DOCSLIB.ORG

Profile of Amisulpride

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text

Load more

Profile of Amisulpride Graylands Hospital Drug Bulletin 2002 Vol 10 No 2 July ISSN 1323-1251 Amisulpride (Solian) will become the Pharmacokinetics latest addition to the range of atypical Absorption antipsychotics available in Australia, Amisulpride is absorbed rapidly, within 3- though it has been available in parts of 4 hours of oral administration. Europe since the late 1980s. It belongs to the benzamide class and will be available Metabolism on the PBS for the treatment of Amisulpride undergoes minimal schizophrenia from 1st August 2002. metabolism to form two metabolites (both inactive). Hepatic metabolism plays a Pharmacology limited role in healthy patients. Although it shares clinical properties that characterise other atypical agents eg. Excretion decreased incidence of extrapyramidal Excretion is primarily via urine (mainly as symptoms (EPS), amisulpride is unusual in unchanged drug). The elimination half- that it lacks the combined antagonism of life is approximately 12 hours. Plasma protein binding is low, therefore drug 5HT2/D2 receptors which usually defines “atypicality”. interactions due to displacement are unlikely. At low doses, amisulpride enhances Efficacy dopaminergic neurotransmission by Recent reviews have concluded that preferentially blocking pre-synaptic D /D 2 3 amisulpride (400 to 1200mg/day) was as dopamine receptors. This may explain its effective as haloperidol (5 to 40mg/day), efficacy in the treatment of negative flupenthixol (25mg/day) and risperidone symptoms in schizophrenia. (8mg/day) in patients with acute exacerbations of schizophrenia with At higher doses, amisulpride antagonises predominantly positive symptoms (1,2). post-synaptic D /D dopamine receptors, 2 3 Amisulpride was found to be more reducing dopaminergic transmission, effective than haloperidol but equally as which may explain its efficacy against the effective as risperidone in controlling positive symptoms of schizophrenia. negative symptoms. Amisulpride has little affinity for other In patients with predominantly persistent dopamine receptor subtypes or other negative symptoms, low dosages of neurotransmitter receptors such as amisulpride (50 to 300mg/day) serotonin, α-adrenergic, histamine and significantly reduced negative symptoms muscarinic. It is selective for dopamine compared to placebo. receptors in the limbic system rather than Amisulpride has been shown to be the striatum, which should reduce its efficacious in long-term studies where it tendency to produce EPS. has been used as maintenance therapy in patients with chronic schizophrenia with Graylands Hospital Drug Bulletin 2002 Vol 10 No 2 July - 1 - mixed symptoms. Long-term use was also Mixed positive and negative symptoms: associated with improvements in measures adjust dose to obtain optimal control of of quality of life and social functioning. positive symptoms. Contraindications Amisulpride has been available in France to These include prolactin-dependant treat schizophrenia since 1986, where a group of clinicians have produced a dosage tumours, phaeochromocytoma and use in (3) combination with medications that may algorithm (see Figure 1 below). This induce torsade de pointes – see drug suggests management strategies according interactions. to symptoms and treatment setting. Due to its lack of sedative properties, it may Precautions be appropriate in the initial stages to use a Amisulpride shares similar warnings with benzodiazepine or sedative antipsychotic to other atypical antipsychotics regarding the help control the symptoms of a very rare events of neuroleptic malignant disturbed or aggressive patient. syndrome, seizures and the need for No specific titration is required for initiation caution in the elderly and Parkinson’s of therapy; adjust dosage to individual disease. response. Where the dose is above or equal In renal impairment, use a decreased dose to 400mg, administer twice daily. and consider intermittent treatment in Preferably give the dose before meals. severe cases. Use with caution in patients with moderate Renal impairment Dosage reduction will be or severe hepatic impairment – limited required in this patient group. data. Hepatic impairment Dosage reduction should not be necessary as the drug is Pregnancy and Lactation Pregnancy Category B3 – Contraindicated. weakly metabolised. Figure 1: Amisulpride dosage algorithm Adverse effects (based on extensive use in France). Similarly to risperidone, amisulpride appears to be linked with dose-related EPS ACUTE EPISODES and hyperprolactinemia. Unlike other Severe & recurrent Mild-moderate First episode atypicals however, sedation and Treated patients Out-patients Untreated patients Initial dose 800mg/d Initial dose 400mg/d Initial dose 600mg/d hypotension