The Neuroprotective Effects of Mood Stabilizers
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Curriculum Vitae Full Name: David M. Marks, M.D. Contact: [email protected] Mobile (619) 822-7117 Credentials: Diplomate, American Board of Psychiatry and Neurology (Psychiatry) Subspecialty Certification in Psychosomatic Medicine Diplomate, American Board of Pain Medicine Position Title: Associate Professor Department of Psychiatry and Behavioral Sciences Department of Community and Family Medicine Duke University Medical Center Duke Clinical Research Institute Duke Pain and Palliative Care Clinic Education: Institution & Location Degree Year Conferred Field of Study University of California at San Diego Fellowship 1999 - 2000 Consultation and San Diego, CA Liaison Psychiatry Medical College of Pennsylvania / Senior 1998 - 1999 Psychiatry Clinical Neuroscience Research Unit Resident Philadelphia, PA University of California at San Diego Resident 1995 - 1998 Psychiatry San Diego, CA University of Texas Medical Branch M.D. 1995 Galveston, TX Rice University B.A. 1991 Psychology Houston, TX Research and Professional Experience: Position Institution/Employer & Location Dates of Employment Attending Faculty Physician Duke Pain and Palliative Care Clinic 09/08-present (Chronic Pain Management) Attending Faculty Physician Duke University Medical Center, 07/06-present Inpatient Psychiatric Service, Emergency Service, Consultation/Liaison Service Attending Faculty Physician Durham Regional Hospital, 09/08-07/11 Consultation/Liaison Service Medical Director, Inpatient and Duke University Medical Center 07/06 – 02/07 Emergency Psychiatry Services Medical Director, CNS Division EStudy Site 05/05 -- 07/06 La Mesa, Oceanside, National City CA Chief Executive Officer/Medical Optimum Health Services 01/02 – 05/05 Director La Mesa, Oceanside CA Chief of Staff Alvarado Parkway Institute 01/04 – 01/05 1 La Mesa, CA Page _____________________________________________________________________ David M. -
Ie-O-JY -CH2 S (56) References Cited Wherein N Is 0 to 6, X" and Y Are Independently H, Cl, F, CH, CH, CH, CH, OCH, OH, CF, OCF, NO, U.S
US005574060A United States Patent (19) 11) Patent Number: 5,574,060 Rothman et al. (45) Date of Patent: Nov. 12, 1996 54 SELECTIVE INHIBITORS OF BIOGENIC "Hydrindene Derivatives as Potential Oral Hypoglycemic AMINE TRANSPORTERS Agents: N-Alkyl 1,2,3,3a,4,8b-Hexahydroindeno1,2-b) pyrroles', De et al., Journal of Pharmaceutical Sciences, vol. (75) Inventors: Richard Rothman, Silver Spring, Md.; 62, No. 8, Aug. 1973, pp. 1363-1364. Frank J. Carroll, Durham, N.C.; Bruce Blough, Raleigh, N.C.; Samuel (List continued on next page.) W. Mascarella, Hillsborough, N.C. Primary Examiner-Mark L. Berch (73) Assignees: The United States of America as Attorney, Agent, or Firm-Morgan & Finnegan LLP represented by the Department of 57) ABSTRACT Health and Human Services, Washington, D.C.; Office of Technology The present invention provides a compound having the Transfer, Bethesda, Md.; Research Structure: Triangle Institue, Research Triangle Park, N.C. (21) Appl. No.: 203,222 22 Filed: Feb. 28, 1994 Related U.S. Application Data H 63 Continuation-in-part of Ser. No. 105,747, Aug. 12, 1993, abandoned. wherein X, Y, and Z are independently H, Cl, Br, F, OCH, I, or an alkyl group having 1 to 6 carbon atoms; and R is (51) Int. Cl." .......................... A61K 31/40; A61K 31/47; C07D 403/06; C07D 471/08 X (52) U.S. Cl. ............................ 514/411; 546/94; 546/146; 54.6/150; 548/427: 548/428 58) Field of Search .............................. 548/427; 514/411 -ie-O-JY -CH2 S (56) References Cited wherein n is 0 to 6, X" and Y are independently H, Cl, F, CH, CH, CH, CH, OCH, OH, CF, OCF, NO, U.S. -
New Drug Evaluation Monograph Template
