
PMID:7905839
The agonist- and cell type-specific activity is predominantly coupled to pertussis toxin-sensitive G(i) and G(o) G alpha proteins, GNAI1, GNAI2, GNAI3 and GNAO1 isoforms Alpha-1 and Alpha-2, and to a lesser extent to pertussis toxin-insensitive G alpha proteins GNAZ and GNA15 .
PMID:12068084
They mediate an array of downstream cellular responses, including inhibition of adenylate cyclase activity and both N-type and L-type calcium channels, activation of inward rectifying potassium channels, mitogen-activated protein kinase (MAPK), phospholipase C (PLC), phosphoinositide/protein kinase (PKC), phosphoinositide 3-kinase (PI3K) and regulation of NF-kappa-B (By similarity). Also couples to adenylate cyclase stimulatory G alpha proteins (By similarity).
The selective temporal coupling to G-proteins and subsequent signaling can be regulated by RGSZ proteins, such as RGS9, RGS17 and RGS4 (By similarity). Phosphorylation by members of the GPRK subfamily of Ser/Thr protein kinases and association with beta-arrestins is involved in short-term receptor desensitization (By similarity). Beta-arrestins associate with the GPRK-phosphorylated receptor and uncouple it from the G-protein thus terminating signal transduction (By similarity).
The phosphorylated receptor is internalized through endocytosis via clathrin-coated pits which involves beta-arrestins (By similarity). The activation of the ERK pathway occurs either in a G-protein-dependent or a beta-arrestin-dependent manner and is regulated by agonist-specific receptor phosphorylation (By similarity). Acts as a class A G-protein coupled receptor (GPCR) which dissociates from beta-arrestin at or near the plasma membrane and undergoes rapid recycling (By similarity).
Receptor down-regulation pathways are varying with the agonist and occur dependent or independent of G-protein coupling (By similarity). Endogenous ligands induce rapid desensitization, endocytosis and recycling (By similarity). Heterooligomerization with other GPCRs can modulate agonist binding, signaling and trafficking properties (By similarity)
Transporters(5)
Proteins that transport this drug across cell membranes
Multidrug and toxin extrusion protein 1
SLC47A1
substrate
inhibitor
Specific functionantiporter activity
Cellular location
Cell membrane
General function & pharmacology
Multidrug efflux pump that functions as a H(+)/organic cation antiporter .
PMID:16330770 PMID:17509534
Plays a physiological role in the excretion of cationic compounds including endogenous metabolites, drugs, toxins through the kidney and liver, into urine and bile respectively .
PMID:16330770 PMID:17495125 PMID:17509534 PMID:17582384 PMID:18305230 PMID:19158817 PMID:21128598 PMID:24961373
Mediates the efflux of endogenous compounds such as creatinine, vitamin B1/thiamine, agmatine and estrone-3-sulfate .
PMID:16330770 PMID:17495125 PMID:17509534 PMID:17582384 PMID:18305230 PMID:19158817 PMID:21128598 PMID:24961373
May also contribute to regulate the transport of cationic compounds in testis across the blood-testis-barrier (Probable)
PMID:16330770 PMID:17509534
Plays a physiological role in the excretion of cationic compounds including endogenous metabolites, drugs, toxins through the kidney and liver, into urine and bile respectively .
PMID:16330770 PMID:17495125 PMID:17509534 PMID:17582384 PMID:18305230 PMID:19158817 PMID:21128598 PMID:24961373
Mediates the efflux of endogenous compounds such as creatinine, vitamin B1/thiamine, agmatine and estrone-3-sulfate .
PMID:16330770 PMID:17495125 PMID:17509534 PMID:17582384 PMID:18305230 PMID:19158817 PMID:21128598 PMID:24961373
May also contribute to regulate the transport of cationic compounds in testis across the blood-testis-barrier (Probable)
Multidrug and toxin extrusion protein 2
SLC47A2
substrate
inhibitor
Specific functionantiporter activity
Cellular location
Cell membrane
General function & pharmacology
Multidrug efflux pump that functions as a H(+)/organic cation antiporter. Mediates the efflux of cationic compounds, such as the model cations, tetraethylammonium (TEA) and 1-methyl-4-phenylpyridinium (MPP+), the platinum-based drug oxaliplatin or weak bases that are positively charged at physiological pH, cimetidine, the platinum-based drugs cisplatin and oxaliplatin or the antidiabetic drug metformin. Mediates the efflux of endogenous compounds such as, creatinine, thiamine and estrone-3-sulfate.