do not prominently feature in (up to 1200mg/d ↑by 200mg/d steps its side-effect profile. for in-patients) Adequate dose : 800mg/d Other commonly reported adverse events in clinical trials included insomnia, anxiety, agitation and weight gain. Cases of QT prolongation have been reported (dose dependant) and very rarely (<0.01%) SHORT-TERM FOLLOW-UP (3 months) torsade de pointes. According to symptom evolution No reference is made in the product Reduce dose Continue treatment Increase dose information to possible disturbances in by 200mg/d steps at same dose by 200mg/d steps glucose metabolism. During the period January 1997 to January 2002, the manufacturers received only 3 reports of this nature worldwide (Personal MAINTENANCE communication, Sanofi-Synthelabo). Modulation according to symptoms No positive symptoms Dosage and administration Patient stable The recommended dose varies according Dose reduced by 100-200mg/d every 2-3 months to which symptoms predominate. Usual maintenance dose: 400mg/d Acute positive symptoms: 400-800mg/day (two divided doses). May be increased to 1200mg/day in individual cases (no If +ve symptoms reappear If -ve symptoms present superior efficacy proven). Increase dose to previous Decrease dose to 100-300mg/d stabilising level for Usual dose 100mg/d Predominantly negative symptoms: 50- several months before 300mg/day given once daily. renewed dose reduction Adapted from Reference 3 Graylands Hospital Drug Bulletin 2002 Vol 10 No 2 July - 2 - Switching to amisulpride be enhanced by amisulpride. Concomitant Taper down existing antipsychotic and during use with levodopa is not recommended due this period, begin amisulpride at the to reciprocal antagonism of effects. therapeutic dose required; no titration is necessary. Overlapping periods of 1-4 weeks Conclusion – place in therapy have been described depending on the Amisulpride appears to offer no significant patient’s clinical state. benefit over the existing atypical agents. It may be associated with the least weight Drug Interactions gain of the atypicals (4) and has less Interactions via the CYP450 system are potential for interaction with other drugs, unlikely as amisulpride is not significantly due to its lack of hepatic metabolism. metabolised by the liver. Further trials are needed comparing it with the other atypical agents. Comparative The potential for increased risk of ventricular data with olanzapine should be available arrhythmias must be borne in mind. Use with later this year. Class IA and III antiarrhythmic agents eg. flecainide and amiodarone respectively, is Presentation contraindicated. Caution is required in the Manufacturer: Sanofi-Synthelabo concomitant use of drugs that may induce Brand name: Solian bradycardia or hypokalemia or other drugs Available in following tablet strengths: known to prolong the QT interval, such as 100mg, 200mg and 400mg (all breakable). thioridazine and droperidol. References Caution is advised when used with other 1. Curran MP and Perry CM. Amisulpride – A Review of its Use in the Management of Schizophrenia. Drugs renally cleared drugs eg. lithium, which may 2001;61(14):2123-2150. interfere with clearance of amisulpride. 2. Leucht S, Pitschel-Walz G, Engel RR, Kissling W. However, a study of the concomitant use of Amisulpride, an Unusual “Atypical” Antipsychotic: a lithium carbonate (500mg twice daily) with Meta-Analysis of Randomised Controlled Trials. Am J Psychiatry 2002;159:180-190. low dose amisulpride (100mg twice daily) in 3. Lecrubier Y, Azorin M, Bottai T, Dalery J, Garreau G, healthy young males, showed no effect of Lemperiere T et al. Consensus on the Practical Use of amisulpride on the pharmacokinetics of Amisulpride, an Atypical Antipsychotic, in the Treatment lithium. of Schizophrenia. Neuropsychobiology 2001;44:41-46. 4. Taylor DM and McAskill R. Atypical Antipsychotics and Weight Gain – a Systematic Review. Acta Psychiatr The effects of CNS depressants eg. Scand. 2000;101(6):416-32. benzodiazepines, narcotics and alcohol may Serotonin syndrome – recognising the signs Serotonin syndrome (SS) is a condition ! concomitant use of agents that caused by drug-induced serotonin promote the release of serotonin from hyperstimulation. It is difficult to diagnose, presynaptic neurons eg. amphetamines usually mild and as a result may go largely ! pharmacokinetic interactions eg. unreported. SS may occur with co- CYP2D6 inhibition of tricyclic administration of drugs or lack of adequate antidepressant (TCA) metabolism by washout period when switching drugs. This agents such as paroxetine, bupropion, increases synaptic serotonin concentration leading to increased TCA plasma levels causing hyperstimulation of mainly 5HT1A ! inhibition of serotonin metabolism eg. receptors (other serotonin receptors may be
Recommended publications
  • Aristada™ (Aripiprazole Lauroxil)

