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References

1. Heal DJ, Smith SL, Gosden J, Nutt DJ (June 2013). "Amphetamine,
past and present – a pharmacological and clinical perspective". J.
Psychopharmacol. 27 (6): 479–
496. doi:10.1177/0269881113482532.PMC 3666194. PMID 2353964
2. The intravenous use of d-amphetamine and other stimulants still
pose major safety risks to the individuals indulging in this practice.
Some of this intravenous abuse is derived from the diversion of
ampoules of d-amphetamine, which are still occasionally prescribed
in the UK for the control of severe narcolepsy and other disorders of
excessive sedation. ... For these reasons, observations of
dependence and abuse of prescription d-amphetamine are rare in
clinical practice, and this stimulant can even be prescribed to
people with a history of drug abuse provided certain controls, such
as daily pick-ups of prescriptions, are put in place (Jasinski and
Krishnan, 2009b).
2. "Pharmacology". Dextroamphetamine. DrugBank. University of
Alberta. 8 February 2013. Retrieved 5 November 2013.
3. "Pharmacology". Amphetamine. DrugBank. University of Alberta. 8
February 2013. Retrieved 5 November 2013.
4. "Adderall XR Prescribing Information" (PDF). United States Food and
Drug Administration. Shire US Inc. December 2013. pp. 12–13.
Retrieved30 December 2013.
5. Glennon RA (2013). "Phenylisopropylamine stimulants:
amphetamine-related agents". In Lemke TL, Williams DA, Roche VF,
Zito W. Foye's principles of medicinal chemistry (7th ed.).
Philadelphia, USA: Wolters Kluwer Health/Lippincott Williams &
Wilkins. pp. 646–648.ISBN 9781609133450. Retrieved 11
September 2015. The simplest unsubstituted phenylisopropylamine,
1-phenyl-2-aminopropane, or amphetamine, serves as a common
structural template for hallucinogens and psychostimulants.
Amphetamine produces central stimulant, anorectic, and
sympathomimetic actions, and it is the prototype member of this
class (39). ... The phase 1 metabolism of amphetamine analogs is
catalyzed by two systems: cytochrome P450 and flavin
monooxygenase. ... Amphetamine can also undergo aromatic
hydroxylation to p-hydroxyamphetamine. ... Subsequent oxidation
at the benzylic position by DA β-hydroxylase affordsphydroxynorephedrine. Alternatively, direct oxidation of
amphetamine by DA β-hydroxylase can afford norephedrine.
6. Taylor KB (January 1974). "Dopamine-beta-hydroxylase.
Stereochemical course of the reaction" (PDF). J. Biol. Chem. 249 (2):
454–458.PMID 4809526. Retrieved 6 November 2014. Dopamine-β-

hydroxylase catalyzed the removal of the pro-R hydrogen atom and
the production of 1-norephedrine, (2S,1R)-2-amino-1-hydroxyl-1phenylpropane, from d-amphetamine.
7. Horwitz D, Alexander RW, Lovenberg W, Keiser HR (May 1973).
"Human serum dopamine-β-hydroxylase. Relationship to
hypertension and sympathetic activity". Circ. Res. 32 (5): 594–
599.doi:10.1161/01.RES.32.5.594. PMID 4713201. Subjects with
exceptionally low levels of serum dopamine-β-hydroxylase activity
showed normal cardiovascular function and normal β-hydroxylation
of an administered synthetic substrate, hydroxyamphetamine.
8. Krueger SK, Williams DE (June 2005). "Mammalian flavin-containing
monooxygenases: structure/function, genetic polymorphisms and
role in drug metabolism". Pharmacol. Ther. 106 (3): 357–
387.doi:10.1016/j.pharmthera.2005.01.001. PMC 1828602. PMID 15
922018.
"Table 5: N-containing drugs and xenobiotics oxygenated by FMO"
9. Cashman JR, Xiong YN, Xu L, Janowsky A (March 1999). "Noxygenation of amphetamine and methamphetamine by the human
flavin-containing monooxygenase (form 3): role in bioactivation and
detoxication". J. Pharmacol. Exp. Ther. 288 (3): 1251–
1260. PMID 10027866.
10."Pharmacology and Biochemistry". Amphetamine. Pubchem
Compound. National Center for Biotechnology Information.
Retrieved 12 October 2013.
11.Santagati NA, Ferrara G, Marrazzo A, Ronsisvalle G (September
2002). "Simultaneous determination of amphetamine and one of its
metabolites by HPLC with electrochemical detection". J. Pharm.
Biomed. Anal. 30 (2): 247–255. doi:10.1016/S0731-7085(02)003308. PMID 12191709.
12."Pharmacology". amphetamine/dextroamphetamine. Medscape.
WebMD. Retrieved 21 January 2016. Onset of action: 30–60 min
13.Millichap JG (2010). "Chapter 9: Medications for ADHD". In Millichap
JG. Attention Deficit Hyperactivity Disorder Handbook: A Physician's
Guide to ADHD (2nd ed.). New York, USA: Springer.
p. 112.ISBN 9781441913968.
Table 9.2 Dextroamphetamine formulations of stimulant medication
Dexedrine [Peak:2–3 h] [Duration:5–6 h] ...
Adderall [Peak:2–3 h] [Duration:5–7 h]
Dexedrine spansules [Peak:7–8 h] [Duration:12 h] ...
Adderall XR [Peak:7–8 h] [Duration:12 h]
Vyvanse [Peak:3–4 h] [Duration:12 h]

14.Brams M, Mao AR, Doyle RL (September 2008). "Onset of efficacy of
long-acting psychostimulants in pediatric attentiondeficit/hyperactivity disorder". Postgrad. Med. 120 (3): 69–
88. doi:10.3810/pgm.2008.09.1909.PMID 18824827.
15."Adderall IR Prescribing Information" (PDF). United States Food and
Drug Administration. Barr Laboratories, Inc. March 2007. pp. 1–5.
Retrieved2 November 2013.
16."Biological Half-Life". AMPHETAMINE. United States National Library
of Medicine – Toxnet. Hazardous Substances Data Bank. Retrieved 5
January2014. Concentrations of (14)C-amphetamine declined less
rapidly in the plasma of human subjects maintained on an alkaline
diet (urinary pH > 7.5) than those on an acid diet (urinary pH < 6).
Plasma half-lives of amphetamine ranged between 16-31 hr & 8-11
hr, respectively, & the excretion of (14)C in 24 hr urine was 45 &
70%.
17.Mignot EJ (October 2012). "A practical guide to the therapy of
narcolepsy and hypersomnia syndromes". Neurotherapeutics 9 (4):
739–752.doi:10.1007/s13311-012-0150-9. PMC 3480574. PMID 2306
5655.
18."Compound Summary". Amphetamine. PubChem Compound.
National Center for Biotechnology Information. 11 April 2015.
Retrieved 17 April2015.
19.Yoshida T (1997). "Chapter 1: Use and Misuse of Amphetamines: An
International Overview". In Klee H. Amphetamine Misuse:
International Perspectives on Current Trends. Amsterdam,
Netherlands: Harwood Academic Publishers.
p. 2. ISBN 9789057020810. Retrieved 1
December2014. Amphetamine, in the singular form, properly
applies to the racemate of 2-amino-1-phenylpropane. ... In its
broadest context, however, the term [amphetamines] can even
embrace a large number of structurally and pharmacologically
related substances.
20."Properties: Predicted – EP|Suite". Amphetamine. Chemspider.
Retrieved6 November 2013.
21."Chemical and Physical Properties". Amphetamine. PubChem
Compound. National Center for Biotechnology Information.
Retrieved 13 October 2013.
22."Identification". Amphetamine. DrugBank. University of Alberta. 8
February 2013. Retrieved 13 October 2013.
23.Greene SL, Kerr F, Braitberg G (October 2008). "Review article:
amphetamines and related drugs of abuse". Emerg. Med.

