How Far Is Too Far? The Ethics of Mini Brain Research
December 11, 2025
Brand Name :
Risperdal, Risperdal M-tab, perseris
Synonyms :
risperidone
Class :
Atypical antipsychotics
Dosage Forms & Strengths
Tablet
0.25mg
0.5mg
1mg
2mg
3mg
4mg
Oral disintegrating tablet
0.5mg
1mg
2mg
3mg
4mg
Oral solution
1mg/ml
Long-acting injectable suspension, Intramuscular injection kit
12.5mg
25mg
37.5mg
50mg
Extended-release injectable suspension
12.5mg
25mg
37.5mg
50mg
Subcutaneous injection kit
90mg
120mg
Orally
Initially:2mg/day
At an interval of 24 hours, may increase the dose from 1-2mg/day
Maintenance dose:2 to 8mg orally/day
Maximum dose:16mg orally/day
Intramuscular
Initial dose:25mg intramuscular every two weeks
Titration dose: may increase up to 37.5mg or 50mg
Maximum dose: 50mg intramuscular every two weeks
Subcutaneous
90mg or 120mg subcutaneously monthly once
Orally
Initial dose:2 to 3mg orally /day
Titration dose: Increase 1mg/day at 24 hours intervals
Maximum dose: 6mg orally /day
Intramuscular
Initial dose:25mg intramuscular every two weeks
Titration dose: may increase up to 37.5mg or 50mg
Maximum dose: 50mg intramuscular every two weeks
Indicated for Post-traumatic stress disorder :
0.5 - 8
mg/day
Orally
Dose Adjustments
Hepatic impairment
The recommended starting dose for patients with mild to moderate liver impairment is 0.5 mg once daily, gradually increasing to a maximum of 2-3 mg daily. For patients with severe liver impairment, the starting dose is typically 0.25 mg once daily, gradually increasing to a maximum of 1-2 mg daily
It's important to note that the pharmacokinetics of risperidone may be affected in patients with liver impairment, and there may be an increased risk of adverse reactions. Therefore, a healthcare provider should closely monitor patients with liver impairment
Renal impairment
It is eliminated primarily by the liver, with a small portion eliminated by the kidneys. Therefore, modifications to the dosing may not typically be necessary for patients with renal impairment
Dosage Forms & Strengths
Tablet
0.25mg
0.5mg
1mg
2mg
3mg
4mg
Oral disintegrating tablet
0.5mg
1mg
2mg
3mg
4mg
Oral solution
1mg/ml
<13 years: Safety and efficacy not established
>13 years:
Initial dose: 0.5mg/day orally in the morning or evening
Titration dose: may increase 0.5mg to 1mg/day at 24 hours intervals
Maintenance dose:3mg orally per day
Maximum dose: 6mg orally per day
<10 years: Safety and efficacy not established
>10 years:
Initial dose: 0.5mg/day orally in the morning or evening
Titration dose: may increase 0.5mg to 1mg/day at 24 hours intervals
Maximum dose: 6mg orally per day
Indicated for autism:
<5 years: Safety and efficacy not established
5-16 years(<20kg)
Initial dose:0.25mg orally once a day
Titration: A following dose increase may be made in increments of 0.25 mg at intervals of 2 weeks or more, as tolerated, after a minimum of 4 days
Maintain this dose for a minimum of 14 days
5-16 years(>20kg)
Initial dose:0.5mg orally once a day
Titration: A following dose increase may be made in increments of 0.5 mg at intervals of 2 weeks or more, as tolerated, after a minimum of 4 days
Maintain this dose for a minimum of 14 days
Dose Adjustments
Renal impairment
Dosage adjustments may be necessary for mild to moderate renal impairment, but no specific guidelines have been provided. Caution is recommended. For severe renal impairment, the initial starting dose is 0.5 mg twice daily, with increments of 0.5 mg or less administered twice a day. For doses above 1.5 mg twice daily, increase in 1 week or more significant intervals. The long-acting intramuscular injection can be used if a total daily oral dose of at least 2 mg once daily is well tolerated, with an initial dose of 25 mg every two weeks by deep intramuscular injection in the deltoid or gluteal muscle
Liver impairment
Dosage adjustments may be necessary for mild to moderate hepatic dysfunction (Child-Pugh less than 10), but no specific guidelines have been provided. Caution is recommended. For severe hepatic dysfunction (Child-Pugh 10 to 15), the initial starting dose is 0.5 mg twice a day, with increments of 0.5 mg or less, administered twice daily. For doses above 1.5 mg twice daily, increase in 1 week or more significant intervals. The long-acting intramuscular injection can be used if a total daily oral dose of at least 2 mg once daily is well tolerated, with an initial dose of 25 mg every two weeks by deep intramuscular injection in the deltoid or gluteal muscle
Orally
Initially:0.5mg/day
At an interval of 24 hours, may increase the dose from 1-2mg/day
Maintenance dose:2 to 8mg orally/day
Maximum dose:16mg orally/day
Intramuscular
Initial dose:25mg intramuscular every two weeks
Titration dose: may increase up to 37.5mg or 50mg
Maximum dose: 50mg intramuscular every two weeks
Orally
Initially:0.5mg/day
At an interval of 24 hours, may increase the dose from 1-2mg/day
Maximum dose:16mg orally/day
Intramuscular
Initial dose:25mg intramuscular every two weeks
Titration dose: may increase up to 37.5mg or 50mg
Maximum dose: 50mg intramuscular every two weeks
may increase the QTc prolonging effect
may decrease the therapeutic effect of anti-parkinson agents
may decrease the therapeutic effect of anti-parkinson agents
