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    Risperidone molecular structure

    Risperidone Stats & Data

    Risperdal
    NPS DataHub
    MW410.49
    FormulaC23H27FN4O2
    CAS106266-06-2
    IUPAC3-[2-[4-(6-fluoro-1,2-benzoxazol-3-yl)piperidin-1-yl]ethyl]-2-methyl-6,7,8,9-tetrahydropyrido[1,2-a]pyrimidin-4-one
    SMILESFc1ccc2c(c1)onc2C1CCN(CC1)CCc1c(C)nc2CCCCn2c1=O
    InChIKeyRAPZEAPATHNIPO-UHFFFAOYSA-N
    Chemical Class Benzodiazepine
    Psychoactive Class Depressant

    Pharmacology

    DrugBank
    State Solid

    Description

    Risperidone is a second-generation antipsychotic (SGA) medication used in the treatment of a number of mood and mental health conditions including schizophrenia and bipolar disorder. It is one of the most widely used SGAs. Paliperidone, another commonly used SGA, is the primary active metabolite of risperidone (i.e. 9-hydroxyrisperidone). Schizophrenia and various mood disorders are thought to be caused by an excess of dopaminergic D2 and serotonergic 5-HT2A activity, resulting in overactivity of central mesolimbic pathways and mesocortical pathways, respectively. Risperidone is thought to reduce this overactivity through inhibition of dopaminergic D2 receptors and serotonergic 5-HT2A receptors in the brain. Risperidone binds with a very high affinity to 5-HT2A receptors, approximately 10-20 fold greater than the drug's binding affinity to D2 receptors, and carries lesser activity at several off-targets which may responsible for some of its undesirable effects.

    Mechanism of Action

    Though its precise mechanism of action is not fully understood, current focus is on the ability of risperidone to inhibit the D2 dopaminergic receptors and 5-HT2A serotonergic receptors in the brain. Schizophrenia is thought to result from an excess of dopaminergic D2 and serotonergic 5-HT2A activity, resulting in overactivity of central mesolimbic pathways and mesocortical pathways, respectively. D2 dopaminergic receptors are transiently inhibited by risperidone, reducing dopaminergic neurotransmission, therefore decreasing positive symptoms of schizophrenia, such as delusions and hallucinations. Risperidone binds transiently and with loose affinity to the dopaminergic D2 receptor, with an ideal receptor occupancy of 60-70% for optimal effect. Rapid dissociation of risperidone from the D2 receptors contributes to decreased risk of extrapyramidal symptoms (EPS), which occur with permanent and high occupancy blockade of D2 dopaminergic receptors. Low-affinity binding and rapid dissociation from the D2 receptor distinguish risperidone from the traditional antipsychotic drugs. A higher occupancy rate of D2 receptors is said to increase the risk of extrapyramidal symptoms and is therefore to be avoided. Increased serotonergic mesocortical activity in schizophrenia results in negative symptoms, such as depression and decreased motivation.

    Pharmacodynamics

    The primary action of risperidone is to decrease dopaminergic and serotonergic pathway activity in the brain, therefore decreasing symptoms of schizophrenia and mood disorders. Risperidone has a high binding affinity for serotonergic 5-HT2A receptors when compared to dopaminergic D2 receptors in the brain. Risperidone binds to D2 receptors with a lower affinity than first-generation antipsychotic drugs, which bind with very high affinity. A reduction in extrapyramidal symptoms with risperidone, when compared to its predecessors, is likely a result of its moderate affinity for dopaminergic D2 receptors.

    Metabolism

    Extensively metabolized by hepatic cytochrome P450 2D6 isozyme to 9-hydroxyrisperidone (i.e. paliperidone), which has approximately the same receptor binding affinity as risperidone. Hydroxylation is dependent on debrisoquine 4-hydroxylase and metabolism is sensitive to genetic polymorphisms in debrisoquine 4-hydroxylase. Risperidone also undergoes N-dealkylation to a lesser extent.

    Absorption

    Well absorbed. The absolute oral bioavailability of risperidone is 70% (CV=25%). The relative oral bioavailability of risperidone from a tablet is 94% (CV=10%) when compared to a solution.