    Aristada™ (Aripiprazole Lauroxil)

    Aristada™ (aripiprazole lauroxil) – New Drug Approval • On October 5, 2015, Alkermes’ announced the FDA approval of Aristada (aripiprazole lauroxil) extended-release injection, an atypical antipsychotic, for the treatment of schizophrenia. • Schizophrenia is a chronic, severe and disabling brain disorder affecting an estimated 2.4 million Americans. Typically, symptoms include hearing voices, believing other people are reading their minds or controlling their thoughts, and being suspicious or withdrawn. • Aristada’s approval was based on data from a double-blind, placebo-controlled 12-week trial involving 622 patients with schizophrenia. In addition, the efficacy of Aristada was established, in part, on the basis of efficacy data from trials with oral aripiprazole. — Aristada significantly improved symptoms of schizophrenia compared to placebo at day 85. • Similar to other atypical antipsychotics, Aristada carries a boxed warning for increased mortality in elderly patients with dementia-related psychosis. • Other warnings and precautions for Aristada include cerebrovascular adverse reactions, including stroke; neuroleptic malignant syndrome; tardive dyskinesia; metabolic changes; orthostatic hypotension; leukopenia, neutropenia, and agranulocytosis; seizures; potential for cognitive and motor impairment; body temperature regulation; and dysphagia. • The most common adverse reaction (≥ 5% and at least twice that for placebo) with Aristada use was akathisia. • Aristada is administered by intramuscular injection in the deltoid (441 mg dose only) or gluteal (441 mg, 662 mg, or 882 mg) muscle by a healthcare professional. — Aristada can be initiated at a monthly dose (441 mg, 662 mg or 882 mg) or every 6 week dose (882 mg). — For patients naïve to aripiprazole, tolerability should be established with oral aripiprazole prior to initiating treatment with Aristada.
  • Product Monograph

    Product Monograph

    PRODUCT MONOGRAPH PrFLUANXOL® Flupentixol Tablets (as flupentixol dihydrochloride) 0.5 mg, 3 mg, and 5 mg PrFLUANXOL® DEPOT Flupentixol Decanoate Intramuscular Injection 2% and 10% flupentixol decanoate Antipsychotic Agent Lundbeck Canada Inc. Date of Revision: 2600 Alfred-Nobel December 12th, 2017 Suite 400 St-Laurent, QC H4S 0A9 Submission Control No : 209135 Page 1 of 35 Table of Contents PART I: HEALTH PROFESSIONAL INFORMATION .........................................................3 SUMMARY PRODUCT INFORMATION ........................................................................3 INDICATIONS AND CLINICAL USE ..............................................................................3 CONTRAINDICATIONS ...................................................................................................4 WARNINGS AND PRECAUTIONS ..................................................................................4 ADVERSE REACTIONS ..................................................................................................10 DRUG INTERACTIONS ..................................................................................................13 DOSAGE AND ADMINISTRATION ..............................................................................15 OVERDOSAGE ................................................................................................................18 ACTION AND CLINICAL PHARMACOLOGY ............................................................19 STORAGE AND STABILITY ..........................................................................................21
  • Pharmacotherapy, Drug-Drug Interactions and Potentially

