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Methadone Information Your Safety and the Safety of Everyone
Methadone Information Your Safety and the Safety of Everyone Methadone, when taken as prescribed is safe. Methadone taken by any individual it is NOT prescribed to, can be deadly; and when mixed with other drugs, can be deadly; and in the hands of a child, is most certainly deadly. Why? Because it is often difficult to know what other drugs including prescription medications others are being prescribed including herbal/ natural medications; and because unless you are a pharmacist or an experienced physician who is knowledgeable about METHADONE you truly don’t know what will happen when medications are mixed. Treatment Rules and Regulations clearly state: “It is extremely important that medication (this means METHADONE!) be stored in a VERY secure place away from children once the patient takes it to their home. It is not advisable to store the medication in the refrigerator unless it is in a locked, childproof container.” “Patients are not to give away… (Take) home medications (methadone).”It is clearly stated in Rules and Regulations that “Children cannot be held while dosing.” “…The mixing of chemicals may be harmful or fatal.” This is why Locked boxes must meet stringent criteria; to protect you, and those around you. Methadone is a Central Nervous System (CNS) Depressant. This means that Methadone slows down all your central nervous systems including breathing, heart rate, Some medications should NEVER be taken with methadone because they too are CNS depressants. These include alcohol, Benzodiazepines, Naltrexone, Soma, other Opiates and Barbiturates. These drugs taken together potentiate or add to each other: 1+1 no longer = 2; it equals 5 or more If you are a child or anyone the drug is NOT prescribed for you may not know you are in danger as your heart slows, and your breathing becomes shallower and then you die. -
Substance Abuse and Dependence
9 Substance Abuse and Dependence CHAPTER CHAPTER OUTLINE CLASSIFICATION OF SUBSTANCE-RELATED THEORETICAL PERSPECTIVES 310–316 Residential Approaches DISORDERS 291–296 Biological Perspectives Psychodynamic Approaches Substance Abuse and Dependence Learning Perspectives Behavioral Approaches Addiction and Other Forms of Compulsive Cognitive Perspectives Relapse-Prevention Training Behavior Psychodynamic Perspectives SUMMING UP 325–326 Racial and Ethnic Differences in Substance Sociocultural Perspectives Use Disorders TREATMENT OF SUBSTANCE ABUSE Pathways to Drug Dependence AND DEPENDENCE 316–325 DRUGS OF ABUSE 296–310 Biological Approaches Depressants Culturally Sensitive Treatment Stimulants of Alcoholism Hallucinogens Nonprofessional Support Groups TRUTH or FICTION T❑ F❑ Heroin accounts for more deaths “Nothing and Nobody Comes Before than any other drug. (p. 291) T❑ F❑ You cannot be psychologically My Coke” dependent on a drug without also being She had just caught me with cocaine again after I had managed to convince her that physically dependent on it. (p. 295) I hadn’t used in over a month. Of course I had been tooting (snorting) almost every T❑ F❑ More teenagers and young adults die day, but I had managed to cover my tracks a little better than usual. So she said to from alcohol-related motor vehicle accidents me that I was going to have to make a choice—either cocaine or her. Before she than from any other cause. (p. 297) finished the sentence, I knew what was coming, so I told her to think carefully about what she was going to say. It was clear to me that there wasn’t a choice. I love my T❑ F❑ It is safe to let someone who has wife, but I’m not going to choose anything over cocaine. -
Phenibut Overdose in Combination with Fasoracetam: Emerging Drugs of Abuse
Open Access Journal of Clinical Intensive Care and Medicine Case Report Phenibut Overdose in Combination ISSN with Fasoracetam: Emerging Drugs 2639-6653 of Abuse Cristian Merchan1*, Ryan Morgan1, John Papadopoulos1,2 and David Fridman2 1Department of Pharmacy, New York University Langone Medical Center, New York, USA 2New York University School of Medicine, New York, USA *Address for Correspondence: Dr. Cristian INTRODUCTION D Merchan, Pharm.D, BCCCP, Critical Care Pharmacotherapist, Department of Pharmacy, The widespread availability of non-traditional dietary supplements and New York University Langone Medical Center, pharmacologically active substances via the Internet