Retrieved 14 March 2014. 11."Adderall XR Prescribing Information" (PDF). methylphenidate.. 24.02. but also on general levels of arousal and.1016/j. Hyman SE (2009). doi:10. International Union of Pure and Applied Chemistry. as stated above..Malenka RC.17426723. 321.x. p. and desipramine.). Beyond these general permissive effects. USA: McGraw-Hill Medical..Australas 20 (5): 391–402. doi:10. and delay fatigue. 25. such as methylphenidate and amphetamine. decrease reaction time. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed. amphetamines. ..pop.E02069. "Nutritional supplements and ergogenic AIDS"...009. .ISBN 9780071481274..PMID 23668655. 26. improve performance on working memory tasks both in normal subjects and those with ADHD. enhance working memory and aspects of attention. In Sydor A. Care 40 (2): 487– 505.. United States Food and Drug Administration. Shire US Inc.2013. Physiologic and performance effects • Amphetamines increase dopamine/norepinephrine release and inhibit their reuptake. stimulants improve performance on effortful but tedious tasks . improve focus. doi:10. atomoxetine. stimulants act not only on working memory function. "Chapter 13: Higher Cognitive Function and Behavioral Control". at optimal levels. Archived from the original on 17 March 2013. Prim. Therapeutic (relatively low) doses of psychostimulants. New York. Connor DJ (June 2013). dopamine (acting via D1 receptors) and norepinephrine (acting at several receptors) can.Liddle DG. Thus. through indirect stimulation of dopamine and norepinephrine receptors. One of a pair of molecular entities which are mirror images of each other and non-superposable. improve the saliency of tasks. Retrieved30 December 2013.01114. IUPAC Goldbook. Nestler EJ.1351/goldbook. December 2013. 318. PMID 18973636. Amphetamines and caffeine are stimulants that increase alertness. ."Enantiomer". p.2008. leading to central nervous system (CNS) stimulation • Amphetamines seem to enhance athletic performance in anaerobic conditions 39 40 • Improved reaction time • Increased muscle strength and delayed muscle fatigue • Increased acceleration • Increased alertness and attention to task 27. Drugs used for this purpose include. allowing for an increased intensity and duration of training .1111/j. Brown RY. within the nucleus accumbens.

Although useful in the treatment of ADHD. In some cases. 61 (3): 288– 323. Child Adolesc. United States Food and Drug Administration. 34. stimulants are controlled II substances with a history of preclinical and human studies showing potential abuse liability. 1997. Utzinger L. National Institutes of Health.Montgomery KA (June 2008)."Evekeo Prescribing Information" (PDF). INNs are selected only for the active part of the molecule which is usually the base. Stimulant misuse appears to occur both for performance enhancement and their euphorogenic effects. Retrieved1 December 2014.0b013e31815a56f1. such as formulation purposes. Adler LA.1097/chi. IR versus ER profile) . Rotrosen J. Retrieved 11 August 2015. Adams J. doi:10. "Making the first anti-depressant: amphetamine in American medicine. 30."Amphetamine". PMC 2695750..Rasmussen N (July 2006). acid or alcohol. United Nations. bioavailability or absorption rate."National Drug Code Amphetamine Search Results". Allied Sci. . Psychiatry (Edgmont) 5 (6): 50–55. Hist. Psychiatry 47 (1): 21– 31. Arbor Pharmaceuticals LLC. names for different salts or esters of the same active substance should differ only with regard to the inactive moiety of the molecule. J . In 1975 the experts designated for the selection of INN decided to adopt a new policy for naming such molecules. 31.. PMID 16492800. 29. Retrieved 11 November 2013. The latter are called modified INNs (INNMs). Retrieved 16 December 2013. United Nations Treaty Collection. World Health Organization. PMID 19727285.1093/jhmas/jrj039.. In future. 35. Medical Subject Headings. Archived from the original on 7 February 2014."Convention on psychotropic substances". . 1929–1950". Am. Sgambati S. In principle. however. National Library of Medicine. Med. Fusillo S (January 2008). "Sexual desire disorders". PMID 18174822. J.g. the latter being related to the intrinsic properties of the stimulants (e. April 2014.28. "Misuse and diversion of stimulants prescribed for ADHD: a systematic review of the literature". Retrieved 16 December 2013. pp. National Drug Code Directory.."Guidelines on the Use of International Nonproprietary Names (INNS) for Pharmaceutical Substances". Acad. Sawtelle R. 33. 32. 1–2.doi:10..Wilens TE. the active molecules need to be expanded for various reasons.

Rev. Li JX (February 2016). Westfall TC (2010). "The emerging role of trace amineassociated receptor 1 in the functional regulation of monoamine transporters and dopaminergic activity". pp. PMI D 21073468. p. ISBN 9780071624428. United States Food and Drug Administration.Grandy DK.. 39. "Treatment for amphetamine psychosis". In such cases. "Stimulant Misuse: Strategies to Manage a Growing Problem" (PDF). "Miscellaneous Sympathomimetic Agonists".2015.1016/j.1111/j. 38. . Findings from one trial indicate use of antipsychotic medications effectively resolves symptoms of acute amphetamine psychosis. ""TAARgeting Addiction"-The Alamo Bears Witness to Another Revolution: An Overview of the Plenary Symposium of the 2015 Behavior. Drug Alcohol Depend.CD003026. 37. symptoms of amphetamine psychosis commonly include paranoid and persecutory delusions as well as auditory and visual hallucinations in the presence of extreme agitation. Archived from the original (PDF) on 3 November 2013.x.drugalcdep. December 2013. 4–8."Adderall XR Prescribing Information" (PDF). Goodman & Gilman's Pharmacological Basis of Therapeutics (12th ed. 116 (2): 164–176. About 5–15% of the users who develop an amphetamine psychosis fail to recover completely (Hofmann 1983) . More common (about 18%) is for frequent amphetamine users to report psychotic symptoms that are sub-clinical and that do not require high-intensity intervention . New York.11. 159: 9– 16. USA: McGraw-Hill.doi:10.07109.).. 41.pub3.Westfall DP.Greydanus D. 20. ed.. American College Health Association (Review Article). In Brunton LL. PMID 19160215 .014.Shoptaw SJ. 40. Ali R.1471-4159. PMC 3005101. Cochrane Database Syst. (1): CD003026. Ling W (January 2009). A minority of individuals who use amphetamines develop full-blown psychosis requiring care at emergency departments or psychiatric hospitals. Retrieved 2 November 2013.2010. Kao U. When considered together with the rapidly growing literature in the field a compelling case emerges in support of developing TAAR1-selective agonists as medications for preventing relapse to psychostimulant abuse.doi:10. Shoptaw SJ.36. doi:10. Retrieved30 December 2013.. Chabner BA.Miller GM (January 2011). J. Biology and Chemistry Conference". Miller GM. ACHA Professional Development Program. Knollmann BC. PMID 26644139. Shire US Inc. Neurochem.1002/14651858.