may decrease the therapeutic effect of anti-parkinson agents
may decrease the therapeutic effect of anti-parkinson agents
may decrease the therapeutic effect of anti-parkinson agents
may increase the CNS depressant effect of CNS depressants
may increase the constipating effects of anticholinergic agents
may increase the serum concentration
may increase the serum concentration
may increase the serum concentration
may increase the serum concentration
may increase the serum concentration
may enhance the serum concentration
may enhance the serum concentration
may enhance the serum concentration
may enhance the serum concentration
may enhance the serum concentration
may increase the CNS depressant effect of CNS depressants
may increase the CNS depressant effect of CNS depressants
may increase the CNS depressant effect of CNS depressants
may increase the CNS depressant effect of CNS depressants
may increase the CNS depressant effect of CNS depressants
may increase the CNS depressant effect of CNS depressants
may increase the QTc prolonging effect
may increase the QTc prolonging effect
may increase the QTc prolonging effect
may increase the QTc prolonging effect
may increase the QTc prolonging effect
may increase the CNS depressant effect of CNS depressants
the efficacy of Dopamine agonists will be decreased when Antipsychotic Agents are used in combination
the efficacy of Dopamine agonists will be decreased when Antipsychotic Agents are used in combination
the efficacy of Dopamine agonists will be decreased when Antipsychotic Agents are used in combination
the efficacy of Dopamine agonists will be decreased when Antipsychotic Agents are used in combination
the efficacy of Dopamine agonists will be decreased when Antipsychotic Agents are used in combination
may decrease the therapeutic effect when combined with anti-parkinson agents
may decrease the therapeutic effect when combined with anti-parkinson agents
may decrease the therapeutic effect when combined with anti-parkinson agents
may decrease the therapeutic effect when combined with anti-parkinson agents
may enhance the CNS depressant effect
may decrease the therapeutic effect of anti-Parkinson agents
may increase the CNS depressant effect of CNS depressants
may increase the toxic effect of antipsychotics
may diminish the therapeutic effect of antipsychotic agents
may increase the anti-cholinergic effect of anti-cholinergic agents
may increase the anti-cholinergic effect of anti-cholinergic agents
may increase the anti-cholinergic effect of anti-cholinergic agents
may increase the CNS depressant effect of CNS depressants
may increase the ulcerogenic effect of anti-cholinergic agents
CYP3A strong enhancers of the small intestine may reduce the bioavailability of risperidone
when used together, entrectinib and risperidone both increase the QTc interval
when used together, encorafenib and risperidone both increase the QTc interval
it increases the effect of CNS depressants
CNS depressants increase the effect of paraldehyde
CNS depressants increase the effect of orphenadrine
may have an increasingly adverse effect when combined with antipsychotic agents
antipsychotic agents increase the effect of arrhythmia of saquinavir
Could potentially reduce the therapeutic efficacy of antipsychotic agents
The potential for increased toxicity of Sulpiride could be amplified by the presence of antipsychotic agents
tiopronin: they may increase the toxic effect of antipsychotic agents
CNS depressants may enhance the CNS depressant effect of cannabinoid-Containing products
CNS depressants may enhance the CNS depressant effect of cannabinoid-Containing products
may increase the QTc prolonging effect
may increase the QTc prolonging effect
may increase the QTc-prolonging effects of QTc-prolonging agents
may increase the QTc-prolonging effects of QTc-prolonging agents
may increase the QTc-prolonging effects of QTc-prolonging agents
may increase the QTc-prolonging effects of QTc-prolonging agents
may increase the constipating effect of anticholinergic agents
may increase the toxic effect of CNS depressants
may increase the toxic effect of antipsychotic agents
may increase the toxic effect of anticholinergic agents
may reduce the therapeutic effect of anti-Parkinson drugs
may reduce the therapeutic effect of anti-Parkinson drugs
may reduce the therapeutic effect of anti-Parkinson drugs
may reduce the therapeutic effect of anti-Parkinson drugs
may reduce the therapeutic effect of anti-Parkinson drugs
may have an increased hypotensive effect when combined with anti-hypertensive agents
may have an increased hypotensive effect when combined with anti-hypertensive agents
may have an increased hypotensive effect when combined with anti-hypertensive agents
may have an increased hypotensive effect when combined with anti-hypertensive agents
may have an increased hypotensive effect when combined with anti-hypertensive agents
It may enhance sedation when combined with a shepherd's purse
It may enhance sedation when combined with codeine
may have an increased QTc-prolonging effect when combined with QT-prolonging antipsychotics
may have an increased QTc-prolonging effect when combined with QT-prolonging antipsychotics
may have an increased QTc-prolonging effect when combined with QT-prolonging antipsychotics