    Pharmacotherapy, Drug-Drug Interactions and Potentially

    medRxiv preprint doi: https://doi.org/10.1101/2021.03.31.21254518; this version posted April 6, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license . Pharmacotherapy, drug-drug interactions and potentially inappropriate medication in depressive disorders Jan Wolff1,2,3, Pamela Reißner4, Gudrun Hefner5, Claus Normann2, Klaus Kaier6, Harald Binder6, Christoph Hiemke7, Sermin Toto8, Katharina Domschke2, Michael Marschollek1, Ansgar Klimke4,9 1 Peter L. Reichertz Institute for Medical Informatics of TU Braunschweig and Hannover Medical School, Germany. 2 Department of Psychiatry and Psychotherapy, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany. 3 Evangelical Foundation NeuerKerode, Germany. 4 Vitos Hochtaunus, Friedrichsdorf, Germany. 5 Vitos Clinic for Forensic Psychiatry, Eltville, Germany 6 Institute of Medical Biometry and Statistics, Medical Center - University of Freiburg, Faculty of Medicine, University of Freiburg, Germany. 7 Department of Psychiatry and Psychotherapy, University Medical Center Mainz, Germany. 8 Department of Psychiatry, Social Psychiatry and Psychotherapy, Hannover Medical School, Germany. 9 Heinrich-Heine-University Düsseldorf, Germany. ___ Correspondence Dr. Jan Wolff, Peter L. Reichertz Institute for Medical Informatics of TU Braunschweig and Hannover Medical School, Hannover, Germany. Address: Karl- Wiechert-Allee 3, 30625 Hannover. Email: [email protected], wolff.jan@mh- hannover.de, ORCID: https://orcid.org/0000-0003-2750-0606 Key words (MeSH) Depression, Polypharmacy, Antidepressants, Hospitals, Drug Interactions, Psychiatry NOTE: This preprint reports new research that has not been certified by peer review and should not be used to guide clinical practice.
  • Amisulpride Tablets I.P. SOLIAN® THERAPEUTIC CATEGORY Anti-Psychotic COMPOSITION Solian® 50 /100 /200 /400 Each Uncoated Tablet Contains Amisulpride IP

    Amisulpride Tablets I.P. SOLIAN® THERAPEUTIC CATEGORY Anti-Psychotic COMPOSITION Solian® 50 /100 /200 /400 Each Uncoated Tablet Contains Amisulpride IP

    For the use only of a Registered Medical Practitioner (Psychiatrist) or a Hospital or a Laboratory Abridged Prescribing Information Amisulpride tablets I.P. SOLIAN® THERAPEUTIC CATEGORY Anti-psychotic COMPOSITION Solian® 50 /100 /200 /400 Each uncoated tablet contains Amisulpride IP. 50mg / 100mg / 200mg Each film coated tablet contains Amisulpride IP 400mg. THERAPEUTIC INDICATIONS Treatment of acute and chronic schizophrenic disorders, in which positive symptoms (such as delusions, hallucinations, and thought disorders) and/or negative symptoms (such as blunted affect, emotional and social withdrawal) are prominent, including patients characterised by predominant negative symptoms. DOSAGE AND ADMINISTRATION For acute psychotic episodes, oral doses between 400 and 800 mg/d are recommended. Doses above 1200 mg/d should not be used. For patients with mixed positive and negative symptoms, doses should be adjusted to obtain optimal control of positive symptoms. Maintenance treatment should be established individually with the minimally effective dose. For patients characterised by predominant negative symptoms, oral doses between 50 mg/d and 300 mg/d are recommended. Doses should be adjusted individually. Solian® can be administered once daily at oral doses up to 300 mg, higher doses should be administered bid. The Minimum effective dose should be used. Caution in elderly. Renal & Hepatic insufficiency: Dose should be reduced. Use of amisulpride from puberty to 18 years is not recommended. SAFETY-RELATED INFORMATION Contraindications: Hypersensitivity to amisulpride or to other ingredients of the product; concomitant prolactin- dependent tumours e.g. pituitary gland prolactinomas and breast cancer; phaeochromocytoma; children up to puberty; lactation; combinations with drugs which could induce torsades de pointes and levodopa.
  • Aripiprazole Augmentation of Clomipramine Therapy In

