Gomez Et Al. V. Pure Nootropics
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Nootropics: Boost Body and Brain? Report #2445
NOOTROPICS: BOOST BODY AND BRAIN? REPORT #2445 BACKGROUND: Nootropics were first discovered in 1960s, and were used to help people with motion sickness and then later were tested for memory enhancement. In 1971, the nootropic drug piracetam was studied to help improve memory. Romanian doctor Corneliu Giurgea was the one to coin the term for this drug: nootropics. His idea after testing piracetam was to use a Greek combination of “nous” meaning mind and “trepein” meaning to bend. Therefore the meaning is literally to bend the mind. Since then, studies on this drug have been done all around the world. One test in particular studied neuroprotective benefits with Alzheimer’s patients. More tests were done with analogues of piracetam and were equally upbeat. This is a small fraction of nootropic drugs studied over the past decade. Studies were done first on animals and rats and later after results from toxicity reports, on willing humans. (Source: https://www.purenootropics.net/general-nootropics/history-of-nootropics/) A COGNITIVE EDGE: Many decades of tests have convinced some people of how important the drugs can be for people who want an enhancement in life. These neuro-enhancing drugs are being used more and more in the modern world. Nootropics come in many forms and the main one is caffeine. Caffeine reduces physical fatigue by stimulating the body’s metabolism. The molecules can pass through the blood brain barrier to affect the neurotransmitters that play a role in inhibition. These molecule messengers can produce muscle relaxation, stress reduction, and onset of sleep. Caffeine is great for short–term focus and alertness, but piracetam is shown to work for long-term memory. -
(19) United States (12) Patent Application Publication (10) Pub
US 20130289061A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2013/0289061 A1 Bhide et al. (43) Pub. Date: Oct. 31, 2013 (54) METHODS AND COMPOSITIONS TO Publication Classi?cation PREVENT ADDICTION (51) Int. Cl. (71) Applicant: The General Hospital Corporation, A61K 31/485 (2006-01) Boston’ MA (Us) A61K 31/4458 (2006.01) (52) U.S. Cl. (72) Inventors: Pradeep G. Bhide; Peabody, MA (US); CPC """"" " A61K31/485 (201301); ‘4161223011? Jmm‘“ Zhu’ Ansm’ MA. (Us); USPC ......... .. 514/282; 514/317; 514/654; 514/618; Thomas J. Spencer; Carhsle; MA (US); 514/279 Joseph Biederman; Brookline; MA (Us) (57) ABSTRACT Disclosed herein is a method of reducing or preventing the development of aversion to a CNS stimulant in a subject (21) App1_ NO_; 13/924,815 comprising; administering a therapeutic amount of the neu rological stimulant and administering an antagonist of the kappa opioid receptor; to thereby reduce or prevent the devel - . opment of aversion to the CNS stimulant in the subject. Also (22) Flled' Jun‘ 24’ 2013 disclosed is a method of reducing or preventing the develop ment of addiction to a CNS stimulant in a subj ect; comprising; _ _ administering the CNS stimulant and administering a mu Related U‘s‘ Apphcatlon Data opioid receptor antagonist to thereby reduce or prevent the (63) Continuation of application NO 13/389,959, ?led on development of addiction to the CNS stimulant in the subject. Apt 27’ 2012’ ?led as application NO_ PCT/US2010/ Also disclosed are pharmaceutical compositions comprising 045486 on Aug' 13 2010' a central nervous system stimulant and an opioid receptor ’ antagonist. -
UFC PROHIBITED LIST Effective June 1, 2021 the UFC PROHIBITED LIST