may have an increased QTc-prolonging effect when combined with QT-prolonging antipsychotics
may have an increased QTc-prolonging effect when combined with QT-prolonging antipsychotics
may have an increased neurotoxic effect when combined with antipsychotic agents
may have an increased neurotoxic effect when combined with antipsychotic agents
may have an increasingly adverse effect when combined with amphetamines
may have an increasingly adverse effect when combined with amphetamines
may have an increasingly adverse effect when combined with amphetamines
may have an increasingly adverse effect when combined with amphetamines
may have an increasingly adverse effect when combined with amphetamines
may have an increased hypotensive effect when combined with beta-blockers
may have an increased hypotensive effect when combined with beta-blockers
may have an increased hypotensive effect when combined with beta-blockers
may have an increased hypotensive effect when combined with beta-blockers
may have an increased hypotensive effect when combined with beta-blockers
it increases the QT-c prolonging effect with gilteritinib
nabilone and risperidone, when used simultaneously, both increase the sedation
it may enhance the neurotoxic (central) effect of antipsychotic Agents
it may enhance the neurotoxic (central) effect of antipsychotic Agents
it may enhance the neurotoxic (central) effect of antipsychotic Agents
it may enhance the neurotoxic (central) effect of antipsychotic Agents
it may enhance the neurotoxic (central) effect of antipsychotic Agents
may enhance the neurotoxic (central) effect of antipsychotic agents
may enhance the neurotoxic (central) effect of antipsychotic agents
may enhance the neurotoxic (central) effect of antipsychotic agents
may enhance the neurotoxic (central) effect of antipsychotic agents
CNS Depressants may enhance the CNS depressant effect of flunarizine
it increases the effect of CNS depressants
may enhance the adverse/toxic effect of antipsychotic agents
may enhance the adverse/toxic effect of antipsychotic agents
may enhance the adverse/toxic effect of antipsychotic agents
may enhance the adverse/toxic effect of antipsychotic agents
may enhance the adverse/toxic effect of antipsychotic agents
it increases the effect of CNS depressants
it increases the effect of CNS depressants
may increase the hypotensive effect of antihypertensives
may enhance the adverse/toxic effect of antipsychotic agents
may enhance the adverse/toxic effect of antipsychotic agents
may enhance the adverse/toxic effect of antipsychotic agents
may enhance the adverse/toxic effect of antipsychotic agents
may enhance the adverse/toxic effect of antipsychotic agents
may diminish the therapeutic effect of antipsychotic agents
may diminish the therapeutic effect of antipsychotic agents
may diminish the therapeutic effect of antipsychotic agents
may diminish the therapeutic effect of antipsychotic agents
may diminish the therapeutic effect of antipsychotic agents
may increase the hypotensive effect of blood pressure-lowering agents
may have an increased hypotensive effect when combined with antipsychotic agents
may have an increased hypotensive effect when combined with antipsychotic agents
may have an increased hypotensive effect when combined with antipsychotic agents
may have an increased hypotensive effect when combined with antipsychotic agents
may have an increased hypotensive effect when combined with antipsychotic agents
may enhance the serum concentrations of P-glycoprotein-ABCB1 inhibitors
may increase the risk of adverse effect
may have an increased neurotoxic effect when combined with antipsychotic agents
may have an increased neurotoxic effect when combined with antipsychotic agents
may have an increasingly adverse effect when combined with antipsychotic agents
may have an increasingly adverse effect when combined with dexmethylphenidate
may increase the QTc-prolonging effect of QT-Prolonging Inhalational Anesthetics
may have an increased hypotensive effect when combined with antipsychotic agents
may increase the QTc-prolonging effect
may increase the QTc-prolonging effect
may increase the QTc-prolonging effect
may increase the QTc-prolonging effect
may increase the QTc-prolonging effect
The Therapeutic efficacy of quinagolide might be reduced
may enhance the risk of hypertension when combined with risperidone
Could potentially amplify the toxicity of antipsychotic agents
lithium: they may increase the neurotoxic effect of antipsychotic agents
mianserin: they may decrease the therapeutic effect of antipsychotics
may have an increased neurotoxic effect when combined with antipsychotic agents
When risperidone is used together in combination with profenamine, this leads to reduction in therapeutic effectiveness of profenamine
Actions and spectrum
Mechanism of action
Risperidone is an antipsychotic drug working on dopamine D2 and serotonin 5-HT2A receptors present in the brain that it decreases the intensity of psychosis which is expressed through delusions and hallucinations. In addition to having some of the activity on the 5HT1A receptor that reduces anxiety and nervousness, it also has the activity on the 5HT2A receptor which calms down fear and psychosis.
