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Impact of CYP2C19 Genotype on Sertraline Exposure in 1200 Scandinavian Patients
www.nature.com/npp ARTICLE Impact of CYP2C19 genotype on sertraline exposure in 1200 Scandinavian patients Line S. Bråten 1,2, Tore Haslemo1,2, Marin M. Jukic3,4, Magnus Ingelman-Sundberg 3, Espen Molden1,5 and Marianne K. Kringen1,2 Sertraline is an (SSRI-)antidepressant metabolized by the polymorphic CYP2C19 enzyme. The aim of this study was to investigate the impact of CYP2C19 genotype on the serum concentrations of sertraline in a large patient population. Second, the proportions of patients in the various CYP2C19 genotype-defined subgroups obtaining serum concentrations outside the therapeutic range of sertraline were assessed. A total of 2190 sertraline serum concentration measurements from 1202 patients were included retrospectively from the drug monitoring database at Diakonhjemmet Hospital in Oslo. The patients were divided into CYP2C19 genotype-predicted phenotype subgroups, i.e. normal (NMs), ultra rapid (UMs), intermediate (IMs), and poor metabolisers (PMs). The differences in dose-harmonized serum concentrations of sertraline and N-desmethylsertraline-to-sertraline metabolic ratio were compared between the subgroups, with CYP2C19 NMs set as reference. The patient proportions outside the therapeutic concentration range were also compared between the subgroups with NMs defined as reference. Compared with the CYP2C19 NMs, the sertraline serum concentration was increased 1.38-fold (95% CI 1.26–1.50) and 2.68-fold (95% CI 2.16–3.31) in CYP2C19 IMs and PMs, respectively (p < 0.001), while only a marginally lower serum concentration (−10%) was observed in CYP2C19 UMs (p = 0.012). The odds ratio for having a sertraline concentration above the therapeutic reference range was 1.97 (95% CI 1.21–3.21, p = 0.064) and 8.69 (95% CI 3.88–19.19, p < 0.001) higher for IMs and PMs vs. -
ZOLOFT® 50 Mg and 100 Mg Tablets
NEW ZEALAND DATA SHEET 1. PRODUCT NAME ZOLOFT® 50 mg and 100 mg tablets 2. QUALITATIVE AND QUANTITATIVE COMPOSITION Each 50 mg tablet contains sertraline hydrochloride equivalent to 50 mg sertraline. Each 100 mg tablet contains sertraline hydrochloride equivalent to 100 mg sertraline. For the full list of excipients, see section 6.1. 3. PHARMACEUTICAL FORM ZOLOFT 50 mg tablets: white film-coated tablets marked with the Pfizer logo on one side and “ZLT” scoreline “50” on the other. Approximate tooling dimensions are 1.03 cm x 0.42 cm x 0.36 cm. ZOLOFT 100 mg tablets: white film-coated tablets marked with the Pfizer logo on one side and “ZLT-100” or “ZLT 100” on the other. Approximate tooling dimensions are 1.31 cm x 0.52 cm x 0.44 cm. 4. CLINICAL PARTICULARS 4.1 Therapeutic indications Adults ZOLOFT is indicated for the treatment of symptoms of depression, including depression accompanied by symptoms of anxiety, in patients with or without a history of mania. Following satisfactory response, continuation with ZOLOFT therapy is effective in preventing relapse of the initial episode of depression or recurrence of further depressive episodes. ZOLOFT is indicated for the treatment of obsessive compulsive disorder (OCD). Following initial response, sertraline has been associated with sustained efficacy, safety and tolerability in up 2 years of treatment of OCD. ZOLOFT is indicated for the treatment of panic disorder, with or without agoraphobia. ZOLOFT is indicated for the treatment of post-traumatic stress disorder (PTSD). ZOLOFT is indicated for the treatment of social phobia (social anxiety disorder). -
Addyi Generic Name: Flibanserin Manufacturer