    Aripiprazole Augmentation of Clomipramine Therapy In

    Dusunen Adam The Journal of Psychiatry and Neurological Sciences 2016;29:167-172 Case Report / Olgu Sunumu DOI: 10.5350/DAJPN2016290209 Aripiprazole Augmentation Filiz Izci1, Murat Yalcin2, Sumeyye Yasemin Kurtulus Calli2, of Clomipramine Therapy in Yagmur Sever3, Rabia Bilici3 1Istanbul Bilim University, Faculty of Medicine, Treatment-Resistant Department of Psychiatry, Istanbul - Turkey 2Kocaeli Derince Training and Research Hospital, Department of Psychiatry, Kocaeli - Turkey Obsessive-Compulsive 3Erenkoy Training and Research Hospital for Psychiatric and Neurological Disorders, Istanbul - Turkey Disorder: Case Series ABSTRACT Aripiprazole augmentation of clomipramine therapy in treatment-resistant obsessive-compulsive disorder: case series Obsessive-compulsive disorder (OCD) is a chronic disorder characterized by recurrent intrusive thoughts and repetitive rituals, causing significant distress and functional loss. Studies show evidence about serotonergic and dopaminergic mechanisms in neuropathogenesis of OCD. Selective serotonin re-uptake inhibitors (SSRI) are considered as first-line treatment in OCDs, but treatment resistance may occur in 40-60% of cases treated with SSRIs. Augmentation of antidepressants with atypical antipsychotics is an important treatment option in treatment-resistant patients with OCD. In this article, we aimed to present five OCD cases with treatment-resistance in which we obtained good outcomes, with addition of aripiprazole 10-30mg per day to clomipramine therapy. Address reprint requests to / Yazışma adresi:
  • Current P SYCHIATRY

    Current P SYCHIATRY

    Current p SYCHIATRY N ew Investigators Tips to manage and prevent discontinuation syndromes Informed tapering can protect patients when you stop a medication Sriram Ramaswamy, MD Shruti Malik, MBBS, MHSA Vijay Dewan, MD Instructor, department of psychiatry Foreign medical graduate Assistant professor Creighton University Department of psychiatry Omaha, NE University of Nebraska Medical Center Omaha, NE bruptly stopping common psychotropics New insights on psychotropic A —particularly antidepressants, benzodi- drug safety and side effects azepines, or atypical antipsychotics—can trigger a discontinuation syndrome, with: This paper was among those entered in the 2005 • rebound or relapse of original symptoms Promising New Investigators competition sponsored • uncomfortable new physical and psycho- by the Neuroleptic Malignant Syndrome Information Service (NMSIS). The theme of this year’s competition logical symptoms was “New insights on psychotropic drug safety and • physiologic withdrawal at times. side effects.” To increase health professionals’ awareness of URRENT SYCHIATRY 1 C P is honored to publish this peer- the risk of these adverse effects, this article reviewed, evidence-based article on a clinically describes discontinuation syndromes associated important topic for practicing psychiatrists. with various psychotropics and offers strategies to NMSIS is dedicated to reducing morbidity and anticipate, recognize, and manage them. mortality of NMS by improving medical and psychiatric care of patients with heat-related disorders; providing
  • Effects of Typical and Atypical Antipsychotics and Receptor