continues to introduce New York, USA, Tel: 516-263-1671; Email: [email protected] mechanisms for inadvertent toxidromes not commonly seen. Consumers are virtually unrestricted in their ability to acquire products purporting augmentation of normal Submitted: 25 October 2016 Approved: 15 December 2016 physiology for the purposes of enhancement, recreation, and/or potential abuse. The Published: 17 December 2016 safety proiles at standard or toxic doses remain largely unknown for many agents that Copyright: 2016 Merchan et al. This is an can be purchased electronically. We report a case of mixed toxicity related to phenibut open access article distributed under the and fosaracetam, both of which are readily available for consumer purchase from Creative Commons Attribution License, which online retailers. Written and verbal consent was obtained for this case presentation. permits unrestricted use, distribution, and reproduction in any medium, provided the CASE REPORT original work is properly cited. Keywords: Nootropic; GABA agonist; Drug of A 27-year-old male with a past medical history of anxiety was discovered abuse; Dietary supplement; Alternative medicine unresponsive on the sidewalk. -
Calcium Channel Blocker As a Drug Candidate for the Treatment of Generalised Epilepsies
UNIVERSITAT DE BARCELONA Faculty of Pharmacy and Food Sciences Calcium channel blocker as a drug candidate for the treatment of generalised epilepsies Final degree project Author: Janire Sanz Sevilla Bachelor's degree in Pharmacy Primary field: Organic Chemistry, Pharmacology and Therapeutics Secondary field: Physiology, Pathophysiology and Molecular Biology March 2019 This work is licensed under a Creative Commons license ABBREVIATIONS AED antiepileptic drug AMPA α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid ANNA-1 antineuronal nuclear antibody 1 BBB blood-brain barrier Bn benzyl BnBr benzyl bromide BnNCO benzyl isocyanate Boc tert-butoxycarbonyl Bu4NBr tetrabutylammonium bromide Ca+2 calcium ion CACNA1 calcium channel voltage-dependent gene cAMP cyclic adenosine monophosphate CCB calcium channel blocker cGMP cyclic guanosine monophosphate CH3CN acetonitrile Cl- chlorine ion Cmax maximum concentration CMV cytomegalovirus CTScan computed axial tomography DCM dichloromethane DIPEA N,N-diisopropylethylamine DMF dimethylformamide DMPK drug metabolism and pharmacokinetics DNET dysembryoplastic neuroepithelial tumours EEG electroencephalogram EPSP excitatory post-synaptic potential FDA food and drug administration Fe iron FLIPR fluorescence imaging plate reader fMRI functional magnetic resonance imaging GABA γ-amino-α-hydroxybutyric acid GAD65 glutamic acid decarboxylase 65 GAERS generalised absence epilepsy rat of Strasbourg GluR5 kainate receptor GTC generalised tonic-clonic H+ hydrogen ion H2 hydrogen H2O dihydrogen dioxide (water) -
Chapter 25 Mechanisms of Action of Antiepileptic Drugs
Chapter 25 Mechanisms of action of antiepileptic drugs GRAEME J. SILLS Department of Molecular and Clinical Pharmacology, University of Liverpool _________________________________________________________________________ Introduction The serendipitous discovery of the anticonvulsant properties of phenobarbital in 1912 marked the foundation of the modern pharmacotherapy of epilepsy. The subsequent 70 years saw the introduction of phenytoin, ethosuximide, carbamazepine, sodium valproate and a range of benzodiazepines. Collectively, these compounds have come to be regarded as the ‘established’ antiepileptic drugs (AEDs). A concerted period of development of drugs for epilepsy throughout the 1980s and 1990s has resulted (to date) in 16 new agents being licensed as add-on treatment for difficult-to-control adult and/or paediatric epilepsy, with some becoming available as monotherapy for newly diagnosed patients. Together, these have become known as the ‘modern’ AEDs. Throughout this period of unprecedented drug development, there have also been considerable advances in our understanding of how antiepileptic agents exert their effects at the cellular level. AEDs are neither preventive nor curative and are employed solely as a means of controlling symptoms (i.e. suppression of seizures). Recurrent seizure activity is the manifestation of an intermittent and excessive hyperexcitability of the nervous system and, while the pharmacological minutiae of currently marketed AEDs remain to be completely unravelled, these agents essentially redress the balance between neuronal excitation and inhibition. Three major classes of mechanism are recognised: modulation of voltage-gated ion channels; enhancement of gamma-aminobutyric acid (GABA)-mediated inhibitory neurotransmission; and attenuation of glutamate-mediated excitatory neurotransmission. The principal pharmacological targets of currently available AEDs are highlighted in Table 1 and discussed further below. -