Brand Name: Addyi Generic Name: Flibanserin Manufacturer: Sprout Pharmaceuticals Drug Class: Central Nervous System Agent, Serotonin Agonist, Dopamine antagonist Uses: Labeled Uses: Indicated for the treatment of premenopausal women with acquired, generalized hypoactive sexual desire disorder (HSDD) as characterized by low sexual desire that causes marked distress or interpersonal difficulty and is NOT due to: A co-existing medical or psychiatric condition, problems within the relationship, or the effects of a medication or other drug substance. Unlabeled Uses: none. Mechanism of Action: The mechanism of action for flibanserin in the treatment of hypoactive sexual desire disorder is unknown. Flibanserin has high affinity for serotonin (5-hydroxytryptamine or 5-HT) 1A receptors, as an agonist, and 5-HT2A receptors, as an antagonist, and moderate affinity for 5- HT2B, 5-HT2C, and dopamine D4 receptors as an antagonist Pharmacokinetics: Absorption: Tmax 0.75 hours Vd 50L t ½ 11 hours Clearance Not reported Protein binding 98% (albumin) Bioavailability 33% Metabolism: Flibanserin is extensively metabolized primarily by CYP3A4 and, to a lesser extent, CYP2C19 to at least 35 metabolites, with most of the metabolites occurring in low concentrations in plasma. Elimination: Flibanserin is primarily excreted through the kidneys in to urine (44%) and feces (51%). Two metabolites could be characterized that showed plasma concentration similar to that achieved with flibanserin: 6,21-dihydroxy-flibanserin-6,21-disulfate and 6- hydroxy-flibanserin-6-sulfate. These two metabolites are inactive. Efficacy: Katz M, DeRogatis LR, Ackerman R, et al. Efficacy of flibanserin in women with hypoactive sexual desire disorder: results from the BEGONIA trial. J Sex Med. -
2015-02 Toxicology Rapid Testing Panel
SOUTH CAROLINA LAW ENFORCEMENT DIVISION NIKKI R. HALEY MARK A. KEEL Governor Chief FORENSIC SERVICES LABORATORY CUSTOMER NOTICE 2015-02 REGARDING TOXICOLOGY RAPID TESTING PANEL August 12, 2015 This notice is to inform the Coroners of South Carolina of a new testing panel available through the SLED Toxicology Department. On Monday, August 17th, the Toxicology Department will begin offering both a Rapid Testing Panel in addition to the already available Expanded Testing Panel. This Rapid Testing Panel is to be utilized in cases where the Expanded Testing Panel is not warranted, specifically where a cause of death has already been established. The Rapid Testing Panel will consist of volatiles analysis, to include, ethanol, acetone, isopropanol and methanol, drug screens, and drug confirmation/quantitation of positive screens. The cases assigned to the Rapid Testing Panel will have an expedited turnaround time. Targeted turn around times will be two weeks for negative cases and six weeks or less for positive cases. While every effort will be made to adhere to these time frames, additional time may be required on occasion due to the nature of postmortem samples. Submitters will be notified if there is a problem with a particular sample. Please see attachment regarding specifically which substances are covered by the Rapid Testing Panel and the Expanded Testing Panel. As always, a detailed case history and list of drugs suspected is appreciated. Rapid Panel and Expanded Panel will be choices available in iLAB. Please contact Lt. Dustin Smith (803-896-7385) with additional questions. ALI-359-T An Accredited Law Enforcement Agency P.O. -
Central Valley Toxicology Drug List