© 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: Second Generation Antidepressant Medications Month/Year of Review: May 2014 Last Oregon Review: April 2012 PDL Classes: Psychiatric: Antidepressants Source Document: OSU College of Pharmacy New drug(s): vortioxetine (Brintellix®) Manufacturer: Takeda & Lundbeck/Forest levomilnacipran extended-release (Fetzima®) Dossier Received: Yes/Pending Current Status of Voluntary PDL Class: Preferred Agents: BUPROPION HCL TABLET/TABLET ER, CITALOPRAM TABLET/SOLUTION, FLUOXETINE CAPSULE/SOLUTION/TABLET, FLUVOXAMINE, MIRTAZEPINE TAB RAPDIS/TABLET, PAROXETINE TABLET, SERTRALINE ORAL CONC/TABLET, VENLAFAXINE TABLET, VENLAFAXINE ER Non-Preferred Agents: BUPROPRION XL, DESVENLAFAXINE (PRISTIQ ER), DULOXETINE (CYMBALTA®), ESCITALOPRAM, FLUOXETINE DF (PROZAC® WEEKLY), NEFAZODONE, PAROXETINE HCL (PAXIL CR®), SELEGILINE PATCH (ENSAM®), VILAZODONE (VIIBRYD®), OLANZAPINE/FLUOXETINE (SYMBYAX®) Status of the Voluntary Mental Health Preferred Drug List Currently, all antidepressants are available without prior authorization for non-preferred placement. Oregon law prohibits traditional methods of PDL enforcement on mental health drugs. Second generation antidepressants have been reviewed for clinical efficacy and safety and specific agents were chosen as clinically preferred; this eliminates a copay. Oregon’s Medicaid program currently -
Can N-Methyl-D-Aspartate Receptor Hypofunction in Schizophrenia Be Localized to an Individual Cell Type?
REVIEW published: 21 November 2019 doi: 10.3389/fpsyt.2019.00835 Can N-Methyl-D-Aspartate Receptor Hypofunction in Schizophrenia Be Localized to an Individual Cell Type? Alexei M. Bygrave 1, Kasyoka Kilonzo 2, Dimitri M. Kullmann 3, David M. Bannerman 4 and Dennis Kätzel 2* 1 Department of Neuroscience, Johns Hopkins University, Baltimore, MD, United States, 2 Institute of Applied Physiology, Ulm University, Ulm, Germany, 3 UCL Queen Square Institute of Neurology, University College London, London, United Kingdom, 4 Department of Experimental Psychology, University of Oxford, Oxford, United Kingdom Hypofunction of N-methyl-D-aspartate glutamate receptors (NMDARs), whether caused by endogenous factors like auto-antibodies or mutations, or by pharmacological or genetic manipulations, produces a wide variety of deficits which overlap with—but do not precisely match—the symptom spectrum of schizophrenia. In order to understand how NMDAR hypofunction leads to different components of the syndrome, it is necessary to take into account which neuronal subtypes are particularly affected by it in terms of detrimental Edited by: functional alterations. We provide a comprehensive overview detailing findings in rodent Bernat Kocsis, Harvard Medical School, models with cell type–specific knockout of NMDARs. Regarding inhibitory cortical cells, United States an emerging model suggests that NMDAR hypofunction in parvalbumin (PV) positive Reviewed by: interneurons is a potential risk factor for this disease. PV interneurons display a selective Margarita Behrens, Salk Institute for Biological Studies, vulnerability resulting from a combination of genetic, cellular, and environmental factors United States that produce pathological multi-level positive feedback loops. Central to this are two Vasileios Kafetzopoulos, antioxidant mechanisms—NMDAR activity and perineuronal nets—which are themselves Harvard Medical School, United States impaired by oxidative stress, amplifying disinhibition. -
Cerebellar Toxicity of Phencyclidine