“GABA” 'Bout? Pregabalin and Gabapentin Abuse
3/19/18 What’s All the “GABA” ‘Bout? Pregabalin and Gabapentin Abuse Courtney Kominek, PharmD, BCPS, CPE Disclosures .Courtney Kominek, PharmD, BCPS, CPE –Axial Healthcare – Consultant .The views and opinions expressed in this presentation are those of the authors and do not necessarily reflect the official policy or position of any agency of the United States government, including the Department of Veterans Affairs. 1 3/19/18 Learning Objectives .Review the proposed mechanisms of action (MOA) for gabapentin and pregabalin. .Explain the proposed rationale as to why gabapentin and pregabalin have become drugs of abuse. .Identify signs and symptoms of withdrawal that an addicted or tolerant patient may experience upon abrupt discontinuation of gabapentin or pregabalin. .Discuss updates on changes in pain management given the increase in gabapentin and pregabalin abuse. Current Situation Opioid overdose public health crisis Rising use of nonopioid medications including gabapentin Opioids and concomitant gabapentin increase risk for overdose Reports of gabapentinoid abuse Changes in PDMP and scheduling at state level http://www.register-herald.com/news/manchin-asks-fda-dea-to-consider-rescheduling-gabapentin/article_442fa04b-7ed9-5bf8-8d19-b5440e9c278b.html 2 3/19/18 Gabapentin and Pregabalin: Pharmacology and Pharmacokinetics Fact or Alternate Fact? .Gabapentin and pregabalin work on GABA. 3 3/19/18 Mechanism of Action Structurally related to GABA and has GABA-mimetic properties Do not • Alter uptake or breakdown • Convert into GABA • Bind to GABAa or GABAB Binds to the α2-δ subunit of the voltage-gated calcium channel Reduces the Ca2+ -dependent release of pro-nociceptive neurotransmitters Decreases release of glutamate, NE, and substance P Dworkin RH et al. -
Conjugation of Tryptamine to Biologically Active Carboxylic Acids in Order to Create Prodrugs
ISSN 2380-5064 | The Arsenal is published by the Augusta University Libraries | http://guides.augusta.edu/arsenal Volume 4, Issue 1 (2021) Special Edition Issue CONJUGATION OF TRYPTAMINE TO BIOLOGICALLY ACTIVE CARBOXYLIC ACIDS IN ORDER TO CREATE PRODRUGS Colin Miller, Jr. and Iryna O. Lebedyeva Citation Miller, C., Jr., & Lebedyeva, I. O. (2021). Conjugation of tryptamine to biologically active carboxylic acids in order to create prodrugs. The Arsenal: The Undergraduate Research Journal of Augusta University, 4(1), 26. http://doi.org/10.21633/issn.2380.5064/s.2021.04.01.26 © Miller, Jr. and Lebedyeva 2021. This open access article is distributed under a Creative Commons Attribution NonCommercial-NoDerivs 2.0 Generic License (https://creativecommons.org/licenses/by-nc-nd/2.0/). Conjugation of Tryptamine to Biologically Active Carboxylic Acids in Order to Create Prodrugs Presenter(s): Colin Miller, Jr. Author(s): Colin Miller Jr. and Iryna O. Lebedyeva Faculty Sponsor(s): Iryna O. Lebedyeva, PhD Affiliation(s): Department of Chemistry and Physics (Augusta Univ.) ABSTRACT A number of blood and brain barrier penetrating neurotransmitters contain polar functional groups. Gamma-aminobutyric acid (GABA) is an amino acid, which is one of the primary inhibitory neurotransmitter in the brain and a major inhibitory neurotransmitter in the spinal cord. Antiepileptic medications such as Gabapentin, Phenibut, and Pregabalin have been developed to structurally represent GABA. These drugs are usually prescribed for the treatment of neuropathic pain. Since these drugs contain a polar carboxylic acid group, it affects their ability to penetrate the blood and brain barrier. To address the low bioavailability and tendency for intramolecular cyclization of Gabapentin, its less polar prodrug Gabapentin Enacarbil has been approved in 2011. -
85 Mv Respectively. When the Membranewas Depolarized, Th