J. Seidman LJ. Costa VM. Fears S. 24 (5): 1345–1357. Carmo H.1196/annals. Curr. Nakao T.2009. Sci. Arch. 47.005."Abuse of amphetamines and structural abnormalities in the brain".1185/030079908X280707. . they are unlikely to yield effects consistent with abuse potential in patients with ADHD. 49. Berlin. doi:10. and age effects". doi:10. "The vascular effects of trace amines and amphetamines". PMC 3801446. Remião F.12r08287. Pharmacol. Valera EM.ISBN 9783540686989. Carvalho F.1007/s00204012-0815-5. 1141: 195– 220. doi:10.Kollins SH (May 2008). Biederman J (September 2013). Y.42.277.x.031.PMID 18991959. "A qualitative review of issues arising in the use of psycho-stimulant medications in patients with ADHD and comorbid substance use disorders". 125 (3): 363– 375. stimulant medication. Mataix-Cols D.PMID 22392347.Berman S. Brown A. Bartzokis G. JAMA Psychiatry 70(2): 185– 198. "Effect of psychostimulants on brain structure and function in ADHD: a qualitative literature review of magnetic resonance imaging-based neuroimaging studies". 78. "Toxicity of amphetamines: an update". PMID 19948186. Encyclopedia of Psychopharmacology. Retrieved 19 October 2013. Opin. Stolerman IP. Skokauskas N (February 2012). Radua J. O'Neill J.Frodl T. London. 125 (2): 114–126. 46. Faraone SV.4088/JCP. PMID 22118249.Hart H. Capela JP. Acta psychiatrica Scand.Broadley KJ (March 2010). Res.1441. Ther.doi:10. 86 (8): 1167–1231. N. Toxicol. 50. Rubia K (February 2013).2011. "Meta-analysis of functional magnetic resonance imaging studies of inhibition and attention in attention-deficit/hyperactivity disorder: exploring task-specific. Psychiatry 74 (9): 902– 917.".pharmthera. When oral formulations of psychostimulants are used at recommended doses and frequencies. Makris N. Clin. Lomedico A. PMC 2769923. 45.doi:10.2013."Amphetamine".16000447. 44. 43.11.1016/j.1111/j.Carvalho M. Pontes H. doi:10.PMID 24107764. p.Stolerman IP (2010). "Meta-analysis of structural MRI studies in children and adults with attention deficit hyperactivity disorder indicates treatment effects.01786.doi:10. PMID 18384709.Spencer TJ. PMID 23247506. 48. Acad. ed. Ann. London ED (October 2008). England: Springer. Med.1001/jamapsychiatry. Germany. Bastos Mde L (August 2012). European Monitoring Centre for Drugs and Drug Addiction.

Chalhoub N. doi:10. New York. Acetylcholine. Nestler EJ. 52. 56.1016/j. Hyman SE (2009). 53. Psychol.51. Among significantly improved outcomes. "Long-term outcomes with medications for attention-deficit hyperactivity disorder: current status of knowledge". Tsai MH (July 2011). the largest effect sizes were found for combination treatment.Huang YS. Pharmacol. Biochem. Hodgkins P.2165/11589380-000000000-00000. Wales G. "Chapter 6: Widely Projecting Systems: Monoamines.PMID 21699268.). Rec ent studies have demonstrated that stimulants. Manag. PMC 3353150.002.S49114. are continuously effective for more than 2-year treatment periods with few and tolerable adverse effects.05. and Orexin". 54. PMID 24082796. 125–127.2147/PRBM. pp.doi:10.Arnold LE. Only one paper53 examining outcomes beyond 36 months met the review criteria. Behav. In Millichap JG. The highest proportion of improved outcomes was reported with combination treatment (83% of outcomes). Caci H. 55. PLoS ONE 10 (2): e0116407.Millichap JG (2010). PMC 4340791.0116407. and has confirmed the effectiveness and safety of the long-term use of medication. 99 (2): 262– 274. inattention..Bidwell LC. PMID 21596055. Harpin V (September 2013). 6: 87– 99. The greatest improvements were associated with academic. "Cognitive enhancers for the treatment of ADHD". PMC 3785407. .2011. Attention Deficit Hyperactivity Disorder Handbook: A Physician's Guide to ADHD (2nd ed.1371/journal. "Chapter 9: Medications for ADHD". along with the nonstimulants atomoxetine and extended-release guanfacine. Kahle J. doi:10. Kollins SH (August 2011). Ongoing research has provided answers to many of the parents’ concerns.Molecular Neuropharmacology: A Foundation for Clinical Neuroscience(2nd ed. ISBN 9781441913968. There is high level evidence suggesting that pharmacological treatment can have a major beneficial effect on the core symptoms of ADHD (hyperactivity. 154–157.PMID 2 5714373. In Sydor A.. 121–123. McClernon FJ.CNS Drugs 25 (7): 539– 554. USA: McGraw-Hill Medical. Brown RY.pone.pbb. "Effect of treatment modality on long-term outcomes in attention-deficit/hyperactivity disorder: a systematic review".). and impulsivity) .ISBN 9780071481274. Behav. self-esteem.Parker J. "The long-term outcomes of interventions for the management of attention-deficit hyperactivity disorder in children and adolescents: a systematic review of randomized controlled trials".Malenka RC. Res. Young S (February 2015). or social function outcomes. USA: Springer. doi:10. pp. New York.

. pp. Pringsheim T.CD007990.1602188.pub2. "Pharmacological treatment for Attention Deficit Hyperactivity Disorder (ADHD) in children with comorbid tic disorders".doi:10.in approximately 80% of cases compared with placebo controls.1002/14651858. 57. Clarke M.ejcn. New York. PMID 25499957. USA: Springer. Hetherington J (August 2005). Collectively.Scholten RJ.1016/j. 59.biopsych. (6): CD007813. . doi:10. PMID 16052183. Shamseer L.Punja S. discussion S195–S196..PMID 26844979. doi:10. 62. Nutr. Eur. Rev. J. Castells X. Cochrane Database Syst. WebMD. 61. the neurobiology of the procognitive actions of psychostimulants has only recently been systematically investigated. Rev. Hartling L. Findings from this research unambiguously demonstrate that the cognition-enhancing effects of psychostimulants involve the preferential elevation of catecholamines in the PFC and the subsequent activation of norepinephrine α2 and dopamine D1 receptors. In Millichap JG.1002/14651858. Devilbiss DM.09.013. Rev. Ramos-Quiroga JA.Pringsheim T. Bosch R. "The Cochrane Collaboration".1002/14651858. Vohra S (February 2016). This differential modulation of PFC-dependent processes across dose appears to be associated with the differential involvement of noradrenergic α2 versus α1 receptors.Spencer RC. ed. "Amphetamines for attention deficit hyperactivity disorder (ADHD) in children and adolescents". 2: CD009996.Castells X. "The CognitionEnhancing Effects of Psychostimulants Involve Direct Action in the Prefrontal Cortex". doi:10. 58. PMID 21491404 . (4): CD007990. Nogueira M.CD007813.1038/sj. "Chapter 9: Medications for ADHD". Steeves T (April 2011). 59 Suppl 1: S147–S149. Urichuk L.Millichap JG (2010). doi:10. PMID 21678370 . Clin. Healthwise. 12 April 2010.ISBN 9781441913968.pub2. despite nearly 80 years of clinical use.CD009996.2014. Psychiatry 77 (11): 940– 950."Stimulants for Attention Deficit Hyperactivity Disorder". "Amphetamines for Attention Deficit Hyperactivity Disorder (ADHD) in adults". Casas M (June 2011). Cochrane Database Syst. Cochrane Database Syst. Surprisingly. The procognitive actions of psychostimulants are only associated with low doses.). Berridge CW (June 2015). ed. Retrieved 12 November 2013. Nikles J. 111– 113. 63. Biol.. 60. Vandermeer B. Attention Deficit Hyperactivity Disorder Handbook: A Physician's Guide to ADHD (2nd ed. this evidence indicates that at low.pub2. in the short term.