Plays a physiological role in the excretion of drugs, toxins and endogenous metabolites through the kidney
Plays a physiological role in the excretion of drugs, toxins and endogenous metabolites through the kidney
ATP-dependent translocase ABCB1
ABCB1
substrate
Specific functionABC-type xenobiotic transporter activity
Cellular location
Cell membrane
General function & pharmacology
Translocates drugs and phospholipids across the membrane .
PMID:2897240 PMID:35970996 PMID:8898203 PMID:9038218 PMID:35507548
Catalyzes the flop of phospholipids from the cytoplasmic to the exoplasmic leaflet of the apical membrane. Participates mainly to the flop of phosphatidylcholine, phosphatidylethanolamine, beta-D-glucosylceramides and sphingomyelins .
PMID:8898203
Energy-dependent efflux pump responsible for decreased drug accumulation in multidrug-resistant cells PMID:2897240 PMID:35970996 PMID:9038218
PMID:2897240 PMID:35970996 PMID:8898203 PMID:9038218 PMID:35507548
Catalyzes the flop of phospholipids from the cytoplasmic to the exoplasmic leaflet of the apical membrane. Participates mainly to the flop of phosphatidylcholine, phosphatidylethanolamine, beta-D-glucosylceramides and sphingomyelins .
PMID:8898203
Energy-dependent efflux pump responsible for decreased drug accumulation in multidrug-resistant cells PMID:2897240 PMID:35970996 PMID:9038218
Broad substrate specificity ATP-binding cassette transporter ABCG2
ABCG2
substrate
Specific functionABC-type xenobiotic transporter activity
Cellular location
Cell membrane
General function & pharmacology
Broad substrate specificity ATP-dependent transporter of the ATP-binding cassette (ABC) family that actively extrudes a wide variety of physiological compounds, dietary toxins and xenobiotics from cells .
PMID:11306452 PMID:12958161 PMID:19506252 PMID:20705604 PMID:28554189 PMID:30405239 PMID:31003562
Involved in porphyrin homeostasis, mediating the export of protoporphyrin IX (PPIX) from both mitochondria to cytosol and cytosol to extracellular space, it also functions in the cellular export of heme .
PMID:20705604 PMID:23189181
Also mediates the efflux of sphingosine-1-P from cells .
PMID:20110355
Acts as a urate exporter functioning in both renal and extrarenal urate excretion .
PMID:19506252 PMID:20368174 PMID:22132962 PMID:31003562 PMID:36749388
In kidney, it also functions as a physiological exporter of the uremic toxin indoxyl sulfate (By similarity). Also involved in the excretion of steroids like estrone 3-sulfate/E1S, 3beta-sulfooxy-androst-5-en-17-one/DHEAS, and other sulfate conjugates .
PMID:12682043 PMID:28554189 PMID:30405239
Mediates the secretion of the riboflavin and biotin vitamins into milk (By similarity). Extrudes pheophorbide a, a phototoxic porphyrin catabolite of chlorophyll, reducing its bioavailability (By similarity).
Plays an important role in the exclusion of xenobiotics from the brain (Probable). It confers to cells a resistance to multiple drugs and other xenobiotics including mitoxantrone, pheophorbide, camptothecin, methotrexate, azidothymidine, and the anthracyclines daunorubicin and doxorubicin, through the control of their efflux .
PMID:11306452 PMID:12477054 PMID:15670731 PMID:18056989 PMID:31254042
In placenta, it limits the penetration of drugs from the maternal plasma into the fetus (By similarity). May play a role in early stem cell self-renewal by blocking differentiation (By similarity).
In inflammatory macrophages, exports itaconate from the cytosol to the extracellular compartment and limits the activation of TFEB-dependent lysosome biogenesis involved in antibacterial innate immune response
PMID:11306452 PMID:12958161 PMID:19506252 PMID:20705604 PMID:28554189 PMID:30405239 PMID:31003562
Involved in porphyrin homeostasis, mediating the export of protoporphyrin IX (PPIX) from both mitochondria to cytosol and cytosol to extracellular space, it also functions in the cellular export of heme .
PMID:20705604 PMID:23189181
Also mediates the efflux of sphingosine-1-P from cells .
PMID:20110355
Acts as a urate exporter functioning in both renal and extrarenal urate excretion .
PMID:19506252 PMID:20368174 PMID:22132962 PMID:31003562 PMID:36749388
In kidney, it also functions as a physiological exporter of the uremic toxin indoxyl sulfate (By similarity). Also involved in the excretion of steroids like estrone 3-sulfate/E1S, 3beta-sulfooxy-androst-5-en-17-one/DHEAS, and other sulfate conjugates .