J. Physiol. (1985), 360, pp. 161-185 161 With 14 text-figurem Printed in Great Britain COMPARISON OF THE ACTION OF BACLOFEN WITH y-AMINOBUTYRIC ACID ON RAT HIPPOCAMPAL PYRAMIDAL CELLS IN VITRO BY N. R. NEWBERRY* AND R. A. NICOLLt From the Departments of Pharmacology and Physiology, University of California, San Francisco, CA 94143, U.S.A. (Received 13 June 1984) SUMMARY 1. Intracellular recordings from CAI pyramidal cells in the hippocampal slice preparation were used to compare the action of baclofen, a y-aminobutyric acid (GABA) analogue, with GABA. 2. Ionophoretic application of GABA or baclofen into stratum (s.) pyramidale evoked hyperpolarizations associated with reductions in the input resistance of the cell. Baclofen responses were easier to elicit in the dendrites than in the cell body layer. 3. Blockade of synaptic transmission, with tetrodotoxin or cadmium, did not reduce baclofen responses, indicating a direct post-synaptic action. 4. (+ )-Bicuculline (10 ,UM) and bicuculline methiodide (100 /SM) had little effect on baclofen responses but strongly antagonized somatic GABA responses of equal amplitude. The bicuculline resistance of the baclofen response was not absolute, as higher concentrations of these compounds did reduce it. Pentobarbitone (100 /M) enhanced somatic GABA responses without affecting baclofen responses. (-)-Baclofen was approximately 200 times more potent than (+ )-baclofen. 5. The reversal potentials for the somatic GABA and baclofen responses were -70 mV and -85 mV respectively. When the membrane was depolarized, the baclofen response was reduced. This apparent voltage sensitivity was not seen with somatic GABA responses. 6. Altering the chloride gradient across the cell membrane altered the reversal potential of the somatic GABA response but not that ofthe baclofen response. -
Assessment of Molecular Action of Direct Gating and Allosteric Modulatory Effects of Carisoprodol (Somartm) on GABA a Receptors
Graduate Theses, Dissertations, and Problem Reports 2015 Assessment of molecular action of direct gating and allosteric modulatory effects of carisoprodol (SomaRTM) on GABA A receptors Manoj Kumar Follow this and additional works at: https://researchrepository.wvu.edu/etd Recommended Citation Kumar, Manoj, "Assessment of molecular action of direct gating and allosteric modulatory effects of carisoprodol (SomaRTM) on GABA A receptors" (2015). Graduate Theses, Dissertations, and Problem Reports. 6022. https://researchrepository.wvu.edu/etd/6022 This Dissertation is protected by copyright and/or related rights. It has been brought to you by the The Research Repository @ WVU with permission from the rights-holder(s). You are free to use this Dissertation in any way that is permitted by the copyright and related rights legislation that applies to your use. For other uses you must obtain permission from the rights-holder(s) directly, unless additional rights are indicated by a Creative Commons license in the record and/ or on the work itself. This Dissertation has been accepted for inclusion in WVU Graduate Theses, Dissertations, and Problem Reports collection by an authorized administrator of The Research Repository @ WVU. For more information, please contact [email protected]. ASSESSMENT OF MOLECULAR ACTION OF DIRECT GATING AND ALLOSTERIC MODULATORY EFFECTS OF MEPROBAMATE (MILTOWN®) ON GABAA RECEPTORS Manish Kumar, MD, MS Dissertation submitted to the School of Pharmacy at West Virginia University in partial fulfillment of Requirements -
Membrane Stabilizer Medications in the Treatment of Chronic Neuropathic Pain: a Comprehensive Review
Current Pain and Headache Reports (2019) 23: 37 https://doi.org/10.1007/s11916-019-0774-0 OTHER PAIN (A KAYE AND N VADIVELU, SECTION EDITORS) Membrane Stabilizer Medications in the Treatment of Chronic Neuropathic Pain: a Comprehensive Review Omar Viswanath1,2,3 & Ivan Urits4 & Mark R. Jones4 & Jacqueline M. Peck5 & Justin Kochanski6 & Morgan Hasegawa6 & Best Anyama7 & Alan D. Kaye7 Published online: 1 May 2019 # Springer Science+Business Media, LLC, part of Springer Nature 2019 Abstract Purpose of Review Neuropathic pain is often debilitating, severely limiting the daily lives of patients who are affected. Typically, neuropathic pain is difficult to manage and, as a result, leads to progression into a chronic condition that is, in many instances, refractory to medical management. Recent Findings Gabapentinoids, belonging to the calcium channel blocking class of drugs, have shown good efficacy in the management of chronic pain and are thus commonly utilized as first-line therapy. Various sodium channel blocking drugs, belonging to the categories of anticonvulsants