Boyd CJ (October 2006). "Pills become an addictive study aid". Farah MJ (January 2015).Molecular Neuropharmacology: A Foundation for Clinical Neuroscience(2nd ed. 266. Pharmacol. In Sydor A. leading to improved recall. Dopamine acts in the nucleus accumbens to attach motivational significance to stimuli associated with reward. Anagnostaras SG (January 2014). Archived from the original on 15 August 2007..Malenka RC. Nestler EJ. 42 (4): 535–542. 68. Rev. In particular. 69. "Psychostimulants and cognition: a continuum of behavioral and cognitive activation". p. J. in both animals and humans.02 ≥ P ≤ 0. "Regional cerebral blood flow response to oral amphetamine challenge in healthy volunteers".).ISBN 9780071481274. 70. USA: McGraw-Hill Medical. Med. LaGrange K. Hyman SE (2009). whereas maximal suppression of overt behavior and facilitation of attentional processes occurs at higher doses. "Prescription Stimulants' Effects on Healthy Inhibitory Control.007054. 67. Hook CJ. PMID 24749160. .Twohey M (26 March 2006).PMC 4471173.Wood S. "Efficacy of stimulants for cognitive enhancement in non-attention deficit hyperactivity disorder youth: a systematic review".Teter CJ. McCabe SE. psychostimulants are devoid of the behavioral and neurochemical actions that define this class of drugs and instead act largely as cognitive enhancers (improving PFCdependent function).1111/add. and Episodic Memory: A Meta-analysis". Kaminer Y (April 2014). Sage JR. doi:10. 66 (1): 193– 221. New York.PMID 24344115. doi:10.12460."Illicit use of specific prescription stimulants among college students: prevalence. 64.Ilieva IP. Cogn.clinically relevant doses. Nucl.112. PMID 11337538. and routes of .05). This information has potentially important clinical implications as well as relevance for public health policy regarding the widespread clinical use of psychostimulants and for the development of novel pharmacologic treatments for attentiondeficit/hyperactivity disorder and other conditions associated with PFC dysregulation. Shuman T. Cranford JA.1124/pr.. Brown RY. Neurosci. Working Memory. "Chapter 10: Neural and Neuroendocrine Control of the Internal Milieu". Addiction 109 (4): 547– 557. Amphe tamine has been shown to improve consolidation of information (0.: 1– 21.1162/jocn_a_00776. JS Online. Rush AJ (April 2001). PMID 25591060. 65. lower doses maximally improve performance in tests of working memory and response inhibition. motives. Retrieved2 December 2007. Trivedi MH.Bagot KS.doi:10. 66. J.Devous MD.

1038/bjp.Parr JW (July 2011).PMID 16999660.Clemow DB. Med. doi:10.26. Retrieved 8 October 2013. and time to exhaustion during maximal oxygen consumption (VO2 max) testing after administration of 15 mg of dextroamphetamine versus placebo.administration". 71. "The potential for misuse and abuse of medications in ADHD: a review". doi:10. Munro BA. 30 (3): 591–610. Roelands and colleagues53 studied the effect of reboxetine. Br. Overall. PMC 4164338.1016/j.1501.09. Oster DR. PMID 18500382. Most of the information to answer this question has been obtained in the past decade through studies of fatigue rather than an attempt to systematically investigate the effect of ADHD drugs on exercise. Pharmacol. "National Study of Substance Use Trends Among NCAA College Student-Athletes" (PDF).10. 74.2147/PRBM. anaerobic capacity. . Res.csm. Behav. doi:10. Marraccini ME. 73. large numbers of students claim to have engaged in the nonmedical use of prescription stimulants. pre-exercise and maximum heart rates. a pure NE reuptake inhibitor. PMID 25228824. 75. In 1980.2801. 154 (3): 606–622. Pharmacotherapy 26(10): 1501– 1510.3810/pgm..Bracken NM (January 2012). depending on the study. "Pharmacology of stimulants prohibited by the World Anti-Doping Agency (WADA)". PMC 1794223. acceleration.03. Kuhar B (September 2014).1592/phco. the data suggest that ADHD medication misuse and diversion are common health care problems for stimulant medications. PMID 25295651.S47013. Gudmundsdottir BG. National Collegiate Athletic Association. 7: 223– 249.2008.doi:10. Walker DJ (September 2014). Clin. . In 2008.2014. Manag. Chandler and Blair47 showed significant increases in knee extension strength.124. time to exhaustion during exercise. Indeed. J. "Attention-deficit hyperactivity disorder and the athlete: new advances and understanding". Zavras BM. PMID 21658550..2011. 126 (5): 64– 81.. similar to atomoxetine. doi:10. . 72. with the prevalence believed to be approximately 5% to 10% of high school students and 5% to 35% of college students. "Pharmacological interventions for adolescents and adults with ADHD: stimulant and nonstimulant medications and misuse of prescription stimulants". Postgrad. Sports Med. Psychol.007. which is reflected in lifetime prevalence rates of prescription stimulant misuse ranging from 5% to nearly 34% of students.Weyandt LL.Docherty JR (June 2008)..mis use of prescription stimulants has become a serious problem on college campuses across the US and has been recently documented in other countries as well. NCAA Publications. PMC 2439527.

Sports Med.3389/fnint. PMC 3813949. Front. Med. Hettinga F. 76. Caetano MS. and bupropion).2013. De Pauw K. or “clock. Dopaminergic drugs appear to override a safety switch and allow athletes to use a reserve capacity that is ‘off-limits’ in a normal (placebo) situation.1007/s40279-013-0030-4. 77. Scand.. "Neurophysiological effects of exercise in the heat".. subjects are able to maintain a higher power output compared with placebo. Integr.in 9 healthy. Argus C. PMC 4362407.PMID 24198770. Retrieved 10 March 2016.. For instance.. whereas antagonists of D2 type dopamine receptors typically slow timing. Foster C. dopaminergic manipulations clearly improve performance. "Is it time to turn our attention toward central mechanisms for postexertional recovery strategies and performance?". 2009) and the greater power output during a RPE matched cycling time trial following amphetamine ingestion (Swart. . which increases concentrations of dopamine at the synaptic cleft advances the start of responding during interval timing. 1996).Parker KL. Dopamine stimulating drugs are known to enhance aspects of exercise performance (Roelands et al. doi:10.. M anipulations of dopaminergic signaling profoundly influence interval timing. Lamichhane D. 78. PMID 23456493. Front. They showed decreased power output and exercise performance at both 18 and 30 degrees centigrade.. A side from accounting for the reduced performance of mentally fatigued participants.” activity. . Sports. Depletion of dopamine in healthy volunteers impairs timing. Martin K.12350.. the depletion of . Physiol.00079.00075. 2008) 79. doi:10. Sci. Neurosci. Their conclusion was that DA reuptake inhibition was the cause of the increased exercise performance seen with drugs that affect both DA and NE (MPH. PMID 25943657. Meeusen R (June 2015). 2009). 25 Suppl 1: 65–78.3389/fphys.. Northey J. They too exercised in both temperate and warm environments. 7: 75. doi:10. "Neurophysiological determinants of theoretical concepts and mechanisms involved in pacing". PMID 25852568.Rattray B. while amphetamine releases synaptic dopamine and speeds up timing. 6: 79.Roelands B.doi:10.Roelands B. de Koning J. Meeusen R (May 2013). leading to the hypothesis that dopamine influences internal pacemaker. amphetamine. 43 (5): 301– 311. Driller M (March 2015). this model rationalizes the reduced RPE and hence improved cycling time trial performance of athletes using a glucose mouthwash (Chambers et al.1111/sms. In highambient temperatures. Narayanan NS (October 2013).Physical fatigue has classically been attributed to peripheral factors within the muscle (Fitts. The distribution of the power output reveals that after dopamine reuptake inhibition."Executive dysfunction in Parkinson's disease and timing deficits".2015. well-trained cyclists.. amphetamine. J.

