AMIABEL Amisulpride 400mg Film-Coated Tablet 1's
RXDRUG-DR-XY41217-1pc
Discreet Packaging
FDA-registered Products
FDA-licensed Pharmacies
Indications/Uses
For the treatment of psychoses, such as acute and chronic schizophrenic disorders, in which positive symptoms (e.g., delusions, hallucinations, thought disorders) and/or negative symptoms (e.g., blunted affect, emotional and social withdrawal) are prominent, including patients characterized by predominant negative symptoms.
Dosage/Direction for Use
Doses should preferably be given before meals.
Amisulpride should be administered twice a day for doses above 400 mg.
Doses should be adjusted based on individual patient response.
There is no specific titration required when initiating treatment with amisulpride.
Maintenance treatment should be established individually with the minimally effective dose.
Recommended Adult Oral Amisulpride Dose: For acute psychotic episodes: Oral doses between 400 mg and 800 mg per day; In individual cases, the daily dose may be increased up to 1,200 mg per day.
Doses above 1,200 mg per day have not been evaluated for safety and should not be used.
For patients with mixed positive and negative symptoms: Initially, 400 mg to 800 mg per day; Doses should then be adjusted to obtain optimal control of positive symptoms.
For patients with predominant negative symptoms: Oral doses between 50 mg and 300 mg per day.
Special Population: Renal Insufficiency: Dose should be reduced to half in patients with creatinine clearance (CLCr) between 30 to 60 mL/min and to a third in patients with CLCr between 10 to 30 mL/min.
As there is no experience in patient with severe renal impairment (CLCr < 10 mL/min), particular care is recommended in these patients.
Hepatic Impairment: Dose reduction is not necessary since amisulpride is weakly metabolized.
Or, as prescribed by a physician.
Amisulpride should be administered twice a day for doses above 400 mg.
Doses should be adjusted based on individual patient response.
There is no specific titration required when initiating treatment with amisulpride.
Maintenance treatment should be established individually with the minimally effective dose.
Recommended Adult Oral Amisulpride Dose: For acute psychotic episodes: Oral doses between 400 mg and 800 mg per day; In individual cases, the daily dose may be increased up to 1,200 mg per day.
Doses above 1,200 mg per day have not been evaluated for safety and should not be used.
For patients with mixed positive and negative symptoms: Initially, 400 mg to 800 mg per day; Doses should then be adjusted to obtain optimal control of positive symptoms.
For patients with predominant negative symptoms: Oral doses between 50 mg and 300 mg per day.
Special Population: Renal Insufficiency: Dose should be reduced to half in patients with creatinine clearance (CLCr) between 30 to 60 mL/min and to a third in patients with CLCr between 10 to 30 mL/min.
As there is no experience in patient with severe renal impairment (CLCr < 10 mL/min), particular care is recommended in these patients.
Hepatic Impairment: Dose reduction is not necessary since amisulpride is weakly metabolized.
Or, as prescribed by a physician.
Overdosage
Experience with amisulpride in overdosage is limited. There have been reports of exaggeration of the known pharmacological and adverse effects of amisulpride. Symptoms include drowsiness, sedation, coma, hypotension and extrapyramidal symptoms.
Fatal outcomes have been reported mainly in combination with other psychotropic agents. In cases of acute overdosage, the possibility of multiple drug intake should be considered.
There is no specific antidote to amisulpride. Appropriate supportive measure should be instituted with close observation of vital functions including continuous cardiac monitoring because of the risk of prolongation of QT interval. If severe extrapyramidal symptoms occur, anticholinergic agents should be administered.
Hemodialysis is not recommended as a method of elimination since amisulpride is weakly dialyzed.
Fatal outcomes have been reported mainly in combination with other psychotropic agents. In cases of acute overdosage, the possibility of multiple drug intake should be considered.
There is no specific antidote to amisulpride. Appropriate supportive measure should be instituted with close observation of vital functions including continuous cardiac monitoring because of the risk of prolongation of QT interval. If severe extrapyramidal symptoms occur, anticholinergic agents should be administered.
Hemodialysis is not recommended as a method of elimination since amisulpride is weakly dialyzed.
Administration
Should be taken on an empty stomach.
Contraindications
Hypersensitivity. Concomitant prolactin-dependent tumors eg, pituitary gland prolactinomas & breast cancer. Pheochromocytoma. In combination w/ levodopa & drugs that induce Torsades de pointes including class Ia antiarrhythmic agents (eg, quinidine, procainamide, disopyramide), class III antiarrhythmic agents (eg, amiodarone, sotalol), certain antipsychotic drugs (eg, sertindole) & other drugs eg, bepridil, cisapride, sultopride, thioridazine, erythromycin IV, vincamine IV, halofantrine, pentamidine & sparfloxacin. Women of childbearing potential. Pregnancy & lactation. Childn <15 yr.