UFC PROHIBITED LIST Effective June 1, 2021 THE UFC PROHIBITED LIST UFC PROHIBITED LIST Effective June 1, 2021 PART 1. Except as provided otherwise in PART 2 below, the UFC Prohibited List shall incorporate the most current Prohibited List published by WADA, as well as any WADA Technical Documents establishing decision limits or reporting levels, and, unless otherwise modified by the UFC Prohibited List or the UFC Anti-Doping Policy, Prohibited Substances, Prohibited Methods, Specified or Non-Specified Substances and Specified or Non-Specified Methods shall be as identified as such on the WADA Prohibited List or WADA Technical Documents. PART 2. Notwithstanding the WADA Prohibited List and any otherwise applicable WADA Technical Documents, the following modifications shall be in full force and effect: 1. Decision Concentration Levels. Adverse Analytical Findings reported at a concentration below the following Decision Concentration Levels shall be managed by USADA as Atypical Findings. • Cannabinoids: natural or synthetic delta-9-tetrahydrocannabinol (THC) or Cannabimimetics (e.g., “Spice,” JWH-018, JWH-073, HU-210): any level • Clomiphene: 0.1 ng/mL1 • Dehydrochloromethyltestosterone (DHCMT) long-term metabolite (M3): 0.1 ng/mL • Selective Androgen Receptor Modulators (SARMs): 0.1 ng/mL2 • GW-1516 (GW-501516) metabolites: 0.1 ng/mL • Epitrenbolone (Trenbolone metabolite): 0.2 ng/mL 2. SARMs/GW-1516: Adverse Analytical Findings reported at a concentration at or above the applicable Decision Concentration Level but under 1 ng/mL shall be managed by USADA as Specified Substances. 3. Higenamine: Higenamine shall be a Prohibited Substance under the UFC Anti-Doping Policy only In-Competition (and not Out-of- Competition). -
Gsk3β: a Master Player in Depressive Disorder Pathogenesis and Treatment Responsiveness
cells Review GSK3β: A Master Player in Depressive Disorder Pathogenesis and Treatment Responsiveness Przemysław Duda * , Daria Hajka , Olga Wójcicka , Dariusz Rakus and Agnieszka Gizak * Department of Molecular Physiology and Neurobiology, University of Wrocław, Sienkiewicza 21, 50-335 Wrocław, Poland; [email protected] (D.H.); [email protected] (O.W.); [email protected] (D.R.) * Correspondence: [email protected] (P.D.); [email protected] (A.G.); Tel.: +48713754135 (A.G.) Received: 4 February 2020; Accepted: 14 March 2020; Published: 16 March 2020 Abstract: Glycogen synthase kinase 3β (GSK3β), originally described as a negative regulator of glycogen synthesis, is a molecular hub linking numerous signaling pathways in a cell. Specific GSK3β inhibitors have anti-depressant effects and reduce depressive-like behavior in animal models of depression. Therefore, GSK3β is suggested to be engaged in the pathogenesis of major depressive disorder, and to be a target and/or modifier of anti-depressants’ action. In this review, we discuss abnormalities in the activity of GSK3β and its upstream regulators in different brain regions during depressive episodes. Additionally, putative role(s) of GSK3β in the pathogenesis of depression and the influence of anti-depressants on GSK3β activity are discussed. Keywords: GSK3β; MDD; depression; anti-depressants; AKT; BDNF; neuroprotection 1. Introduction 1.1. Major Depressive Disorder According to the World Health Organization’s statistics for March 2018, depression is a major contributor to the overall global burden of diseases. Globally, more than 300 million people suffer from depression. In the Diagnostic and Statistical Manual of Mental Disorders (DMS-5), major depressive disorder (MDD), the principal form of depression, is characterized by the following key symptoms: depressed mood and anhedonia (which are the fundamental symptoms), suicidal ideation, plan or attempt, fatigue, sleep deprivation, loss of weight and appetite, and psychomotor retardation [1]. -