The Journal of Neuroscience, March 1995, 75(3): 2097-2108 Cerebellar Toxicity of Phencyclidine Riitta N&kki, Jari Koistinaho, Frank Ft. Sharp, and Stephen M. Sagar Department of Neurology, University of California, and Veterans Affairs Medical Center, San Francisco, California 94121 Phencyclidine (PCP), clizocilpine maleate (MK801), and oth- Phencyclidine (PCP), dizocilpine maleate (MK801), and other er NMDA antagonists are toxic to neurons in the posterior NMDA receptor antagonistshave attracted increasing attention cingulate and retrosplenial cortex. To determine if addition- becauseof their therapeutic potential. These drugs have neuro- al neurons are damaged, the distribution of microglial ac- protective properties in animal studies of focal brain ischemia, tivation and 70 kDa heat shock protein (HSP70) induction where excitotoxicity is proposedto be an important mechanism was studied following the administration of PCP and of neuronal cell death (Dalkara et al., 1990; Martinez-Arizala et MK801 to rats. PCP (10-50 mg/kg) induced microglial ac- al., 1990). Moreover, NMDA antagonists decrease neuronal tivation and neuronal HSP70 mRNA and protein expression damage and dysfunction in other pathological conditions, in- in the posterior cingulate and retrosplenial cortex. In ad- cluding hypoglycemia (Nellgard and Wieloch, 1992) and pro- dition, coronal sections of the cerebellar vermis of PCP (50 longed seizures(Church and Lodge, 1990; Faingold et al., 1993). mg/kg) treated rats contained vertical stripes of activated However, NMDA antagonists are toxic to certain neuronal microglial in the molecular layer. In the sagittal plane, the populations in the brain. Olney et al. (1989) demonstratedthat microglial activation occurred in irregularly shaped patch- the noncompetitive NMDA antagonists,PCP, MK801, and ke- es, suggesting damage to Purkinje cells. -
RTI-4793-14, a New Ligand with High Affinity and Selectivity For
SYNAPSE 16:59-65 (1994) RTI-4793-14, a New Ligand With High Affinity and Selectivity for the ( +)-MK801-Insensitive [3H]1 -[ 1 -( 2- thienyl)cyclohexyl]piperidine Binding Site (PCP Site 2) of Guinea Pig Brain CARL B. GOODMAN, D. NIGEL THOMAS, AGU PERT, BETSEY EMILIEN, JEAN L. CADET, F. IVY CARROLL, BRUCE E. BLOUGH, S. WAYNE MASCARELLA, MICHAEL A. ROGAWSKI, SWAMINATHAN SUBRAMANIAM, AM) RICHARD B. ROTHMAN Clinical Psychopharmacology Section, NIDMNIH Addiction Research Center, Baltimore, Maryland 21224 (C.B.G., B.E., J.L.C., R.B.R.); Biological Psychiatry Branch, NZMH (D.N.T., A.P.) and Neuronal Excitability Section, Epilepsy Research Branch, NINDS (M.A.R., S.S.), NIH, Bethesda, Maryland 20892; and Chemistry and Life Sciences, Organic and Medicinal Chemistry, Research Triangle Institute, Research Triangle Park, North Carolina 27709-2194 (F.I.C., B.E.B., S.W.M.) KEY WORDS Phencyclidine receptor, RTI-4793-14, PCP, Biogenic amine reuptake carrier, ( + )-MK801, Guinea pig brain ABSTRACT L3HlTCP, an analog of the dissociative anesthetic phencyclidine (PCP), binds with high affinity to two sites in guinea pig brain membranes, one that is MK-801 sensitive and one that is not. The MK-801-sensitive site (PCP site 1) is associated with NMDA receptors, whereas the MK-801-insensitive site (PCP site 2) may be associated with biogenic amine transporters (BAT).Although several “BAT ligands” are known that bind selectively to PCP site 2 and not to PCP site 1 (such as indatraline), these corn- pounds have low affinity for site 2 (K, values > 1 pM). Here we demonstrate that the novel pyrrole RTI-4793-14 is a selective, high affinity ligand for PCP site 2. -
United States Patent (10 ) Patent No.: US 10,660,887 B2 Javitt (45 ) Date of Patent: *May 26 , 2020
US010660887B2 United States Patent (10 ) Patent No.: US 10,660,887 B2 Javitt (45 ) Date of Patent : *May 26 , 2020 (54 ) COMPOSITION AND METHOD FOR (56 ) References Cited TREATMENT OF DEPRESSION AND PSYCHOSIS IN HUMANS U.S. PATENT DOCUMENTS 6,228,875 B1 5/2001 Tsai et al. ( 71 ) Applicant : Glytech , LLC , Ft. Lee , NJ (US ) 2004/0157926 A1 * 8/2004 Heresco - Levy A61K 31/198 514/561 (72 ) Inventor: Daniel C. Javitt , Ft. Lee , NJ (US ) 2005/0261340 Al 11/2005 Weiner 2006/0204486 Al 9/2006 Pyke et al . 2008/0194631 Al 8/2008 Trovero et al. ( 73 ) Assignee : GLYTECH , LLC , Ft. Lee , NJ (US ) 2008/0194698 A1 8/2008 Hermanussen et al . 