Chloroform ~F~ Lithium ~A~ Chlorpheniramine Loratadine Famotidine Acebutolol Chlorpromazine Lorazepam Fenoprofen Acetaminophen Cimetidine Loxapine Fentanyl Acetone Citalopram LSD (Lysergide) Fexofenadine 6-mono- Clomipramine acetylmorphine Flecainide ~M~ Clonazepam a-Hydroxyalprazolam Fluconazole Maprotiline Clonidine a-Hydroxytriazolam Flunitrazepam MDA Clorazepate Albuterol Fluoxetine MDMA Clozapine Alprazolam Fluphenazine Medazepam Cocaethylene Amantadine Flurazepam Meperidine Cocaine 7-Aminoflunitrazepam Fluvoxamine Mephobarbital Codeine Amiodarone Fosinopril Meprobamate Conine Amitriptyline Furosemide Mesoridazine Cotinine Amlodipine Methadone Cyanide ~G~ Amobarbital Methanol Cyclobenzaprine Gabapentin Amoxapine d-Methamphetamine Cyclosporine GHB d-Amphetamine l-Methamphetamine Glutethamide l-Amphetamine ~D~ Methapyrilene Guaifenesin Aprobarbital Demoxepam Methaqualone Atenolol Desalkylfurazepam ~H~ Methocarbamol Atropine Desipramine Halazepam Methylphenidate ~B~ Desmethyldoxepin Haloperidol Methyprylon Dextromethoraphan Heroin Metoclopramide Baclofen Diazepam Hexobarbital Metoprolol Barbital Digoxin Hydrocodone Mexiletine Benzoylecgonine Dihydrocodein Hydromorphone Midazolam Benzphetamine Dihydrokevain Hydroxychloroquine Mirtazapine Benztropine Diltiazem Hydroxyzine Morphine (Total/Free) Brodificoum Dimenhydrinate Bromazepam ~N~ Diphenhydramine ~I~ Bupivacaine Nafcillin Disopyramide Ibuprofen Buprenorphine Naloxone Doxapram Imipramine Bupropion Naltrexone Doxazosin Indomethacin Buspirone NAPA Doxepin Isoniazid Butabarbital Naproxen -
Supplementary Materials
Supplementary Materials Table S1. The significant drug pairs in potential DDIs examined by the two databases. Micromedex Drugs.com List of drugs paired PK-PD Mechanism details 1. Amiodarone— PD Additive QT-interval prolongation Dronedarone 2. Amiodarone— PK CYP3A inhibition by Ketoconazole Ketoconazole 3. Ciprofloxacin— PD Additive QT-interval prolongation Dronedarone 4. Cyclosporine— PK CYP3A inhibition by Cyclosporine Dronedarone 5. Dronedarone— PK CYP3A inhibition by Erythromycin Erythromycin 6. Dronedarone— PD Additive QT-interval prolongation Flecainide 7. Dronedarone— PK CYP3A4 inhibition by Itraconazole Itraconazole 8. Dronedarone— PK Contraindication Major CYP3A inhibition by Ketoconazole Ketoconazole 9. Dronedarone— PD Additive QT-interval prolongation Procainamide PD 10. Dronedarone—Sotalol Additive QT-interval prolongation 11. Felodipine— PK CYP3A inhibition by Itraconazole Itraconazole 12. Felodipine— PK CYP3A inhibition by Ketoconazole Ketoconazole 13. Itraconazole— PK CYP3A inhibition by Itraconazole Nisoldipine 14. Ketoconazole— PK CYP3A inhibition by Ketoconazole Nisoldipine 15. Praziquantel— PK CYP induction by Rifampin Rifampin PD 1. Amikacin—Furosemide Additive or synergistic toxicity 2. Aminophylline— Decreased clearance of PK Ciprofloxacin Theophylline by Ciprofloxacin 3. Aminophylline— PK Decreased hepatic metabolism Mexiletine 4. Amiodarone— PD Additive effects on QT interval Ciprofloxacin 5. Amiodarone—Digoxin PK P-glycoprotein inhibition by Amiodarone 6. Amiodarone— PD, PK Major Major Additive effects on QT Erythromycin prolongation, CYP3A inhibition by Erythromycin 7. Amiodarone— PD, PK Flecainide Antiarrhythmic inhibition by Amiodarone, CYP2D inhibition by Amiodarone 8. Amiodarone— PK CYP3A inhibition by Itraconazole Itraconazole 9. Amiodarone— PD Antiarrhythmic inhibition by Procainamide Amiodarone 10. Amiodarone— PK CYP induction by Rifampin Rifampin PD Additive effects on refractory 11. Amiodarone—Sotalol potential 12. Amiodarone— PK CYP3A inhibition by Verapamil Verapamil 13. -
Appendix 13C: Clinical Evidence Study Characteristics Tables