NINDS Custom Collection II
ACACETIN ACEBUTOLOL HYDROCHLORIDE ACECLIDINE HYDROCHLORIDE ACEMETACIN ACETAMINOPHEN ACETAMINOSALOL ACETANILIDE ACETARSOL ACETAZOLAMIDE ACETOHYDROXAMIC ACID ACETRIAZOIC ACID ACETYL TYROSINE ETHYL ESTER ACETYLCARNITINE ACETYLCHOLINE ACETYLCYSTEINE ACETYLGLUCOSAMINE ACETYLGLUTAMIC ACID ACETYL-L-LEUCINE ACETYLPHENYLALANINE ACETYLSEROTONIN ACETYLTRYPTOPHAN ACEXAMIC ACID ACIVICIN ACLACINOMYCIN A1 ACONITINE ACRIFLAVINIUM HYDROCHLORIDE ACRISORCIN ACTINONIN ACYCLOVIR ADENOSINE PHOSPHATE ADENOSINE ADRENALINE BITARTRATE AESCULIN AJMALINE AKLAVINE HYDROCHLORIDE ALANYL-dl-LEUCINE ALANYL-dl-PHENYLALANINE ALAPROCLATE ALBENDAZOLE ALBUTEROL ALEXIDINE HYDROCHLORIDE ALLANTOIN ALLOPURINOL ALMOTRIPTAN ALOIN ALPRENOLOL ALTRETAMINE ALVERINE CITRATE AMANTADINE HYDROCHLORIDE AMBROXOL HYDROCHLORIDE AMCINONIDE AMIKACIN SULFATE AMILORIDE HYDROCHLORIDE 3-AMINOBENZAMIDE gamma-AMINOBUTYRIC ACID AMINOCAPROIC ACID N- (2-AMINOETHYL)-4-CHLOROBENZAMIDE (RO-16-6491) AMINOGLUTETHIMIDE AMINOHIPPURIC ACID AMINOHYDROXYBUTYRIC ACID AMINOLEVULINIC ACID HYDROCHLORIDE AMINOPHENAZONE 3-AMINOPROPANESULPHONIC ACID AMINOPYRIDINE 9-AMINO-1,2,3,4-TETRAHYDROACRIDINE HYDROCHLORIDE AMINOTHIAZOLE AMIODARONE HYDROCHLORIDE AMIPRILOSE AMITRIPTYLINE HYDROCHLORIDE AMLODIPINE BESYLATE AMODIAQUINE DIHYDROCHLORIDE AMOXEPINE AMOXICILLIN AMPICILLIN SODIUM AMPROLIUM AMRINONE AMYGDALIN ANABASAMINE HYDROCHLORIDE ANABASINE HYDROCHLORIDE ANCITABINE HYDROCHLORIDE ANDROSTERONE SODIUM SULFATE ANIRACETAM ANISINDIONE ANISODAMINE ANISOMYCIN ANTAZOLINE PHOSPHATE ANTHRALIN ANTIMYCIN A (A1 shown) ANTIPYRINE APHYLLIC -
Aniracetam Reduces Glutamate Receptor Desensitization and Slows
Proc. Natl. Acad. Sci. USA Vol. 88, pp. 10936-10940, December 1991 Neurobiology Aniracetam reduces glutamate receptor desensitization and slows the decay of fast excitatory synaptic currents in the hippocampus (non-N-methyl-D-aspartate receptor/synapse) JEFFRY S. ISAACSON*t AND ROGER A. NICOLLtt *Physiology Graduate Program and the Departments of SPharmacology and tPhysiology, University of California, San Francisco, CA 94143-0450 Communicated by Floyd E. Bloom, September 16, 1991 ABSTRACT Aniracetam is a nootropic drug that has been and DL-2-amino-5-phosphonovaleric acid (50 ,uM) were shown to selectively enhance quisqualate receptor-mediated added to the medium to block y-aminobutyric acid type A responses inXenopus oocytes injected with brain mRNA and in (GABAA) receptors and NMDA receptors, respectively. In hippocampal pyramidal cells [Ito, I., Tanabe, S., Kohda, A. & the majority of experiments examining iontophoretic re- Sugiyama, H. (1990) J. Physiol. (London) 424, 533-544]. We sponses, tetrodotoxin (0.5-1 1uM) was included to block have used patch clamp recording techniques in hippocampal sodium-dependent action potentials. Currents were recorded slices to elucidate the mechanism for this selective action. We with an Axopatch 1B amplifier from neurons in the CA1 and find that aniracetam enhances glutamate-evoked currents in CA3 pyramidal cell layers and granule cell layer of the whole-cell recordings and, in outside-out patches, strongly dentate gyrus using the "blind" whole-cell recording tech- reduces glutamate receptor desensitization. In addition, nique (15, 16). Patch electrodes (tip diameter = 2 Ium) aniracetam selectively prolongs the time course and increases contained (in mM) either a CsF (110 CsF, 10 CsCl, 10 Hepes, the peak amplitude of fast synaptic currents. -
Neuroenhancement in Healthy Adults, Part I: Pharmaceutical