2010/0069399 A1 * 3/2010 Gant CO7D 401/12 ( * ) Notice : Subject to any disclaimer, the term of this 514 / 253.07 patent is extended or adjusted under 35 2010/0216805 Al 8/2010 Barlow 2011/0207776 Al 8/2011 Buntinx U.S.C. 154 ( b ) by 95 days . 2011/0237602 A1 9/2011 Meltzer This patent is subject to a terminal dis 2011/0306586 Al 12/2011 Khan claimer . 2012/0041026 A1 2/2012 Waizumi ( 21 ) Appl. No.: 15 /650,912 FOREIGN PATENT DOCUMENTS CN 101090721 12/2007 ( 22 ) Filed : Jul. 16 , 17 KR 2007 0017136 2/2007 WO 2005/065308 7/2005 (65 ) Prior Publication Data WO 2005/079756 9/2005 WO 2011044089 4/2011 US 2017/0312275 A1 Nov. 2 , 2017 WO 2012/104852 8/2012 WO 2005/000216 9/2013 WO 2013138322 9/2013 Related U.S. Application Data (63 ) Continuation of application No. -
Current Phase III Clinical Trials
Toolbox: Current phase III clinical trials Tiffany-Jade Kreys, PharmD1 1Assistant Professor of Pharmacy Practice University of the Incarnate Word Feik School of Pharmacy, San Antonio, Texas KEYWORDS clinical trials, depression, bipolar, schizophrenia, medications Table 1. Novel Agents for Major Depression, Bipolar Disorder, and/or Schizophrenia Product Name Sponsor Indication Mechanism of Action (previous name) Downloaded from http://meridian.allenpress.com/mhc/article-pdf/2/6/138/2094102/mhc_n129046.pdf by guest on 26 September 2021 Amitifadine Euthymics MDD Triple Reuptake Inhibitor (EB-1010) Bioscience (1:2:8 ratio of serotonin: norepinephrine: dopamine inhibition) Bitopertin Roche Schizophrenia Glycine reuptake inhibitor (RG1678) Enhances NMDA receptor activity Brexpiprazole Lundbeck MDD, Claimed to have "broad activity across multiple monoamine (OPC-34712) Otsuka America Schizophrenia systems and exhibits reduced partial agonist activity at D2 Pharmaceuticals receptors and enhanced affinity for specific serotonin receptors" Cariprazine Forest Laboratories BPAD, MDD adjunct D3-preferring/D2 receptor partial agonist (RGH-188) therapy, Schizophrenia Citalopram/ PharmaNeuro- MDD 5HT2A/D4 antagonist Pipamperone Boost (PNB01) Edivoxetine Eli Lilly MDD adjunct therapy Norepinephrine reuptake inhibitor (LY2216684) Vortioxetine Lundbeck MDD In vitro studies: 5HT3 and 7 receptor antagonist, 5HT1B partial (LUAA21004) Takeda agonist, 5HT1A agonist, serotonin transporter inhibitor Pharmaceuticals In vivo: Increases serotonin, norepinephrine, dopamine, -
Patent Application Publication ( 10 ) Pub . No . : US 2019 / 0192440 A1
US 20190192440A1 (19 ) United States (12 ) Patent Application Publication ( 10) Pub . No. : US 2019 /0192440 A1 LI (43 ) Pub . Date : Jun . 27 , 2019 ( 54 ) ORAL DRUG DOSAGE FORM COMPRISING Publication Classification DRUG IN THE FORM OF NANOPARTICLES (51 ) Int . CI. A61K 9 / 20 (2006 .01 ) ( 71 ) Applicant: Triastek , Inc. , Nanjing ( CN ) A61K 9 /00 ( 2006 . 01) A61K 31/ 192 ( 2006 .01 ) (72 ) Inventor : Xiaoling LI , Dublin , CA (US ) A61K 9 / 24 ( 2006 .01 ) ( 52 ) U . S . CI. ( 21 ) Appl. No. : 16 /289 ,499 CPC . .. .. A61K 9 /2031 (2013 . 01 ) ; A61K 9 /0065 ( 22 ) Filed : Feb . 28 , 2019 (2013 .01 ) ; A61K 9 / 209 ( 2013 .01 ) ; A61K 9 /2027 ( 2013 .01 ) ; A61K 31/ 192 ( 2013. 01 ) ; Related U . S . Application Data A61K 9 /2072 ( 2013 .01 ) (63 ) Continuation of application No. 16 /028 ,305 , filed on Jul. 5 , 2018 , now Pat . No . 10 , 258 ,575 , which is a (57 ) ABSTRACT continuation of application No . 15 / 173 ,596 , filed on The present disclosure provides a stable solid pharmaceuti Jun . 3 , 2016 . cal dosage form for oral administration . The dosage form (60 ) Provisional application No . 62 /313 ,092 , filed on Mar. includes a substrate that forms at least one compartment and 24 , 2016 , provisional application No . 62 / 296 , 087 , a drug content loaded into the compartment. The dosage filed on Feb . 17 , 2016 , provisional application No . form is so designed that the active pharmaceutical ingredient 62 / 170, 645 , filed on Jun . 3 , 2015 . of the drug content is released in a controlled manner. Patent Application Publication Jun . 27 , 2019 Sheet 1 of 20 US 2019 /0192440 A1 FIG . -