    Effects of Typical and Atypical Antipsychotics and Receptor

    Effects of Typical and Atypical Antipsychotics and Receptor Selective Compounds on Acetylcholine Efflux in the Hippocampus of the Rat Sudabeh Shirazi-Southall, M.A., Dana Ellen Rodriguez, A.H.T., George G. Nomikos, M.D., Ph.D. Some atypical antipsychotic drugs appear to improve 100,907), the 5-HT2C (SB 242,084), the 5-HT6 (Ro 04-6790), ␣ cognitive function in schizophrenia and since acetylcholine the D2 (raclopride) receptors, and the 1-adrenoceptors (ACh) is of importance in cognition, we used in vivo (prazosin) modestly increased ACh by about 50%. The ϩ ␣ microdialysis to examine the effects of antipsychotics 5-HT1A agonist R-( )-8-OH-DPAT and the 2- administered acutely (SC or IP) at pharmacologically adrenoceptor antagonist yohimbine significantly increased comparable doses on ACh outflow in the hippocampus of the ACh by about 100% and 50%, respectively. Thus, olanzapine rat. The atypical antipsychotics olanzapine and clozapine and clozapine increased ACh to a greater extent than other tested produced robust increases in ACh up to 1500% and 500%, antipsychotics, explaining perhaps their purported beneficial respectively. The neuroleptics haloperidol, thioridazine, and effect in cognitive function in schizophrenia. It appears that chlorpromazine, as well as the atypical antipsychotics selective activity at each of the monoaminergic receptors studied risperidone and ziprasidone produced modest increases in is not the sole mechanism underlying the olanzapine and ACh by about 50–100%. Since most atypical antipsychotics clozapine induced increases in hippocampal ACh. affect a variety of monoaminergic receptors, we examined [Neuropsychopharmacology 26:583–594, 2002] whether selective ligands for some of these receptors affect © 2002 American College of Neuropsychopharmacology.
  • SAFETY of the ELECTROCONVULSIVE THERAPY and AMISULPRIDE COMBINATION Rozália Takács1, Zsolt Iványi2, Gabor S

    SAFETY of the ELECTROCONVULSIVE THERAPY and AMISULPRIDE COMBINATION Rozália Takács1, Zsolt Iványi2, Gabor S

    Psychiatria Danubina, 2013; Vol. 25, No. 1, pp 76-79 Brief report © Medicinska naklada - Zagreb, Croatia SAFETY OF THE ELECTROCONVULSIVE THERAPY AND AMISULPRIDE COMBINATION Rozália Takács1, Zsolt Iványi2, Gabor S. Ungvari3, 4 & Gábor Gazdag1,5 1Department of Psychiatry and Psychotherapy, Faculty of Medicine, Semmelweis University, Budapest, Hungary 2 Department of Anesthesiology and Intensive Therapy, Faculty of Medicine, Semmelweis University, Budapest, Hungary 3University of Notre Dame, Australia 4Marian Centre, Perth, Australia 5Consultation–Liaison Psychiatric Service, Szent István and Szent László Hospitals, Budapest, Hungary received: 21.10.2011; revised: 16.1.2012; accepted: 2.12.2012 SUMMARY Background: Electroconvulsive therapy is frequently considered when pharmacotherapy is ineffective. In such cases the combination of the two treatment modalities are commonly used. Amisulpiride, a second generation antipsychotic drug is used in the treatment of schizophrenia and psychotic depression. When amisulpiride is ineffective as a monotherapy, combination with ECT could be an option to enhance its efficacy. To the best of our knowledge, to date there have been no data about the safety of this combination. Subjects and methods: Medical notes of all patients who were given ECT while on amisulpiride were selected from the archives of the Department of Psychiatry, Semmelweis University Medical School, Budapest, covering a 10-year period. A randomly selected matched control group was formed from patients who underwent ECT but were not taking amisulpiride. Patients in both groups also received a variety of psychotropic drugs other than amisulpide. Side effects were compared between the two groups of patients. Results: Twenty patients received amisulpride with ECT. The most common side effects were headache, hypertension, tachycardia, nausea, dizziness, confusion, psychomotor agitation, sialorrhea, and prolonged seizure activity.
  • Atypical Antipsychotics