l Rese ca arc ni h li & C f B o i o l e Journal of a t h n Fond et al., J Clinic Res Bioeth 2015, 6:2 r i c u s o J DOI: 10.4172/2155-9627.1000213 ISSN: 2155-9627 Clinical Research & Bioethics Review Article Open Access Neuroenhancement in Healthy Adults, Part I: Pharmaceutical Cognitive Enhancement: A Systematic Review Fond G1,2*, Micoulaud-Franchi JA3, Macgregor A2, Richieri R3,4, Miot S5,6, Lopez R2, Abbar M7, Lancon C3 and Repantis D8 1Université Paris Est-Créteil, Psychiatry and Addiction Pole University Hospitals Henri Mondor, Inserm U955, Eq 15 Psychiatric Genetics, DHU Pe-psy, FondaMental Foundation, Scientific Cooperation Foundation Mental Health, National Network of Schizophrenia Expert Centers, F-94000, France 2Inserm 1061, University Psychiatry Service, University of Montpellier 1, CHU Montpellier F-34000, France 3POLE Academic Psychiatry, CHU Sainte-Marguerite, F-13274 Marseille, Cedex 09, France 4 Public Health Laboratory, Faculty of Medicine, EA 3279, F-13385 Marseille, Cedex 05, France 5Inserm U1061, Idiopathic Hypersomnia Narcolepsy National Reference Centre, Unit of sleep disorders, University of Montpellier 1, CHU Montpellier F-34000, Paris, France 6Inserm U952, CNRS UMR 7224, Pierre and Marie Curie University, F-75000, Paris, France 7CHU Carémeau, University of Nîmes, Nîmes, F-31000, France 8Department of Psychiatry, Charité-Universitätsmedizin Berlin, Campus Benjamin Franklin, Eschenallee 3, 14050 Berlin, Germany *Corresponding author: Dr. Guillaume Fond, Pole de Psychiatrie, Hôpital A. Chenevier, 40 rue de Mesly, Créteil F-94010, France, Tel: (33)178682372; Fax: (33)178682381; E-mail: [email protected] Received date: January 06, 2015, Accepted date: February 23, 2015, Published date: February 28, 2015 Copyright: © 2015 Fond G, et al. -
NIH Public Access Author Manuscript Addict Biol
NIH Public Access Author Manuscript Addict Biol. Author manuscript; available in PMC 2014 January 01. Published in final edited form as: Addict Biol. 2013 January ; 18(1): 54–65. doi:10.1111/adb.12000. Enhanced AMPA Receptor Activity Increases Operant Alcohol Self-administration and Cue-Induced Reinstatement $watermark-text $watermark-text $watermark-text Reginald Cannadya,b, Kristen R. Fishera, Brandon Duranta, Joyce Besheera,b,c, and Clyde W. Hodgea,b,c,d aBowles Center for Alcohol Studies, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599 bCurriculum in Neurobiology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599 cDepartment of Psychiatry, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599 dDepartment of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599 Abstract Long-term alcohol exposure produces neuroadaptations that contribute to the progression of alcohol abuse disorders. Chronic alcohol consumption results in strengthened excitatory neurotransmission and increased AMPA receptor signaling in animal models. However, the mechanistic role of enhanced AMPA receptor activity in alcohol reinforcement and alcohol- seeking behavior remains unclear. This study examined the role of enhanced AMPA receptor function using the selective positive allosteric modulator, aniracetam, in modulating operant alcohol self-administration and cue-induced reinstatement. Male alcohol-preferring (P-) rats, trained to self-administer alcohol (15%, v/v) versus water were pretreated with aniracetam to assess effects on maintenance of alcohol self-administration. To determine reinforcer specificity, P-rats were trained to self-administer sucrose (0.8%, w/v) versus water, and effects of aniracetam were tested. -
Prohibited Substances List