Special Precautions
Patients w/ stroke risk factors. Neuroleptic malignant syndrome (hyperthermia, muscle rigidity, autonomic instability, altered consciousness & elevated creatinine phosphokinase). Monitor patients w/ history of epilepsy. Acute dystonia, extrapyramidal symptoms eg, tremor, rigidity, hypokinesia & akathisia. Tardive dyskinesia. Patients w/ DM should be monitored for hyperglycemia. Increased plasma prolactin levels, QT interval prolongation & venous thromboembolism may occur, monitor & assess ECG. Patients w/ risk factors for thromboembolism. Patients w/ Parkinson's disease, severe renal insufficiency, moderate or severe hepatic impairment. Concomitant use w/ other renally-excreted drugs including lithium. Avoid abrupt w/drawal. May affect ability to drive or operate machinery. Elderly especially w/ dementia-related psychosis.
Use In Pregnancy & Lactation
Use in Pregnancy: Pregnancy Category B3: The safety of amisulpride during human pregnancy has not been established. Therefore, use of this drug is not recommended during pregnancy unless the benefits justify the potential risk to the fetus.
Neonates exposed to antipsychotic drugs during the third trimester of pregnancy are at risk for extrapyramidal and/or withdrawal symptoms after delivery. There have been reports of agitation, hypertonia, hypotonia, tremor, somnolence, respiratory distress and feeding disorder in these neonates. These complications have varied in severity; while in some cases symptoms have been self-limited, in other cases neonates have required intensive care unit support and prolonged hospitalization.
Use in Lactation: It is not known whether amisulpride or its metabolites are excreted in animal or human breast milk. Therefore, breastfeeding during amisulpride treatment is not recommended.
Neonates exposed to antipsychotic drugs during the third trimester of pregnancy are at risk for extrapyramidal and/or withdrawal symptoms after delivery. There have been reports of agitation, hypertonia, hypotonia, tremor, somnolence, respiratory distress and feeding disorder in these neonates. These complications have varied in severity; while in some cases symptoms have been self-limited, in other cases neonates have required intensive care unit support and prolonged hospitalization.
Use in Lactation: It is not known whether amisulpride or its metabolites are excreted in animal or human breast milk. Therefore, breastfeeding during amisulpride treatment is not recommended.
Adverse Reactions
Hypotension, bradycardia, QT interval prolongation, ventricular arrhythmias eg, torsades de pointes, ventricular tachycardia which may result to ventricular fibrillation or cardiac arrest, sudden death, venous thromboembolism eg, cases of pulmonary embolism & DVT. Allergic reaction, angioedema, urticaria. Wt gain, increased plasma prolactin levels which may result in galactorrhea, amenorrhea, gynecomastia, breast pain, orgasmic dysfunction & impotency; hyperglycemia. Constipation, nausea, vomiting, dry mouth. Hepatic enzymes elevations. Insomnia, anxiety, agitation, somnolence, extrapyramidal symptoms (eg, tremor, rigidity, hypokinesia, hypersalivation, akathisia, dyskinesia), acute dystonia (eg, spasm torticollis, oculogyric crisis, trismus), tardive dyskinesia (characterized by rhythmic, involuntary movements primarily of the tongue &/or face), NMS, seizures.
Drug Interactions
Reciprocal antagonism of effects between levodopa & antipsychotics. May enhance the effects of alcohol. May enhance the risk of Torsades de pointes w/ bradycardia-inducing drugs eg, β-blockers (eg, bisoprolol, carvedilol, metoprolol), Ca channel blockers (eg, diltiazem & verapamil), guanfacine, clonidine & digitalis; hypokalemic diuretics, stimulant laxatives, amphotericin B IV, glucocorticoids & tetracosactides; antipsychotics. May enhance the effects of CNS depressants, antihypertensives & other hypotensive drugs.
Storage
Store at temperatures not exceeding 30°C.
Action
Pharmacology: Amisulpride is a substituted benzamide atypical antipsychotic. It binds selectively with a high affinity to human dopaminergic D2 and D3 receptor subtypes while having no affinity for D1, D4 and D5 receptor subtypes. Unlike conventional and other atypical antipsychotics, amisulpride has no affinity for serotonin, α-adrenergic, histamine H1, and cholinergic receptors. It does not bind to sigma sites.
In animal studies, at high doses, amisulpride antagonizes postsynaptic dopamine D2 and D3 receptors, preferentially in the limbic system rather than those in the striatum, thereby reducing dopaminergic transmission. In addition, amisulpride does not induce catalepsy and does not produce D2 hypersensitivity after repeated treatment. At low doses, it enhances dopaminergic neurotransmission by preferentially blocking presynaptic D2/D3 dopamine receptors, producing dopamine release responsible for its disinhibitory effects.