APPENDIX 13C: CLINICAL EVIDENCE STUDY CHARACTERISTICS TABLES: PHARMACOLOGICAL INTERVENTIONS Abbreviations ............................................................................................................ 3 APPENDIX 13C (I): INCLUDED STUDIES FOR INITIAL TREATMENT WITH ANTIPSYCHOTIC MEDICATION .................................. 4 ARANGO2009 .................................................................................................................................. 4 BERGER2008 .................................................................................................................................... 6 LIEBERMAN2003 ............................................................................................................................ 8 MCEVOY2007 ................................................................................................................................ 10 ROBINSON2006 ............................................................................................................................. 12 SCHOOLER2005 ............................................................................................................................ 14 SIKICH2008 .................................................................................................................................... 16 SWADI2010..................................................................................................................................... 19 VANBRUGGEN2003 .................................................................................................................... -
And N-Demethylation of Venlafaxine in Vitro by Human Liver Microsomes
O- and N-demethylation of Venlafaxine In Vitro by Human Liver Microsomes and by Microsomes from cDNA-Transfected Cells: Effect of Metabolic Inhibitors and SSRI Antidepressants Steven M. Fogelman, Jürgen Schmider, Karthik Venkatakrishnan, Lisa L. von Moltke, Jerold S. Harmatz, Richard I. Shader, and David J. Greenblatt The biotransformation of venlafaxine (VF) into its two to the formation of NDV for all four livers tested. major metabolites, O-desmethylvenlafaxine (ODV) and Parameters determined by applying a single-enzyme model 5 / / 5 N-desmethylvenlafaxine (NDV) was studied in vitro with were Vmax 2.14 nmol min mg protein, and Km 2504 human liver microsomes and with microsomes containing mM. Ketoconazole was a potent inhibitor of NDV individual human cytochromes from cDNA-transfected production, although its inhibitory activity was not as great human lymphoblastoid cells. VF was coincubated with as observed with pure 3A substrates. NDV formation was selective cytochrome P450 (CYP) inhibitors and several also reduced by 42% by a polyclonal rabbit antibody against selective serotonin reuptake inhibitors (SSRIs) to assess rat liver CYP3A1. Studies using expressed cytochromes their inhibitory effect on VF metabolism. Formation rates showed that NDV was formed by CYP2C9, 22C19, and for ODV incubated with human microsomes were 23A4. The highest intrinsic clearance was attributable to consistent with Michaelis-Menten kinetics for a single- CYP2C19 and the lowest to CYP3A4. However the high in enzyme mediated reaction with substrate inhibition. Mean vivo abundance of 3A isoforms will magnify the 5 parameters determined by non-linear regression were: Vmax importance of this cytochrome. Fluvoxamine (FX), at a / / 5 m m 0.36 nmol min mg protein, Km 41 M, and Ks 22901 concentration of 20 M, decreased NDV production by m M (Ks represents a constant which reflects the degree of 46% consistent with the capacity of FX to inhibit CYP3A, substrate inhibition). -
Comprehensive Panel, Blood