For instance, it can aid in the treatment of a range of psychiatric battles. Schizophrenia is not the only way antipsychotic works. It is also helpful for bipolar disorder and certain depressed symptoms. It is also applied as second line management in the treatment of major depression.
Frequency defined:
>10%
Insomnia
Anxiety
Rhinitis
Parkinsonism
Increased appetite
Drooling
Tremor
Enuresis
1-10%
Dyspepsia
Abdominal pain
Facial edema
Dizziness
Gynecomastia in children
Constipation
Nausea
<1%
Cholesterol increased
Ketoacidosis
Seizures
Agranulocytosis
Delirium
Orthostatic hypotension
Frequency not defined
Hyperthermia
Hypothermia
Neuroleptic malignant syndrome
Prolonged QT interval
Dysphagia
Black box warning
The United States Food and Drug Administration recently issued a black box caution due to higher mortality risk in psychosis patients with dementia whose extreme age is the essential factor.
Contraindications/caution
Contraindications
Hypersensitivity
Caution
Increased risk of death in elderly patients with dementia-related psychosis
Cardiovascular risks
Extrapyramidal symptoms
Pregnancy/Lactation
Pregnancy consideration: Insufficient data available
Lactation: Excretion of the drug in human breast milk is unknown
Pregnancy category:
Pharmacology
Risperidone exerts its antagonistic effects on histamine H1, dopamine D2, serotonin 5-HT2, alpha-adrenergic, and muscarinic acetylcholine receptors. Its effectiveness in treating psychotic symptoms is derived from the antagonistic actions on the dopamine receptors particularly the D2 subtype which regulates the dopamine transmission in multiple brain areas. It interacts with serotonin receptors belonging to the group of 5-HT2A especially those that could be potentially beneficial in stabilizing the mood. Caution should be exercised when driving an automobile or operating a device requiring alertness because of the possible effects of drowsiness and hypotension due to its actions as an antagonist on alpha-adrenergic receptors, specifically the alpha-1 subtype.
Pharmacodynamics
The main method that risperidone works is by slowing down the brain’s dopaminergic and serotonergic pathways which lessens the symptoms of schizophrenia and other mood disorders. When it comes to serotonergic 5-HT2A receptors and it binds more strongly than dopaminergic D2 receptors. Risperidone has a lesser affinity for D2 receptors than first-generation antipsychotic medications. It has a modest affinity for D2 receptors.
Pharmacokinetics
Absorption
Risperidone is well-absorbed orally with an absolute oral bioavailability of 70% and a relative oral bioavailability of 94% when compared to a tablet or solution with a 10% variation coefficient.
Distribution
It is rapidly distributed, has a Volume of distribution of 1 to 2 L/kg and is mostly protein bound at 90%
Metabolism
Risperidone is metabolized by the hepatic cytochrome P450 2D6 isozyme, forming 9-hydroxyrisperidone or paliperidone. Its receptor binding affinity is like risperidone. The hydroxylation process relies on debrisoquine 4-hydroxylase which is influenced by genetic polymorphisms. It also undergoes N-dealkylation to a lesser extent. The half-life is 3 to 6 days for intramuscular administration and 3 hours for extensive metabolizers and 20 hr for poor metabolizers when taken orally
Elimination/excretion
It is primarily eliminated through renal clearance with a significant reduction in clearance in elderly individuals and those with a creatinine clearance of 15 to 59 mL/min. It is excreted mainly in the urine (70%) and feces (14%)
Administration
It is administered in the form of tablets
Patient information leaflet
Generic Name: risperidone
Pronounced: [ ris-PER-i-done ]
Why do we risperidone?
Risperidone is an antipsychotic medication which functions by altering the actions of brain chemicals. It is prescribed for schizophrenia in individuals aged 13 and above. It is utilized to treat symptoms of bipolar disorder in individuals aged 10 and above.