This pharmacological profile explains the clinical efficacy of amisulpride against both negative and positive symptoms of schizophrenia.
Amisulpride's reduced tendency to produce extrapyramidal side effects may be related to its preferential limbic activity.
Pharmacokinetics: In humans, amisulpride shows two absorption peaks: One which is attained rapidly one hour post-dose and a second between 3 and 4 hours after oral administration. Corresponding plasma concentrations are 39±3 and 54±4 ng/mL after a 50 mg dose.
A high-carbohydrate low-fat meal significantly decreases the area under the drug curve (AUC), time to reach maximum concentration (Tmax) and maximum concentration (Cmax) of amisulpride, but no changes were seen after a high-fat meal. The significance of these findings in routine clinical use in not known.
Amisulpride's volume of distribution is 5.8 L/kg. Plasma protein-binding is low (16%) and drug interactions due to displacement are unlikely. The absolute bioavailability of amisulpride is 48%.
Amisulpride is weakly metabolized: two inactive metabolites, accounting for approximately 4% of the dose, have been identified. There is no accumulation of amisulpride and its pharmacokinetics remains unchanged after the administration of repeated doses. Amisulpride is eliminated unchanged in the urine. Amisulpride's elimination half-life (t½) is approximately 12 hrs after an oral dose.
Amisulpride is very weakly dialyzed.
Special Population: Renal Insufficiency: The elimination t½ is unchanged in patients with renal insufficiency while systemic clearance is reduced by a factor of 2.5 to 3. The AUC of amisulpride increased two-fold in mild renal failure and almost tenfold in moderate renal failure. There are no data with doses greater than 50 mg.
Geriatric: Limited pharmacokinetic data in elderly patients (>65 years) showed that a 10 to 30% increase occurs in Cmax, t½, and AUC after a single oral 50 mg dose. No data are available after repeated dosing.
In animal studies, at high doses, amisulpride antagonizes postsynaptic dopamine D2 and D3 receptors, preferentially in the limbic system rather than those in the striatum, thereby reducing dopaminergic transmission. In addition, amisulpride does not induce catalepsy and does not produce D2 hypersensitivity after repeated treatment. At low doses, it enhances dopaminergic neurotransmission by preferentially blocking presynaptic D2/D3 dopamine receptors, producing dopamine release responsible for its disinhibitory effects.
This pharmacological profile explains the clinical efficacy of amisulpride against both negative and positive symptoms of schizophrenia.
Amisulpride's reduced tendency to produce extrapyramidal side effects may be related to its preferential limbic activity.
Pharmacokinetics: In humans, amisulpride shows two absorption peaks: One which is attained rapidly one hour post-dose and a second between 3 and 4 hours after oral administration. Corresponding plasma concentrations are 39±3 and 54±4 ng/mL after a 50 mg dose.
A high-carbohydrate low-fat meal significantly decreases the area under the drug curve (AUC), time to reach maximum concentration (Tmax) and maximum concentration (Cmax) of amisulpride, but no changes were seen after a high-fat meal. The significance of these findings in routine clinical use in not known.
Amisulpride's volume of distribution is 5.8 L/kg. Plasma protein-binding is low (16%) and drug interactions due to displacement are unlikely. The absolute bioavailability of amisulpride is 48%.
Amisulpride is weakly metabolized: two inactive metabolites, accounting for approximately 4% of the dose, have been identified. There is no accumulation of amisulpride and its pharmacokinetics remains unchanged after the administration of repeated doses. Amisulpride is eliminated unchanged in the urine. Amisulpride's elimination half-life (t½) is approximately 12 hrs after an oral dose.
Amisulpride is very weakly dialyzed.
Special Population: Renal Insufficiency: The elimination t½ is unchanged in patients with renal insufficiency while systemic clearance is reduced by a factor of 2.5 to 3. The AUC of amisulpride increased two-fold in mild renal failure and almost tenfold in moderate renal failure. There are no data with doses greater than 50 mg.
Geriatric: Limited pharmacokinetic data in elderly patients (>65 years) showed that a 10 to 30% increase occurs in Cmax, t½, and AUC after a single oral 50 mg dose. No data are available after repeated dosing.
MedsGo Class
Antipsychotics
Features
Brand
Amiabel
Full Details
Dosage Strength
400mg
Drug Ingredients
- Amisulpride
Drug Packaging
Film-Coated Tablet 1's
Generic Name
Amisulpride
Dosage Form
Film-Coated Tablet
Registration Number
DR-XY41217
Drug Classification
Prescription Drug (RX)
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