    Atypical Antipsychotics

    Pharmacy Policy Bulletin Category: Managed Rx Coverage Number: J-307 Subject: Atypical Antipsychotics Effective Date Begin: September 1, 2010 Effective Date End: Original Date: March 4, 2009 Review Date(s): March 3, 2010 September 2, 2009 March 4, 2009 NOTE: This version of the policy is effective 9/1/2010, the previous version is effective up to 8/31/20. Please click version 002 of J- 307 below for more details. Policy Applies to: Commercial Plans. Agents addressed in this policy: Abilify (aripiprazole), Symbyax (olanzapine & fluoxetine), Seroquel XR (quetiapine) Background: Antipsychotics are used to treat a myriad of mental health conditions. There are two categories of antipsychotics, first generation or typical antipsychotics and second generation or atypical antipsychotics. Typical antipsychotics (e.g, chlorpromazine) exhibit a high incidence of adverse reactions such as extrapyramidal signs (EPS) and tardive dyskinesia at clinically effective doses. Atypical antipsychotics (e.g. quetiapine, risperidone, olanzapine) may exhibit adverse reactions mentioned above but the incidence is much less often. It is important that both classes of drugs are utilized in appropriate patient populations. The US Food and Drug Administration has required manufacturers of all antipsychotic drugs to add a boxed warning to the drugs' prescribing information about the risk of mortality in elderly patients treated for dementia-related psychosis. Abilify (aripiprazole) is an atypical antipsychotic that is approved for the treatment of schizophrenia, bipolar mania, and as adjunctive treatment of major depressive disorder (MDD). The mechanism of action is unknown but it has been proposed that aripiprazole acts as a partial agonist against D2 and 5-HT1A receptors and antagonist activity at 5-HT2A receptors.
  • Antipsychotics

    Antipsychotics

    © Copyright 2012 Oregon State University. All Rights Reserved Drug Use Research & Management Program Oregon State University, 500 Summer Street NE, E35 Salem, Oregon 97301-1079 Phone 503-947-5220 | Fax 503-947-1119 Class Update with New Drug Evaluations: Antipsychotics Date of Review: May 2016 End Date of Literature Search: February 2016 New Drugs: brexpiprazole Brand Names (Manufacturer): Rexulti® (Otsuka) cariprazine Vraylar™ (Actavis) Dossiers Received: yes PDL Classes: Antipsychotics, First generation Antipsychotics, Second generation Antipsychotics, Parenteral Current Status of PDL Class: See Appendix 1. Purpose for Class Update: Several new antipsychotic drug products have been approved by the U.S. Food and Drug Administration since these drug classes were last reviewed by the Oregon Health Plan (OHP) Pharmacy and Therapeutics Committee. Research Questions: 1. Is there new comparative evidence of meaningful difference in efficacy or effectiveness outcomes for schizophrenia, bipolar mania or major depressive disorders (MDD) between oral antipsychotic agents (first‐ or second‐generation) or between parenteral antipsychotic agents (first‐ or second‐generation)? 2. Is there new comparative evidence of meaningful difference in harms between oral antipsychotic agents (first‐ or second‐generation) or between parenteral antipsychotic agents (first‐ or second‐generation)? 3. Is there new comparative evidence of meaningful difference in effectiveness or harms in certain subpopulations based on demographic characteristics? Conclusions: There is insufficient evidence of clinically meaningful differences between antipsychotic agents in efficacy or effectiveness or harms between antipsychotic agents for schizophrenia, bipolar mania or MDD. There is insufficient evidence to determine if brexpiprazole and cariprazine offer superior efficacy or safety to other antipsychotic agents for schizophrenia. There is insufficient evidence to determine if brexpiprazole offers superior efficacy or safety to other antipsychotic agents for MDD.
  • Pharmacogenetic Studies Investigating the Adverse Effects of Antipsychotics