AHRQ Healthcare Horizon Scanning System – Status Update
AHRQ Healthcare Horizon Scanning System – Status Update Horizon Scanning Status Update: January 2014 Prepared for: Agency for Healthcare Research and Quality U.S. Department of Health and Human Services 540 Gaither Road Rockville, MD 20850 www.ahrq.gov Contract No. HHSA290201000006C Prepared by: ECRI Institute 5200 Butler Pike Plymouth Meeting, PA 19462 January 2014 Statement of Funding and Purpose This report incorporates data collected during implementation of the Agency for Healthcare Research and Quality (AHRQ) Healthcare Horizon Scanning System by ECRI Institute under contract to AHRQ, Rockville, MD (Contract No. HHSA290201000006C). The findings and conclusions in this document are those of the authors, who are responsible for its content, and do not necessarily represent the views of AHRQ. No statement in this report should be construed as an official position of AHRQ or of the U.S. Department of Health and Human Services. A novel intervention may not appear in this report simply because the System has not yet detected it. The list of novel interventions in the Horizon Scanning Status Update Report will change over time as new information is collected. This should not be construed as either endorsements or rejections of specific interventions. As topics are entered into the System, individual target technology reports are developed for those that appear to be closer to diffusion into practice in the United States. A representative from AHRQ served as a Contracting Officer’s Technical Representative and provided input during the implementation of the horizon scanning system. AHRQ did not directly participate in the horizon scanning, assessing the leads or topics, or provide opinions regarding potential impact of interventions. -
Lääkeaineiden Yleisnimet (INN-Nimet) 21.6.2021
Lääkealan turvallisuus- ja kehittämiskeskus Säkerhets- och utvecklingscentret för läkemedelsområdet Finnish Medicines Agency Lääkeaineiden yleisnimet (INN-nimet) 21.6. -
The Long-Term Effects of Fluoxetine on Stress- Related Behaviour and Acute Monoaminergic
The long-term effects of fluoxetine on stress- related behaviour and acute monoaminergic stress response in stress sensitive rats Nico Johan Badenhorst BChD 24307734 Dissertation submitted in partial fulfilment of the requirements for the degree Magister Scientiae in Pharmacology at the Potchefstroom Campus of North-West University Supervisor: Prof C.B. Brink Co-supervisor: Prof L. Brand Assisting Supervisor: Prof B.H. Harvey November 2014 Abstract: Fluoxetine and escitalopram are the only antidepressants approved by the Food and Drug Administration of the United States of America (FDA) for treatment of major depression in children and adolescents. Both drugs are selective serotonin reuptake inhibitors (SSRIs). In recent years there has been a growing concern over the long-term developmental effects of early-life exposure to SSRIs. The current study employed male Flinders Sensitive Line (FSL) rats, a well described and validated translational model of depression, to investigate the long term effects of pre- pubertal fluoxetine exposure. First we examined the effect of such early-life exposure on the development of depressive-like behaviour, locomotor activity and anxiety-like behaviour as manifested in early adulthood. Next, the current study investigated the effect of pre-pubertal fluoxetine exposure on the acute monoaminergic stress response, as displayed later in life. Animals received either saline (vehicle control), or 10 mg/kg/day fluoxetine from postnatal day (ND+) 21 to ND+34 (pre-puberty). The treatment period was chosen to coincide with a developmental phase where the serotonergic system’s neurodevelopment had been completed, yet the noradrenergic and dopaminergic systems had not, a scenario comparable to neurodevelopment in human adolescents.