PMID:12682043 PMID:28554189 PMID:30405239
Mediates the secretion of the riboflavin and biotin vitamins into milk (By similarity). Extrudes pheophorbide a, a phototoxic porphyrin catabolite of chlorophyll, reducing its bioavailability (By similarity).
Plays an important role in the exclusion of xenobiotics from the brain (Probable). It confers to cells a resistance to multiple drugs and other xenobiotics including mitoxantrone, pheophorbide, camptothecin, methotrexate, azidothymidine, and the anthracyclines daunorubicin and doxorubicin, through the control of their efflux .
PMID:11306452 PMID:12477054 PMID:15670731 PMID:18056989 PMID:31254042
In placenta, it limits the penetration of drugs from the maternal plasma into the fetus (By similarity). May play a role in early stem cell self-renewal by blocking differentiation (By similarity).
In inflammatory macrophages, exports itaconate from the cytosol to the extracellular compartment and limits the activation of TFEB-dependent lysosome biogenesis involved in antibacterial innate immune response
Solute carrier family 22 member 1
SLC22A1
substrate
Specific function(R)-carnitine transmembrane transporter activity
Cellular location
Basolateral cell membrane
General function & pharmacology
Electrogenic voltage-dependent transporter that mediates the transport of a variety of organic cations such as endogenous bioactive amines, cationic drugs and xenobiotics .
PMID:11388889 PMID:11408531 PMID:12439218 PMID:12719534 PMID:15389554 PMID:16263091 PMID:16272756 PMID:16581093 PMID:19536068 PMID:21128598 PMID:23680637 PMID:24961373 PMID:34040533 PMID:9187257 PMID:9260930 PMID:9655880
Functions as a pH- and Na(+)-independent, bidirectional transporter (By similarity). Cation cellular uptake or release is driven by the electrochemical potential (i.e. membrane potential and concentration gradient) and substrate selectivity (By similarity). Hydrophobicity is a major requirement for recognition in polyvalent substrates and inhibitors (By similarity).
Primarily expressed at the basolateral membrane of hepatocytes and proximal tubules and involved in the uptake and disposition of cationic compounds by hepatic and renal clearance from the blood flow (By similarity). Most likely functions as an uptake carrier in enterocytes contributing to the intestinal elimination of organic cations from the systemic circulation .
PMID:16263091
Transports endogenous monoamines such as N-1-methylnicotinamide (NMN), guanidine, histamine, neurotransmitters dopamine, serotonin and adrenaline .
PMID:12439218 PMID:24961373 PMID:35469921 PMID:9260930
Also transports natural polyamines such as spermidine, agmatine and putrescine at low affinity, but relatively high turnover .
PMID:21128598
Involved in the hepatic uptake of vitamin B1/thiamine, hence regulating hepatic lipid and energy metabolism .
PMID:24961373
Mediates the bidirectional transport of acetylcholine (ACh) at the apical membrane of ciliated cell in airway epithelium, thereby playing a role in luminal release of ACh from bronchial epithelium .
PMID:15817714
Transports dopaminergic neuromodulators cyclo(his-pro) and salsolinol with lower efficency .
PMID:17460754
Also capable of transporting non-amine endogenous compounds such as prostaglandin E2 (PGE2) and prostaglandin F2-alpha (PGF2-alpha) .
PMID:11907186
May contribute to the transport of cationic compounds in testes across the blood-testis-barrier (Probable). Also involved in the uptake of xenobiotics tributylmethylammonium (TBuMA), quinidine, N-methyl-quinine (NMQ), N-methyl-quinidine (NMQD) N-(4,4-azo-n-pentyl)-quinuclidine (APQ), azidoprocainamide methoiodide (AMP), N-(4,4-azo-n-pentyl)-21-deoxyajmalinium (APDA) and 4-(4-(dimethylamino)styryl)-N-methylpyridinium (ASP) PMID:11408531 PMID:15389554 PMID:35469921 PMID:9260930
PMID:11388889 PMID:11408531 PMID:12439218 PMID:12719534 PMID:15389554 PMID:16263091 PMID:16272756 PMID:16581093 PMID:19536068 PMID:21128598 PMID:23680637 PMID:24961373 PMID:34040533 PMID:9187257 PMID:9260930 PMID:9655880
Functions as a pH- and Na(+)-independent, bidirectional transporter (By similarity). Cation cellular uptake or release is driven by the electrochemical potential (i.e. membrane potential and concentration gradient) and substrate selectivity (By similarity). Hydrophobicity is a major requirement for recognition in polyvalent substrates and inhibitors (By similarity).