state ments on package inserts are not intended to limit medical practice. metabolic. 1967) or increased cardiovascular. certainly when ambient temperature is increased .Kessler S (January 1996). United States Food and Drug Administration. United States Food and Drug Administration. October 2013. Retrieved 24 June 2014. Retrieved4 November 2013.. South. 2008b). and thermoregulatory strain (Abbiss & Laursen. and enable an individual to continue maintaining a high power output 80. The combined effects of DA and NA on performance in the heat were studied by our research group on a number of occasions.. 2006b)... DA. 83. 2010). "Amphetamine (PIM 934)". International Programme on Chemical Safety. PMID 8545689. Retrieved30 December 2013. "Drug therapy in attention-deficit hyperactivity disorder". pp. Interestingly. the FDA asserts explicitly. J. 5-HT. 82.. and the courts have upheld that clinical decisions are to be made by physicians and patients in individual situations. certainly since their neurons innervate the hypothalamus (Roelands & Meeusen. without any change in the perception of effort.. Rather they are intended to limit claims by pharmaceutical companies. INCHEM. Taken together.. Amedra Pharmaceuticals LLC. 4–6. December 2013. This indicates that subjects did not feel they were producing more power and consequently more heat. these data indicate strong ergogenic effects of an increased DA concentration in the brain. and NA have all been implicated in the control of thermoregulation and are thought to mediate thermoregulatory responses. . 2005. . Ailakis J.. In recent decennia however.. it became clear that the central nervous system plays an important role in the onset of fatigue during prolonged exercise (Klass et al. Shire US Inc.muscle glycogen (Bergstrom & Hultman.1097/00007611-199601000-00005.... the authors observed core temperatures that were much higher compared with the placebo situation. . The authors concluded that the “safety switch” or the mechanisms existing in the body to prevent harmful effects are overridden by the drug administration (Roelands et al. Med. . Meeusen et al.. bupropion may dampen or override inhibitory signals arising from the central nervous system to cease exercise because of hyperthermia. . Similar to the methylphenidate study (Roelands et al. this occurred without any change in the subjective feelings of thermal sensation or perceived exertion. 2008).Heedes G. Coinciding with this ergogenic effect. 89 (1): 33– 38. the administration of bupropion (DA/NA reuptake inhibitor) significantly improved performance. 81. doi:10. 2008b)."Adderall XR Prescribing Information" (PDF)."Dexedrine Prescribing Information" (PDF)..

J. Engl. The most common (≥2% in the DYANAVEL XR group and greater than placebo) adverse reactions reported in the Phase 3 controlled study conducted in 108 patients with ADHD (aged 6–12 years) were: epistaxis.Cooper WO.05.1056/NEJMoa1110212. doi:10. doi:10.PMID 22043968. Cheetham TC.84.. Psychiatr. Connell FA. pp. Immunol. Stein CM. 15 December 2011. 20 December 2011. J. Clin.4088/jcp.J. Tris Pharmaceuticals. Table 2. 167: 148– 152. Psychiatry 65 (11): 1520– 1524. 16 (3): 148–155. .1016/j. DYANAVEL XR contains d-amphetamine and l-amphetamine in a ratio of 3. "ADHD drugs and serious cardiovascular events in children and young adults". Ray WA (November 2011). Retrieved 29 April 2015.11.1016/j.010.chc.. Bailen E. "Combining stimulants with monoamine oxidase inhibitors: a review of uses and one possible additional indication". Murray KT. Am. Clin."Dyanavel XR Prescribing Information" (PDF). 91. Lockey RF (2006).. Allergol. 90. Affect. Sox CM. PMID 16784007."FDA Drug Safety Communication: Safety Review Update of Medications used to treat Attention-Deficit/Hyperactivity Disorder (ADHD) in adults". Retrieved4 November 2013.PMID 15554766. 87. . Chan KA. Clin. "Rhinitis medicamentosa" (PDF). PMID 18295156. Kirshner HS. Quinn VP. United States Food and Drug Administration. Child Adolesc. 365 (20): 1896– 1904. Med. PMID 24972362. "How treatable is refractory depression?"..047. DOSAGE FORMS AND STRENGTHS Extended-release oral suspension contains 2."FDA Drug Safety Communication: Safety Review Update of Medications used to treat Attention-Deficit/Hyperactivity Disorder (ADHD) in children and young adults". 85. N. Retrieved 4 November 2013. PMC 2408826.v65n1113. McGrath PJ (June 2014). J. 86.United States Food and Drug Administration. October 2015.2 to 1 .2014.Vitiello B (April 2008). doi:10.5 mg amphetamine base per mL. 1–16. Callahan ST. Disord. Fish FA. allergic rhinitis and upper abdominal pain. O'Duffy A.doi:10. Fireman BH.Ramey JT. Retrieved 23 November 2015. Habel LA. N.2007. Deliyannides DA. "Understanding the risk of using medications for attention deficit hyperactivity disorder with respect to physical growth and cardiovascular function". Arbogast PG. Decongestants Causing Rhinitis Medicamentosa – Nasal decongestants: – Sympathomimetic: • Amphetamine 89. Investig. 88.Stewart JW.Feinberg SS (November 2004).jad. 17 (2): 459– 474.