and local anesthetics, have demonstrated varying degrees of efficacy in the in the treatment of neurogenic pain. Summary Though there is limited medical literature as to efficacy of any one drug, individualized multimodal therapy can provide significant analgesia to patients with chronic neuropathic pain. Keywords Neuropathic pain . Chronic pain . Ion Channel blockers . Anticonvulsants . Membrane stabilizers Introduction Neuropathic pain, which is a result of nervous system injury or lives of patients who are affected. Frequently, it is difficult to dysfunction, is often debilitating, severely limiting the daily manage and as a result leads to the progression of a chronic condition that is, in many instances, refractory to medical This article is part of the Topical Collection on Other Pain management. -
Pregabalin Abuse: a Case Report Ilhan Yargic1, Filiz Alyanak Ozdemiroglu2
Olgu Sunumları / Case Reports DOI: 10.5350/KPB-BCP201121110 Pregabalin Abuse: A Case Report Ilhan Yargic1, Filiz Alyanak Ozdemiroglu2 ÖZET: ABS TRACT: Pregabalin kötüye kullanımı: Bir olgu sunumu Pregabalin abuse: a case report Pregabalin epilepsi, nöropatik ağrı ve yaygın anksiyete Pregabalin is a gamma-amino butyric acid (GABA) analogue bozukluğunun tedavilerinde kullanılan bir gama-aminobu- used in the treatment of epilepsy, neuropathic pain, and tirik asit (GABA) analoğudur. Pregabalin Türkiye’de kontrole generalized anxiety disorder. Although pregabalin is not tabi ilaçlardan olmamasına karşın kötüye kullanılma potan- a controlled medication in Turkey, it has a potential risk 1M.D., Professor of Psychiatry, Istanbul siyeline sahiptir. Türkiye’de yaygın anksiteye bozukluğu gibi of abuse. It has not been approved for the treatment of University, Istanbul Faculty of Medicine, Psychiatry Department, Istanbul-Turkey psikiyatrik hastalıkların tedavisi için ruhsatlandırılmış olma- psychiatric disorders (such as generalized anxiety disorder) 2M.D., Istinye Devlet Hastanesi, Psikiyatri AD, dığı için henüz psikiyatri hastaları arasında popüler değildir. in Turkey, so it is not yet popular as a drug of abuse among Istinye, Istanbul-Turkey 37 yaşında, bipolar bozukluğu ve benzodiyazepin kötüye psychiatric patients. We report the first case of pregabalin Ya zış ma Ad re si / Add ress rep rint re qu ests to: kullanımı öyküsü olan bir erkek hastada Türkiye’den ilk pre- abuse in Turkey in a 37 year old male patient who has a İlhan Yargıç, M.D., Istanbul -
Gamma-Aminobutyric Acid (GABA) Is a Major NeuroTransmitter Widely Distributed Throughout the Central Nervous System (CNS)
Alternative Medicine Review Volume 12, Number 3 2007 Monograph GABA Gamma-Aminobutyric O + Acid (GABA) H3N O- Introduction Gamma-aminobutyric acid (GABA) is a major neuro transmitter widely distributed throughout the central nervous system (CNS). Because too much excitation can lead to irritability, restlessness, insomnia, seizures, and movement disorders, it must be balanced with inhibition. GABA – the most important inhibitory neurotransmitter in the brain – provides this inhibition, acting like a “brake” during times of runaway stress. Medications for anxiety, such as benzodiazepines, stimulate GABA receptors and induce relaxation. Either low GABA levels or decreased GABA function in the brain is associated with several psy- chiatric and neurological disorders, including anxiety, depression, insomnia, and epilepsy. Studies indicate GABA can improve relaxation and enhance sleep. Both synthetic and natural GABA are available as dietary supplements in the United States. Natural GABA is produced via a fermentation process that utilizes Lactobacillus hilgardii – the bacteria used to ferment vegetables in the preparation of the traditional Korean dish known as kimchi. Biochemistry and Pharmacokinetics Within the brain, glutamic acid is converted to GABA via the enzyme glutamate decarboxylase and its cofac- tor pyridoxal 5’ phosphate (P5P; active vitamin B6). GABA is metabolized by gamma-aminobutyrate transaminase, also a P5P-dependent enzyme, forming an intermediate metabolite succinate semialdehyde. This metabolite can then be reduced to gamma-hydroxybutyrate, or oxidized to succinate and eventually converted to CO2 and water via the citric acid cycle. When plasma membrane depolarization induces the release of GABA from nerve terminals, GABA binds to GABA receptors – such as the GABAA and GABAB receptors – that are distributed on post-synaptic cell membranes.