COMPREHENSIVE PANEL, BLOOD Blood Specimens (Order Code 70510) Alcohols Analgesics, cont. Anticonvulsants, cont. Antihistamines Acetone Norbuprenorphine Gabapentin Brompheniramine Ethanol Nortramadol Lamotrigine Cetirizine Isopropanol Oxaprozin Levetiracetam Chlorpheniramine Methanol Pentoxifylline Methsuximide Cyclizine Amphetamines Phenacetin Phenytoin Diphenhydramine Amphetamine Phenylbutazone Pregabalin Doxylamine BDB Piroxicam Primidone Fexofenadine Benzphetamine Salicylic Acid* Topiramate Guaifenesin Ephedrine Sulindac* Zonisamide Hydroxyzine MDA Tapentadol Antidepressants Loratadine MDMA Tizanidine Amitriptyline Oxymetazoline* Mescaline* Tolmetin Amoxapine Pyrilamine Methcathinone Tramadol Bupropion Tetrahydrozoline Methamphetamine Anesthetics Citalopram Triprolidine Phentermine Benzocaine Clomipramine Antipsychotics PMA Bupivacaine Desipramine 9-hydroxyrisperidone Phenylpropanolamine Etomidate Desmethylclomipramine Aripiprazole Pseudoephedrine Ketamine Dosulepin Buspirone Analgesics Lidocaine Doxepin Chlorpromazine Acetaminophen Mepivacaine Duloxetine Clozapine Baclofen Methoxetamine Fluoxetine Fluphenazine Buprenorphine Midazolam Fluvoxamine Haloperidol Carisoprodol Norketamine Imipramine Mesoridazine Cyclobenzaprine Pramoxine* 1,3-chlorophenylpiperazine (mCPP) Norclozapine Diclofenac Procaine Mianserin* Olanzapine Etodolac Rocuronium Mirtazapine Perphenazine Fenoprofen Ropivacaine Nefazodone Pimozide Hydroxychloroquine Antibiotics Norclomipramine Prochlorperazine Ibuprofen Azithromycin* Nordoxepin Quetiapine Ketoprofen Chloramphenicol* -
Toxicology Report Division of Toxicology Daniel D
Franklin County Forensic Science Center Office of the Coroner Anahi M. Ortiz, M.D. 2090 Frank Road Columbus, Ohio 43223 Toxicology Report Division of Toxicology Daniel D. Baker, Chief Toxicologist Casey Goodson Case # LAB-20-5315 Date report completed: January 28, 2021 A systematic toxicological analysis has been performed and the following agents were detected. Postmortem Blood: Gray Top Thoracic ELISA Screen Acetaminophen Not Detected ELISA Screen Barbiturates Not Detected ELISA Screen Benzodiazepines Not Detected ELISA Screen Benzoylecgonine Not Detected ELISA Screen Buprenorphine Not Detected ELISA Screen Cannabinoids See Confirmation ELISA Screen Fentanyl Not Detected ELISA Screen Methamphetamine Not Detected ELISA Screen Naltrexone/Naloxone Not Detected ELISA Screen Opiates Not Detected ELISA Screen Oxycodone/Oxymorphone Not Detected ELISA Screen Salicylates Not Detected ELISA Screen Tricyclics Not Detected Page 1 of 4 Casey Goodson Case # LAB-20-5315 GC/FID Ethanol Not Detected GC/MS Acidic/Neutral Drugs None Detected GC/MS Nicotine Positive GC/MS Cotinine Positive Reference Lab Delta-9-THC 13 ng/mL Reference Lab 11-Hydroxy-Delta-9-THC 1.2 ng/mL Reference Lab 11-Nor-9-Carboxy-Delta-9-THC 15 ng/mL Postmortem Urine: Gray Top Urine GC/MS Cotinine Positive This report has been verified as accurate and complete by ______________________________________ Daniel D. Baker, M.S., F-ABFT Cannabinoid quantitations in blood were performed by NMS Labs, Horsham, PA. Page 2 of 4 Casey Goodson Case # LAB-20-5315 Postmortem Toxicology Scope of Analysis Franklin County Coroner’s Office Division of Toxicology Enzyme Linked Immunosorbant Assay (ELISA) Blood Screen: Qualitative Presumptive Compounds/Classes: Acetaminophen (cut-off 10 µg/mL), Benzodiazepines (cut-off 20 ng/mL), Benzoylecgonine (cut-off 50 ng/mL), Cannabinoids (cut-off 40 ng/mL), Fentanyl (cut-off 1 ng/mL), Methamphetamine/MDMA (cut-off 50 ng/mL), Opiates (cut-off 40 ng/mL), Oxycodone/Oxymorphone (cut-off 40 ng/mL), Salicylates (50 µg/mL). -
Determination of Sertraline and Its Metabolite by High-Pressure Liquid Chromatography in Plasma