1016/j. 93. Merck. "Global.O'Connor PG (February 2012).145) 98. 94.Lancet 385 (9963): 117– 171. In Sydor A. Andrade SE. Fireman BH. Sox CM. Selby JV (December 2011). PMID 2553 0442. 364– 375.2008. Ray WA. "Amphetamine-induced place preference in humans". 1990–2013: a systematic analysis for the Global Burden of Disease Study 2013" (PDF). Magnes.Collaborators (2015).1830. PMID 18557129. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed. 97. 95. norepinephrine. "Chapter 15: Reinforcement and Addictive Disorders". PMID 19111 278. Arbogast PG. Amphetamine use disorders . Hays HL. Retrieved 31 October 2014.Nechifor M (March 2008).). "Overdose of drugs for attention-deficit hyperactivity disorder: clinical presentation.doi:10. .Childs E. mechanisms of toxicity.11. Merck Manual for Health Care Professionals.92. Hyman SE (2009). and methylphenidate act as substrates for the cellular monoamine transporter. "ADHD medications and risk of serious cardiovascular events in young and middle-aged adults". and serotonin. Retrieved 8 May 2012. PMID 23757186. Psychiatry 65 (10): 900– 904. Smith DH.016. Boudreau DM. 3. Biol. Retrieved 3 March 2015. and national age-sex specific all-cause and cause-specific mortality for 240 causes of death. PMID 22161946.Kanehisa Laboratories (10 October 2014).Habel LA. Quinn VP. KEGG Pathway..1001/jama. Uratsu C.2011.425–4. dextroamphetamine. Res. Brown RY..PMC 3350308. Amphetamin e.788 (3. de Wit H (May 2009). like nonhumans. "Amphetamines". ISBN 9780071481274. Sidney S. "Amphetamine – Homo sapiens (human)". New York: McGraw-Hill Medical. Go AS. Dublin S. Aleguas A (June 2013). doi:10. JAMA 306 (24): 2673– 2683. 21 (1): 5–15. Raebel MA. doi:10. PMC 2693956. CNS Drugs 27 (7): 531– 543. These findings support the idea that subjective responses to a drug contribute to its ability to establish place conditioning. and management". pp. 99. Chan KA. Nguyen-Huynh MN. regional. prefer a place associated with amphetamine administration.1007/s40263-013-0084-8. Pawloski PA.Malenka RC.1016/S0140-6736(14)61682-2. Achacoso N. especially the dopamine transporter (DAT) and less so the norepinephrine (NET) and serotonin transporter. Nestler EJ. The mechanism of toxicity is primarily related to excessive extracellular dopamine.biopsych. Cooper WO. "Magnesium in drug dependences".doi:10. Cheetham TC. 96.Spiller HA.PMC 4340604.This study demonstrates that humans.

. PMID 21989194.2014. . Smith MA (September 2013). "Transcriptional and epigenetic mechanisms of addiction". 2008). 2007. PMID 25083822. 103.doi:10. Neurosci. In humans. PMC 3139704. 2008)...These findings suggest that exercise may “magnitude”dependently prevent the development of an addicted phenotype possibly by blocking/reversing behavioral and neuroadaptive changes that develop during and following extended access to the drug.933840. J. 2005). Lynch WJ. Robison AJ. PMC 3898681. .doi:10. This syndrome is characterized by a medication-induced increase in (or compulsive) engagement in non-drug rewards such as gambling. Neurosci.Dialogues Clin. PMC 3272277. "Molecular neurobiology of addiction: what's all the (Δ)FosB about?". 102. neuroplasticity..100. and non-drug addictions". 12 (11): 623–637.Similar to environmental enrichment. Neuropharmacology 61 (7): 1109– 1122. or sex (Evans et al. and one drug recovery program has seen success in participants that train for and compete in a marathon as part of the program (Butler. 37 (8): 1622– 1644. Peterson AB. Ruffle JK (November 2014). Sanchez V. as exercise reduces withdrawal symptoms and relapse in abstinent smokers (Daniel et al.. There is also some evidence that these preclinical findings translate to human populations. Abel J. studies have found that exercise reduces self-administration and relapse to drugs of abuse (Cosgrove et al.06. Olsen CM (December 2011). ΔFosB is an essential transcription factor implicated in the molecular and behavioral pathways of addiction following repeated drug exposure. "Cellular basis of memory for addiction". Nat.doi:10. Rev. "Natural rewards.010. Exercise has been proposed as a treatment for drug addiction that may reduce drug craving and risk of relapse. PMC 3788047. 15 (4): 431– 443.03.PMID 24459410. ΔFos B serves as one of the master control proteins governing this structural plasticity. Am. Prochaska et al. Neurosci.1016/j.2011. Biobehav.neuropharm. the role of dopamine signaling in incentive-sensitization processes has recently been highlighted by the observation of a dopamine dysregulation syndrome in some patients taking dopaminergic drugs. 2006. Lader. Nestler EJ (November 2011). 2006. shopping. Nestler EJ (December 2013). PMID 238 06439. Zlebnik et al.2013.. 101.1016/j. 2010)..011. Although few clinical studies have investigated the efficacy of exercise for preventing relapse. Drug Alcohol Abuse 40 (6): 428– 437..3109/00952990. 2002."Exercise as a novel treatment for drug addiction: a neurobiological and stage-dependent hypothesis". Aiken. Rev.1038/nrn3111. the few studies that have been .neubiorev. 104. PMID 2 1459101..doi:10.

neurobiological. Albertson TE (2011). Nestler EJ. Collectively. J. In Olson KR. In Sydor A. New York.. theory.ISBN 9780071668330. . Anderson IB. Brown RY.. Poisoning & Drug Overdose (6th ed.976708. Kim-Katz SY. . Kearney TE. . and practicality". 77–79. particularly for relapse to psychostimulants. In contrast to the scarce intervention trials to date. nearly universal safety profile. Malenka RC. The limited research conducted suggests that exercise may be an effective adjunctive treatment for SUDs. . Drug Alcohol Abuse 41 (1): 7– 15. including psychological. Benowitz NL. doi:10. Hyman SE (2009). more studies on the neurobiological mechanism of exercise and its roles in preventing and treating drug addiction are needed. a relative abundance of literature on the theoretical and practical reasons supporting the investigation of this topic has been published.PMID 25397661. Zhou Y. "Exercise-based treatments for substance use disorders: evidence. Blanc PD. Front. Taken together. a large number of human and rodent studies clearly show that there are sex differences in drug addiction and exercise.3109/00952990. The postulate that exercise serves as an ideal intervention for drug addiction has been widely recognized and used in human and animal rehabilitation..07. cognitive–behavioral therapies are the most successful treatment available for preventing the relapse of psychostimulant use. "Chapter 15: Reinforcement and Addictive Disorders".yfrne.conducted generally report a reduction in drug craving and better treatment outcomes . Li R (July 2015). 105. Ussher M (January 2015). As briefly reviewed above.PMID 26182835.. Wu AHB. and overall positive health effects..). Neuroendocrinol. these data suggest that the potential benefits of exercise during relapse. USA: McGraw-Hill Medical. 108. behavioral. New York: McGraw-Hill Medical. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed. as well as underlying neurobiological mechanisms. numerous theoretical and practical reasons support exercise-based treatments for SUDs. 107.. 106. p. "Sex differences in drug addiction and response to exercise intervention: From human to animal studies".2014. Zhou C. ISBN 9780071481274.. Linke SE.001. "Amphetamines". Am. may be mediated via chromatin remodeling and possibly lead to greater treatment outcomes.1016/j.2015. In particular. pp. these findings demonstrate that exercise may serve as a substitute or competition for drug abuse by changing ΔFosB or cFos immunoreactivity in the reward system to protect against later or previous drug use. Zhao M. doi:10..). 386. The sex differences are also found in the effectiveness of exercise on drug addiction prevention and treatment.Currently.