Prohibited Substances List This is the Equine Prohibited Substances List that was voted in at the FEI General Assembly in November 2009 alongside the new Equine Anti-Doping and Controlled Medication Regulations(EADCMR). Neither the List nor the EADCM Regulations are in current usage. Both come into effect on 1 January 2010. The current list of FEI prohibited substances remains in effect until 31 December 2009 and can be found at Annex II Vet Regs (11th edition) Changes in this List : Shaded row means that either removed or allowed at certain limits only SUBSTANCE ACTIVITY Banned Substances 1 Acebutolol Beta blocker 2 Acefylline Bronchodilator 3 Acemetacin NSAID 4 Acenocoumarol Anticoagulant 5 Acetanilid Analgesic/anti-pyretic 6 Acetohexamide Pancreatic stimulant 7 Acetominophen (Paracetamol) Analgesic/anti-pyretic 8 Acetophenazine Antipsychotic 9 Acetylmorphine Narcotic 10 Adinazolam Anxiolytic 11 Adiphenine Anti-spasmodic 12 Adrafinil Stimulant 13 Adrenaline Stimulant 14 Adrenochrome Haemostatic 15 Alclofenac NSAID 16 Alcuronium Muscle relaxant 17 Aldosterone Hormone 18 Alfentanil Narcotic 19 Allopurinol Xanthine oxidase inhibitor (anti-hyperuricaemia) 20 Almotriptan 5 HT agonist (anti-migraine) 21 Alphadolone acetate Neurosteriod 22 Alphaprodine Opiod analgesic 23 Alpidem Anxiolytic 24 Alprazolam Anxiolytic 25 Alprenolol Beta blocker 26 Althesin IV anaesthetic 27 Althiazide Diuretic 28 Altrenogest (in males and gelidngs) Oestrus suppression 29 Alverine Antispasmodic 30 Amantadine Dopaminergic 31 Ambenonium Cholinesterase inhibition 32 Ambucetamide Antispasmodic 33 Amethocaine Local anaesthetic 34 Amfepramone Stimulant 35 Amfetaminil Stimulant 36 Amidephrine Vasoconstrictor 37 Amiloride Diuretic 1 Prohibited Substances List This is the Equine Prohibited Substances List that was voted in at the FEI General Assembly in November 2009 alongside the new Equine Anti-Doping and Controlled Medication Regulations(EADCMR). -
Summer 2017 P
In this Issue: • Toxicology Results Timelines Explained • Collection of Blood and Urine Samples for Tox Testing • New Opioid Drugs Implicated in Oregon Deaths • A New Tox Instrument Promises Improved Analysis • Tox Top 24: 2016 vs. 2011 SUMMER 2017 P a g OREGON STATE POLICE e Forensic Services Division Newsletter | TOXICOLOGY TOPICS STILL WAITING FOR THOSE TOX RESULTS? WHY DOES IT TAKE SO LONG? By Jeff Eitner, Springfield Lab The answer is more complicated than you may imagine. We know it can be frustrating to wait six months or longer for the results of a urine analysis. This timeline is a reflection of our backlog rather than the time required for analysis. Toxicology analysis takes place in the Portland Metro and Springfield Forensic Labs, and it typically requires two weeks or less to do the analysis and issue a report. The long waiting times are a function of a large backlog of old cases that has been created by chronic understaffing. A common misconception is that our analysis is equivalent to workplace drug testing, which only gives results on the potential presence of certain common drug classes, such as amphetamines, opiates, or benzodiazepines. Those results do not distinguish between controlled and non-controlled substances—a necessary part of DUII litigation. Our analysis specifically identifies the individual drugs present in a urine sample. For a toxicologist, the majority of the analytical time is spent reviewing large quantities of instrumental data. Each sample is first screened for general drug classes, and then analyzed on our gas chromatograph/ mass spectrometers (GC/MS) at least once. -
Designing a Formulation of the Nootropic Drug Aniracetam Using 2-Hydroxypropyl-Β-Cyclodextrin Suitable for Parenteral Administration