    Pharmacogenetic Studies Investigating the Adverse Effects of Antipsychotics

    online © ML Comm 0REVIEW ARTICLE0 Psychiatry Investig 2007;4:66-75 Print ISSN 1738-3684 / On-line ISSN 1976-3026 Pharmacogenetic Studies Investigating the Adverse Effects of Antipsychotics Heon-Jeong Lee, MD, PhD The pharmacogenetic study of antipsychotics has been developed along with the develop- Department of Psychiatry, ment of general techniques of genetic analysis. Because there are no significant differences Division of Brain Korea in the clinical efficacy of the various antipsychotics, it is important to prevent the adverse 21 for Biomedical Science, Korea University College of Medicine, effects of antipsychotics. Therefore, pharmacogenetic studies concerning antipsychotics have Seoul, Korea been primarily focused on their adverse effects. The most significant finding of the previous studies is the association between drug effects and drug metabolic polymorphisms, mainly in the cytochrome P450 (CYP) genes. Patients with genetically determined to be CYP poor metabolizers (PMs) may require lower doses of antipsychotic medications. On the other hand, CYP ultrarapid matabolizers (UMs) will need an increased dosage in order to obtain a therapeutic response. Genetic variations in the dopamine and serotonin receptor genes have been reported to be associated with the adverse effects of antipsychotics, reflecting the affinities that most antipsychotics have for these receptors. In particular, there is evidence to suggest an association between dopamine 2 receptor polymorphisms and a dopamine 3 receptor polymorphism and antipsychotic-induced tardive dyskinesia. Several studies were recently performed to determine the genetic susceptibility to antipsychotic-induced weight gain and metabolic syndrome. Adrenergic 2a receptor, leptin gene, and serotonin 2C receptor gene variants have been reported to be associated with drug-induced weight gain.
  • HALDOL Decanoate 50 (Haloperidol)

    HALDOL Decanoate 50 (Haloperidol)

    HALDOL® Decanoate 50 (haloperidol) HALDOL® Decanoate 100 (haloperidol) For IM Injection Only WARNING Increased Mortality in Elderly Patients with Dementia-Related Psychosis Elderly patients with dementia-related psychosis treated with antipsychotic drugs are at an increased risk of death. Analyses of seventeen placebo-controlled trials (modal duration of 10 weeks), largely in patients taking atypical antipsychotic drugs, revealed a risk of death in drug-treated patients of between 1.6 to 1.7 times the risk of death in placebo-treated patients. Over the course of a typical 10-week controlled trial, the rate of death in drug-treated patients was about 4.5%, compared to a rate of about 2.6% in the placebo group. Although the causes of death were varied, most of the deaths appeared to be either cardiovascular (e.g., heart failure, sudden death) or infectious (e.g., pneumonia) in nature. Observational studies suggest that, similar to atypical antipsychotic drugs, treatment with conventional antipsychotic drugs may increase mortality. The extent to which the findings of increased mortality in observational studies may be attributed to the antipsychotic drug as opposed to some characteristic(s) of the patients is not clear. HALDOL Decanoate is not approved for the treatment of patients with dementia-related psychosis (see WARNINGS). DESCRIPTION Haloperidol decanoate is the decanoate ester of the butyrophenone, HALDOL (haloperidol). It has a markedly extended duration of effect. It is available in sesame oil in sterile form for intramuscular (IM) injection. The structural formula of haloperidol decanoate, 4-(4-chlorophenyl)-1-[4-(4-fluorophenyl)-4-oxobutyl]-4 piperidinyl decanoate, is: Haloperidol decanoate is almost insoluble in water (0.01 mg/mL), but is soluble in most organic solvents.