ACADEMIA ROMÂNĂ Rev. Roum. Chim., Revue Roumaine de Chimie 2015, 60(5-6), 543-548 http://web.icf.ro/rrch/ DETERMINATION OF SERTRALINE AND ITS METABOLITE BY HIGH-PRESSURE LIQUID CHROMATOGRAPHY IN PLASMA Nazan YUCE-ARTUN,a Erguvan Tuğba ÖZEL KIZIL,b Bora BASKAK,b Halise Devrimci ÖZGÜVEN,b Yalçın DUYDUc and Halit Sinan SUZENc,* aBiotechnology Institute, Ankara University, Golbasi, Ankara, Turkey bDepartment of Psychiatry, School of Medicine, Ankara University, Dikimevi, Ankara, Turkey cDepartment of Toxicology, Faculty of Pharmacy, Ankara University, Tandogan, Ankara, Turkey Received November 10, 2014 A fast, simple and sensitive high-pressure liquid chromatography (HPLC) method with UV detection was developed for frequently prescribed antidepressant, sertraline (SERT) and its main B metabolite N-desmethylsertraline (DSERT), in human plasma. SERT and DSERT were extracted by an optimized solid phase chromatographic (SPE) method using C-18 cartridges and DSE SER Clomipramine was used as external standard (ES). The analytes ES were separated on C18, 4.6 mm × 150 mm, 5 µm column at 50 °C with a mobile phase of 45% acetonitrile + 55% NaH2PO4 at a flow rate of 0.4 mL/min. Detector responses monitored at 4 different wave-lengths; 200-205-210-215 nm. The method proved to be rapid and effective for the plasma sample analyses of therapeutic drug monitoring for sertraline treated patients. INTRODUCTION* depression, panic disorder, generalised anxiety disorder, and social phobia.2 Like other SSRIs, it High rates of poor compliance, considerable has a wide therapeutic index and seems to be better genetic variability in metabolism, and the clinical tolerated than tricyclic antidepressants.3 The drug heterogeneity of depression are the main problems is slowly absorbed with a time to peak plasma for the practical application of selective serotonin concentration of approximately 4–8 h and an reuptake inhibitors (SSRI).1 Therapeutic drug elimination half life of 22–35 h. -
Clinical Trial of the Neuroprotectant Clomethiazole in Coronary Artery Bypass Graft Surgery a Randomized Controlled Trial Robert S
Anesthesiology 2002; 97:585–91 © 2002 American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins, Inc. Clinical Trial of the Neuroprotectant Clomethiazole in Coronary Artery Bypass Graft Surgery A Randomized Controlled Trial Robert S. Kong, F.R.C.A.,* John Butterworth, M.D.,† Wynne Aveling, F.R.C.A.,‡ David A. Stump, M.D.,† Michael J. G. Harrison, F.R.C.P.,§ John Hammon, M.D.,ʈ Jan Stygall, M.Sc.,# Kashemi D. Rorie, Ph.D.,** Stanton P. Newman, D.Phil.†† Background: The neuroprotective property of clomethiazole THE efficacy of coronary artery bypass surgery in the has been demonstrated in several animal models of global and relief of angina and in some circumstances in enhancing Downloaded from http://pubs.asahq.org/anesthesiology/article-pdf/97/3/585/335909/0000542-200209000-00011.pdf by guest on 29 September 2021 focal brain ischemia. In this study the authors investigated the life expectation is now accepted. It is a tribute to the low effect of clomethiazole on cerebral outcome in patients under- mortality of the procedure that interest is now focused going coronary artery bypass surgery. Methods: Two hundred forty-five patients scheduled for on the neurologic and neuropsychological complica- 1–3 coronary artery bypass surgery were recruited at two centers tions. Adverse neurologic outcomes have been found and prospectively randomized to clomethiazole edisilate to occur in 2–6% of patients and neuropsychological (0.8%), 225 ml (1.8 mg) loading dose followed by a maintenance deficits in 10–30%.4–6 These complications are consid- dose of 100 ml/h (0.8 mg/h) during surgery, or 0.9% NaCl ered to be ischemic in nature, being a consequence of (placebo) in a double-blind trial.