pharmaceutics Article Designing a Formulation of the Nootropic Drug Aniracetam Using 2-Hydroxypropyl-β-Cyclodextrin Suitable for Parenteral Administration Sebastian D. Goldsmith and Arlene McDowell * School of Pharmacy, University of Otago, Dunedin 9054, New Zealand; [email protected] * Correspondence: [email protected]; Tel.: +64-3479-7145 Received: 17 October 2018; Accepted: 15 November 2018; Published: 18 November 2018 Abstract: The nootropic drug aniracetam is greatly limited in its application by low aqueous solubility and a poor oral bioavailability. The primary aim of this study was to design a parenteral formulation of aniracetam that can be administered intravenously. Complexation of aniracetam with 2-hydroxypropyl-β-cyclodextrin (HP-β-CD) was investigated as a strategy to enhance solubility. A phase solubility analysis was performed to quantify the extent of improvement. An 819% increase in the solubility of aniracetam was obtained, reaching 36.44 mg/mL. This marked increase enables aniracetam to exist in an aqueous solvent at levels sufficient for parenteral dosing. A stability test was then devised using a design of experiment approach. The aniracetam-HP-β-CD formulation was subjected to different relative humidity and temperature and cyclodextrin concentrations over a 12-week period. Key changes in FTIR vibrational frequencies suggest the benzene moiety of aniracetam was introduced into the hydrophobic cavity of HP-β-CD. These results are highly supportive of the formation of a predictable 1:1 molar stoichiometric inclusion complex, explaining the improvement seen in physiochemical properties of aniracetam following formulation with HP-β-CD. This novel formulation of aniracetam suitable for parenteral administration will have utility in future studies to further elucidate the pharmacokinetics of this drug. -
Mechanism of Positive Allosteric Modulators Acting on AMPA Receptors
The Journal of Neuroscience, September 28, 2005 • 25(39):9027–9036 • 9027 Cellular/Molecular Mechanism of Positive Allosteric Modulators Acting on AMPA Receptors Rongsheng Jin,1 Suzanne Clark,4 Autumn M. Weeks,4 Joshua T. Dudman,2 Eric Gouaux,1,3 and Kathryn M. Partin4 1Department of Biochemistry and Molecular Biophysics, 2Center for Neurobiology and Behavior, and 3Howard Hughes Medical Institute, Columbia University, New York, New York 10032, and 4Department of Biomedical Sciences, Division of Neuroscience, Colorado State University, Fort Collins, Colorado 80523 Ligand-gated ion channels involved in the modulation of synaptic strength are the AMPA, kainate, and NMDA glutamate receptors. Small molecules that potentiate AMPA receptor currents relieve cognitive deficits caused by neurodegenerative diseases such as Alzheimer’s disease and show promise in the treatment of depression. Previously, there has been limited understanding of the molecular mechanism of action for AMPA receptor potentiators. Here we present cocrystal structures of the glutamate receptor GluR2 S1S2 ligand-binding domain in complex with aniracetam [1-(4-methoxybenzoyl)-2-pyrrolidinone] or CX614 (pyrrolidino-1,3-oxazino benzo-1,4-dioxan-10- one), two AMPA receptor potentiators that preferentially slow AMPA receptor deactivation. Both potentiators bind within the dimer interface of the nondesensitized receptor at a common site located on the twofold axis of molecular symmetry. Importantly, the poten- tiator binding site is adjacent to the “hinge” in the ligand-binding core “clamshell” that undergoes conformational rearrangement after glutamatebinding.Usingrapidsolutionexchange,patch-clampelectrophysiologyexperiments,weshowthatpointmutationsofresidues that interact with potentiators in the cocrystal disrupt potentiator function. We suggest that the potentiators slow deactivation by stabilizing the clamshell in its closed-cleft, glutamate-bound conformation.