Primarily expressed at the basolateral membrane of hepatocytes and proximal tubules and involved in the uptake and disposition of cationic compounds by hepatic and renal clearance from the blood flow (By similarity). Most likely functions as an uptake carrier in enterocytes contributing to the intestinal elimination of organic cations from the systemic circulation .
PMID:16263091
Transports endogenous monoamines such as N-1-methylnicotinamide (NMN), guanidine, histamine, neurotransmitters dopamine, serotonin and adrenaline .
PMID:12439218 PMID:24961373 PMID:35469921 PMID:9260930
Also transports natural polyamines such as spermidine, agmatine and putrescine at low affinity, but relatively high turnover .
PMID:21128598
Involved in the hepatic uptake of vitamin B1/thiamine, hence regulating hepatic lipid and energy metabolism .
PMID:24961373
Mediates the bidirectional transport of acetylcholine (ACh) at the apical membrane of ciliated cell in airway epithelium, thereby playing a role in luminal release of ACh from bronchial epithelium .
PMID:15817714
Transports dopaminergic neuromodulators cyclo(his-pro) and salsolinol with lower efficency .
PMID:17460754
Also capable of transporting non-amine endogenous compounds such as prostaglandin E2 (PGE2) and prostaglandin F2-alpha (PGF2-alpha) .
PMID:11907186
May contribute to the transport of cationic compounds in testes across the blood-testis-barrier (Probable). Also involved in the uptake of xenobiotics tributylmethylammonium (TBuMA), quinidine, N-methyl-quinine (NMQ), N-methyl-quinidine (NMQD) N-(4,4-azo-n-pentyl)-quinuclidine (APQ), azidoprocainamide methoiodide (AMP), N-(4,4-azo-n-pentyl)-21-deoxyajmalinium (APDA) and 4-(4-(dimethylamino)styryl)-N-methylpyridinium (ASP) PMID:11408531 PMID:15389554 PMID:35469921 PMID:9260930
Carriers(1)
Proteins that carry this drug through the body
Erythrocyte
binder
Scientific references(9)
Rosenzweig P., Canal M., Patat A., Bergougnan L., Zieleniuk I., Bianchetti G.
A review of the pharmacokinetics, tolerability and pharmacodynamics of amisulpride in healthy volunteers.
Human Psychopharmacology: Clinical and Experimental
200217(1):1-13. doi: 10.1002/hup.320
Moller H.J.
Amisulpride: limbic specificity and the mechanism of antipsychotic atypicality.
Progress in Neuro-Psychopharmacology and Biological Psychiatry
200327(7):1101-1111. doi: 10.1016/j.pnpbp.2003.09.006
Weizman T., Pick C.G., Backer M.M., Rigai T., Bloch M., Schreiber S.
The antinociceptive effect of amisulpride in mice is mediated through opioid mechanisms.
European Journal of Pharmacology
2003478(2-3):155-159. doi: 10.1016/j.ejphar.2003.08.049
Leucht S., Pitschel-Walz G., Engel R.R., Kissling W.
Amisulpride, an Unusual “Atypical” Antipsychotic: A Meta-Analysis of Randomized Controlled Trials.
American Journal of Psychiatry
2002159(2):180-190. doi: 10.1176/appi.ajp.159.2.180
Rehni A.K., Singh T.G., Chand P.
Amisulpride-induced seizurogenic effect: a potential role of opioid receptor-linked transduction systems.
Basic & Clinical Pharmacology & Toxicology
2011 May108(5):310-7. doi: 10.1111/j.1742-7843.2010.00655.x. Epub 2010 Dec 22
Curran M.P., Perry C.M.
Amisulpride: a review of its use in the management of schizophrenia.
Drugs
200161(14):2123-50. doi: 10.2165/00003495-200161140-00014
MacDougall M.R., Sharma S.
Chemoreceptor Trigger Zone. Encyclopedia of Molecular Pharmacology. :355-355.
doi: 10
1007/978-3-540-38918-7_5386
Abbas A.I., Hedlund P.B., Huang X.P., Tran T.B., Meltzer H.Y., Roth B.L.
Amisulpride is a potent 5-HT7 antagonist: relevance for antidepressant actions in vivo.