    Toxicity

    Symptoms of overdose include lethargy, dystonia/spasm, tachycardia, bradycardia, and seizures. LD50=57.7 mg/kg (rat, oral) and 34 mg/kg (rat, intravenous).

    Indication

    Risperidone is indicated for the treatment of schizophrenia and irritability associated with autistic disorder. It is also indicated as monotherapy, or adjunctly with lithium or valproic acid, for the treatment of acute mania or mixed episodes associated with bipolar I disorder. Risperidone is additionally indicated in Canada for the short-term symptomatic management of aggression or psychotic symptoms in patients with severe dementia of the Alzheimer type unresponsive to nonpharmacological approaches. Risperidone is also used off-label for a number of conditions including as an adjunct to antidepressants in treatment-resistant depression.

    Half-life

    3 hours in extensive metabolizers Up to 20 hours in poor metabolizers

    Protein Binding

    Risperidone and its active metabolite, 9-hydroxyrisperidone, are ~88% and ~77% protein-bound in human plasma, respectively. They each bind to both serum albumin and alpha-1-acid glycoprotein.

    Elimination

    Risperidone is extensively metabolized in the liver. In healthy elderly subjects, renal clearance of both risperidone and 9-hydroxyrisperidone was decreased, and elimination half-lives are prolonged compared to young healthy subjects.

    Volume of Distribution

    The volume of distribution of risperidone is approximately 1 to 2 L/kg.

    Clearance

    Risperidone is cleared by the kidneys. Clearance is decreased in the elderly and those with a creatinine clearance (ClCr) between 15-59 mL/min, in whom clearance is decreased by approximately 60%.

    Effect Profile

    Curated + 33 Reports
    Benzodiazepine 7.0

    Strong euphoria with moderate anxiolysis and sedation, mild cognitive impairment

    Anxiolysis×3
    7
    Sedation / Relaxation×2
    63.6
    Motor / Cognitive Impairment×1
    41.5
    Euphoria / Mood Lift×1
    102.7
    Catalog Erowid

    Tolerance & Pharmacokinetics

    drugs.wiki

    Tolerance Decay

    Full tolerance 3d Half tolerance 37d Baseline ~60d

    Experience Report Analysis

    Erowid
    33 Reports
    1999–2019 Date Range
    13 With Age Data
    17 Effects Detected

    Demographics

    Gender Distribution

    Age Distribution

    Reports Over Time

    Effect Analysis

    Erowid

    Effects aggregated from 33 experience reports (33 Erowid)

    33 Reports
    17 Effects Detected
    6 Positive
    6 Adverse
    5 Neutral

    Effect Sentiment Distribution

    Confidence Distribution

    Positive Effects 6

    Anxiety Suppression 51.5% 70%
    Sedation 24.2% 70%
    Stimulation 21.2% 70%
    Euphoria 18.2% 70%
    Empathy 18.2% 70%
    Music Enhancement 15.2% 70%

    Adverse Effects 6

    Psychosis 39.4% 70%
    Confusion 30.3% 70%
    Nausea 15.2% 70%
    Memory Suppression 9.1% 70%
    Increased Heart Rate 9.1% 70%
    Muscle Tension 9.1% 70%

    Dosage Distribution

    Dose distribution from experience reports

    Median: 2.0 mg IQR: 1.0–8.0 mg n=17

    Real-World Dose Distribution

    62K Doses

    From 45 individual dose entries

    Oral (n=35)

    Median: 2.0mg 25th: 1.0mg 75th: 3.0mg 90th: 4.0mg
    mg/kg median: 0.035 mg/kg 75th: 0.057

    Common Combinations

    Most co-occurring substances in experience reports

    Form / Preparation

    Most common forms and preparations reported

    Body-Weight Dosing

    Dose relative to body weight from reports with weight data

    Median: 0.044 mg/kg IQR: 0.017–0.18 mg/kg n=16

    Redose Patterns

    Redosing behavior across 25 reports

    4.0% Redosed
    1.1 Avg Doses
    15m Median Interval
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