9758/cpn. Neurosci.. Perez-Mana C. Riad M. Nestler EJ (October 2008). PMID 18042492. February 2003. . Retrieved 9 February 2015. "Amphetamine – Homo sapiens (human)". As a result of its stability. Merck Manual Home Edition. 115. Nestler EJ (July 2006). "Review.brainresrev. Bo GD. 9: CD009695.. "Co-transmission of dopamine and glutamate". "Neural mechanisms of addiction: the role of reward-related learning and memory". PMID 23996457 . .1016/j. J.doi:10. 11 (3): 257–268. Clin. 29: 565– . Lond. 112. 58 (2): 290– 302.PMC 2834246. Retrieved 28 February 2007. 139 (1): 93– 96. Trans.CD009695. Rev.doi:10. Gen.pub2.PMC 3250102.2012. 111. PMID 19877494. 114. Renthal W. Nestler EJ (December 2012). Descarries L. Dialogues Clin.136. Soc. Transcriptional mechanisms of addiction: role of DeltaFosB". Cochrane Database Syst. Mount Sinai School of Medicine.005. PMID 22200950.363 (1507): 3245– 3255. ΔFosB overexpression in nucleus accumbens induces NFκB 116. PMC 2607320. Capella D. Hyman SE. "Glossary of Terms". Annu. The 35-37 kD ΔFosB isoforms accumulate with chronic drug exposure due to their extraordinarily long half-lives. the ΔFosB protein persists in neurons for at least several weeks after cessation of drug exposure.10. Pérez-Mañá C. 10 (3): 136– 143. "Transcriptional mechanisms of drug addiction".1002/14651858. Physiol. PMC 3569166. Biol. PMID 23430970. ed.109.201110659. Berube-Carriere N.1085/jgp. Torrens M. Sci.. Rev. Neurosci. Neurosci.3. Farre M (September 2013). Psychopharmacol.1098/rstb. Retrieved 31 October 2014. Brain Res. Castells X.PMID 18640924. KEGG Pathway. Rev. doi:10.0067.2007.2008.. Nestler EJ (September 2009).10.. Broussard JI (January 2012). 113. doi:10. "Amphetamines: Drug Use and Abuse". B. Trudeau LE (August 2008). doi:10. Kanehisa Laboratories (10 October 2014). 117. Malenka RC. Department of Neuroscience. Mendez JA. Retrieved 21 July 2014. "Efficacy of psychostimulant drugs for amphetamine abuse or dependence". 110. 118. Archived from the original on 17 February 2007. Merck. "Glutamate in dopamine neurons: synaptic versus diffuse transmission". "Chromatin regulation in drug addiction and depression". R. Philos.

Sci. "Chapter 4: Signal Transduction in the Brain".neuropharm.1523/JNEUROSCI.2012. 33 (8): 3434– 3442. 123. Vialou V. Hyman SE (2009). doi:10. 122. other psychostimulants". Casey GR. and rock 'n' roll: hypothesizing common mesolimbic activation as a function of reward gene polymorphisms".1016/j. 121. 124. Webb IC. 126.2013. PMC 2650365. Proc. Blum K. 106 (8): 2915– 2920. PMID 22641 964. Nat. New York. Neurobiol. Malenka RC. PMID 23085 425.1146/annurev.2012.4881-12. Kanehisa Laboratories (29 October 2014). "Methylphenidate-induced dendritic spine formation and DeltaFosB expression in nucleus accumbens". Kim Y.113009.04. PMID 23 643695.001. "Transcriptional and epigenetic mechanisms of addiction". Coolen LM (February 2013). "Addiction-related gene regulation: risks of exposure to cognitive enhancers vs. Coolen LM (February 2016).1016/j. Steiner H. Pitchers KK. 119. 76 Pt B: 259– 268. Weems PW.10. Oscar-Berman M.051605.neuro. Carnes S. p.pneurobio.1038/nrn3111. Beloate LN. 125. Nestler EJ. Gold M (March 2012). drugs. Nestler EJ (January 2014).Neuropharmacology. Lehman MN. Giordano J.doi:10. "Sex.0813179106. USA: McGraw-Hill Medical. Robison AJ.PMC 3525776. PMC 4040958. Nestler EJ (November 2011). Van Waes V (January 2013).2013.PMID 19202072 . Werner T. Nestler EJ. Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.29. Greengard P (February 2009). Natl. doi:10. PMC 3766384.598. J.). 100: 60– 80. "Natural and drug rewards act on common neural plasticity mechanisms with ΔFosB as a key mediator". Nairn AC. Retrieved 31 October 2014. Baron M. J.1073/pnas. doi:10. Neurosci.004. Acad. "Nucleus accumbens NMDA receptor activation . 94.PMID 16776597 . Teylan MA. 120. In Sydor A. PMID 21989194.S. Neurosci. PMC 3272277. Sands A. Laviolette SR. Psychoactive Drugs 44 (1): 38– 55. PMC 3865508.doi:10.662112. "Epigenetic mechanisms of drug addiction". U.1080/02791072. "Alcoholism – Homo sapiens (human)". Bowirrat A. Carnes P. 127.doi:10.PMID 23 426671. ISBN 9780071481274. Prog. doi:10. Rev.A. KEGG Pathway. 12 (11): 623–637.

Perez-Mana C. "Future pharmacological treatments for substance use disorders".2015.doi:10. J. 761: 345– 352. Expert Rev Clin Pharmacol 7 (3): 363– 374.019. 129. PMID 24716825. Rush CR (May 2014). Clin.pub2. 2010).regulates amphetamine cross-sensitization and deltaFosB expression following sexual experience in male rats". Pharmacol. Torrens M. Given that TAAR1 is primarily located in the intracellular compartments and existing TAAR1 agonists are proposed to get access to the receptors by translocation to the cell interior (Miller. 131.023. Stoops WW. 128. Neuropharmacology 101: 154– 164. Cochrane Database Syst. Farre M (September 2013).ejphar.doi:10.909283.. .the data reviewed here strongly support that TAAR1 is implicated in the functional regulation of monoaminergic systems. To date. Sofuoglu M (February 2014). "Efficacy of psychostimulant drugs for amphetamine abuse or dependence"..x.1111/j.2012. future drug design and development efforts may need to take strategies of drug delivery into consideration (Rajendran et al.1016/j. especially dopaminergic system. 77 (2): 382–400. "Combination pharmacotherapies for stimulant use disorder: a review of clinical findings and recommendations for future research". PMID 23039267.CD009695.2014. Taken together. Li JX (August 2015). Rev. Results of this review do not support the use of psychostimulant medications at the tested doses as a replacement therapy 130. PMC 4014020. and that TAAR1 serves as a homeostatic “brake” system that is involved in the modulation of dopaminergic activity. Pharmacol.1016/j. . "Trace amine-associated receptor 1: A promising target for the treatment of psychostimulant addiction".doi:10. and psychotherapy remains the mainstay of treatment. Existing data provided robust preclinical evidence supporting the development of TAAR1 agonists as potential treatment for psychostimulant abuse and addiction. Br. no pharmacological treatment has been approved for [addiction].1002/14651858. Eur. Castells X.13652125.06.PMID 26092759. 2011). PMID 23996457. doi:10. J. Forray A. 9: CD009695. no widely effective medications have been approved. Capella D.04474.09. . PMID 26391065.doi:10....2015. Jing L.1586/17512433. Despite concerted efforts to identify a pharmacotherapy for managing stimulant use disorders.neuropharm.