Psychopharmacology (Berl)
2009 Jul205(1):119-28. doi: 10.1007/s00213-009-1521-8. Epub 2009 Apr 1
Brisch R., Saniotis A., Wolf R., Bielau H., Bernstein H.G., Steiner J., Bogerts B., Braun K., Jankowski Z., Kumaratilake J., Henneberg M., Gos T.
The role of dopamine in schizophrenia from a neurobiological and evolutionary perspective: old fashioned, but still in vogue.
Front Psychiatry
2014 May 195:47. doi: 10.3389/fpsyt.2014.00047. eCollection 2014
ATC classification(1 code)
ATC N05AL05
Affected organisms(1)
Humans and other mammals
International brands(2)
Experimental properties(4)
Commercial products(1)
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Show
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Amisulpride
Additional database identifiers
ChemSpider
2074
BindingDB
81790
Guide to Pharmacology
963
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5302
GenAtlas
HTR7
GeneCards
HTR7
GenBank Gene Database
U68487
GenBank Protein Database
1857143
Guide to Pharmacology
12
UniProt Accession
5HT7R_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5293
GenAtlas
HTR2A
GeneCards
HTR2A
GenBank Gene Database
S42168
GenBank Protein Database
36431
Guide to Pharmacology
6
UniProt Accession
5HT2A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3023
GenAtlas
DRD2
GeneCards
DRD2
GenBank Gene Database
M30625
GenBank Protein Database
181432
Guide to Pharmacology
215
UniProt Accession
DRD2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3024
GenAtlas
DRD3
GeneCards
DRD3
GenBank Gene Database
U32499
GenBank Protein Database
927342
Guide to Pharmacology
216
UniProt Accession
DRD3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8156
GenAtlas
OPRM1
GeneCards
OPRM1
GenBank Gene Database
L25119
GenBank Protein Database
452073
Guide to Pharmacology
319
UniProt Accession
OPRM_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8153
GenAtlas
OPRD1
GeneCards
OPRD1
GenBank Gene Database
U07882
GenBank Protein Database
27545517
Guide to Pharmacology
317
UniProt Accession
OPRD_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8154
GenAtlas
OPRK1
GeneCards
OPRK1
GenBank Gene Database
U11053
GenBank Protein Database
532060
Guide to Pharmacology
318
UniProt Accession
OPRK_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:25588
GeneCards
SLC47A1
GenBank Gene Database
AK001709
GenBank Protein Database
7023138
Guide to Pharmacology
1216
UniProt Accession
S47A1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:26439
GeneCards
SLC47A2
Guide to Pharmacology
1217
UniProt Accession
S47A2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:40
GenAtlas
ABCB1
GeneCards
ABCB1
GenBank Gene Database
M14758
GenBank Protein Database
307180
Guide to Pharmacology
768
UniProt Accession
MDR1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:74
GenAtlas
ABCG2
GeneCards
ABCG2
GenBank Gene Database
AF103796
GenBank Protein Database
4185796
Guide to Pharmacology
792
UniProt Accession
ABCG2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10963
GeneCards
SLC22A1
GenBank Gene Database
X98332
GenBank Protein Database
2511670
Guide to Pharmacology
1019
UniProt Accession
S22A1_HUMAN
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Source: DrugBank · CC BY-NC 4.0. Patent data sourced from national patent offices. Expiry dates may not reflect extensions, regulatory exclusivity periods, or legal challenges.
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
Knox C., Wilson M., Klinger C.M., et al
DrugBank 6.
0: the DrugBank Knowledgebase for 2024
Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
Wishart D.S., Feunang Y.D., Guo A.C., et al
DrugBank 5.
0: a major update to the DrugBank database for 2018
Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
Show earlier publications
Law V., Knox C., Djoumbou Y., et al
DrugBank 4.
0: shedding new light on drug metabolism
Nucleic Acids Res. 2014 Jan 142(1):D1091-7
Knox C., Law V., Jewison T., et al
DrugBank 3.
0: a comprehensive resource for 'omics' research on drugs
Nucleic Acids Res. 2011 Jan39(Database issue):D1035-41
Wishart D.S., Knox C., Guo A.C., et al
DrugBank: a knowledgebase for drugs, drug actions and drug targets.
Nucleic Acids Research
2008 Jan36(Database issue):D901-6
Wishart D.S., Knox C., Guo A.C., et al
DrugBank: a comprehensive resource for in silico drug discovery and exploration.
Nucleic Acids Research
2006 Jan 134(Database issue):D668-72
Source: go.drugbank.comCC BY-NC 4.0
Updated 26 days ago(8 Mar 2026)