National Library of Medicine. 137. "Update on amphetamine neurotoxicity and its relevance to the treatment of ADHD". pp. "Amphetamine". Hyman SE (2009). 329. methamphetamine is directly toxic to midbrain dopamine neurons. Nestler EJ. Acta Med. "Adderall XR Prescribing Information" (PDF).pub2. 124–125. "Treatment for amphetamine withdrawal". 11 (1): 8–16.). March 2007. "Dopaminergic neuronspecific oxidative stress caused by dopamine itself". Kao U. December 2013.). Rev.1177/1087054706295605. Atten. Brown RY.doi:10. 140. USA: McGraw-Hill Medical. Cochrane Database Syst. Retrieved 26 February 2014. Shire US Inc.CD003021.1002/14651858. A Handbook on Drug and Alcohol Abuse: The Biomedical Aspects (2nd ed. Neurotox. USA: Oxford University Press. p.(2): CD003021. ed. Nestler EJ. In Sydor A. 141. Hofmann FG (1983). Advokat C (July 2007). Direct toxic damage to vessels seems unlikely because of the dilution that occurs before the drug reaches the cerebral circulation. Heinzerling K. 370. "Chapter 5: Excitatory and Inhibitory Amino Acids". Miyazaki I. 136.132. "Intraneuronal dopaminequinone synthesis: a review". Hazardous Substances Data Bank. Retrieved 4 November2013. Zecca L (February 2000).1007/BF03033289. Barr Laboratories. In Sydor A. 138.doi:10. Malenka RC. 139. J. PMID 19370579 . "Adderall IR Prescribing Information" (PDF). p. 135. PMID 12835101. USA: McGraw-Hill Medical. Res. Shoptaw SJ. PMID 17606768. PMID 18596830. New York. Retrieved 30 December2013. New York. Brown RY. Malenka RC.Unlike cocaine and amphetamine. Asanuma M (June 2008).ISBN 9780071481274. . Hyman SE (2009). 133. Sulzer D. Shoptaw SJ. Ling W (April 2009). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed. Okayama 62 (3): 141–150. 134. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). 1 (3): 181– 195. New York. "Chapter 15: Reinforcement and addictive disorders". Disord. United States Food and Drug Administration. United States Food and Drug Administration. ISBN 9780195030570. ISBN 9780071481274. doi:10. Inc.

doi:10. Artymyshyn R.PMC 4183197. IUPHAR database. Gerald C (July 2001). Maguire JJ. Davoli A."Trace amines: identification of a family of mammalian G protein-coupled receptors". Pu X. Retrieved 8 December 2014. mct (28 January 2012). 147. Shire US Inc..neuron. "VMAT2: a dynamic regulator of brain monoaminergic neuronal function interacting with drugs of abuse". Sci. Mercuri NB (July 2011). "Electrophysiological effects of trace amines on mesencephalic dopaminergic neurons". Durkin MM. Retrieved29 May 2014. Ochoa FY. pp. "Adderall XR Prescribing Information" (PDF). 2006. Borowsky B. 144. Bonini JA. Front. Trends Pharmacol. Davenport AP (2 December 2014).1749-6632. 2012). 148. which reduces the basal firing frequency of dopamine (DA) neurons of the ventral tegmental area (VTA) 146.. U. doi:10. Retrieved30 December 2013. AMPH also increases intracellular calcium (Gnegy et al. • tonically activates inwardly rectifying K(+) channels. . 2007) and modulation and trafficking of the DAT (Fog et al. 143. 145. Ann. Underhill SM.PMID 250331 83. PMID 114599 29. Ledonne A. Sakrikar et al..05.043. Weihe E (January 2011). Li M. Neurosci.. PMID 21772817. "Amphetamine modulates excitatory neurotransmission through endocytosis of the glutamate transporter EAAT3 in dopamine neurons".005. Natl.2010. 98 (16): 8966–8971. PMC 3831354. University of Paris. Sci. Branchek TA.x.05906.1016/j.07.1016/j. December 2013. "TAAR1". United States Food and Drug Administration. Bernardi G.Neuron 83 (2): 404– 416. PMID 212 72013. doi:10. GenAtlas.34 (9): 489– 496.2013. Acad.2014.A. Ogozalek KL. 1216: 86– 98. PMC 55357. Lakhlani PP. Raddatz R. Rizzo GR. Eiden LE. Y. Berretta N.S. 149.PMID 23968642.00056. Watts SD.tips. Syst. Sci. Amara SG (July 2014).3389/fnsys. Proc. doi:10. N.2011. Adham N.1111/j. PMC 4159050. Lichtblau H.142. "Mechanisms of dopamine transporter regulation in normal and disease states".doi:10. Foster JD (September 2013). International Union of Basic and Clinical Pharmacology.151105198. Acad. Jones KA. "TA1 receptor". 8– 10. Wheeler DS. Kouranova E. 2004) that is associated with calmodulin/CamKII activation (Wei et al. Vaughan RA. Pathirana S. PMC 3131148.1073/pnas. Boyle N. Ingram SL. 5: 56.

member 1 [ Homo sapiens (human) ]". system Xag). National Center for Biotechnology Information. Jones DC (February 2007). PMID 20 402963.105. Amphetamine. "[The role of glial monoamine transporters in the central nervous system]". These studies suggest that DA plays a role in regulating CART gene expression possibly via the activation of CREB. 154. 151. dopaminergic nerve terminals in the NAc synapse on CARTcontaining neurons (Koylu et al. NCBI Gene. Inazu M. 153. Audus KL (January 2005). Ther. doi:10. J. 312 (1): 192–198.. 152.1124/jpet.. Pharmacol. "Interaction of organic cation transporter 3 (SLC22A3) and amphetamine". IUPHAR database. doi:10. "Biomolecular Interactions and Pathways". Neurochem. J. Pharmacol. Retrieved13 November 2015. 2004). . PMID 13677912. internalization of EAAT3 triggered by amphetamine increases glutamatergic signaling and thus contributes to the effects of amphetamine on neurotransmission.PMID 15316089.. Markowitz JS (July 2010). Vicentic A. 320 (2): 499– 506.x.1111/j. J. PubChem Compound. Retrieved13 October 2013. Zhu HJ. 155. National Center for Biotechnology Information.072363.1124/jpet. Amphetamine modulates excitatory neurotransmission through endocytosis of the glutamate transporter EAAT3 in dopamine neurons. Exp.PMC 3775896. CART and DA receptor transcripts colocalize (Beaudry et al. Nihon Shinkei Seishin Yakurigaku Zasshi (in Japanese) 23 (4): 171– 178. .1471-4159.. Ther.2010. Colocalization studies also support a role for CART in the actions of psychostimulants. "SLC1A1 solute carrier family 1 (neuronal/epithelial high affinity glutamate transporter. .150. International Union of Basic and Clinical Pharmacology. 1999). "The CART (cocaineand amphetamine-regulated transcript) system in appetite and drug addiction". doi:10. "Novel organic cation transporter 2-mediated carnitine uptake in placental choriocarcinoma (BeWo) cells". Exp... Gründemann D. Retrieved11 November 2014. "SLC18 family of vesicular amine transporters". 114 (1): 142– 149. Takeda H.. Rytting E. Appel DI.104.PMID 16840648. Matsumiya T (August 2003)..091512.06738. 156. hence providing the proximity required for neurotransmitter signaling. The physiological importance of CART was further substantiated in numerous human studies demonstrating a role of CART in both feeding and psychostimulant addiction. . Second.

initiates downstream cascades and finally exerts its neuroprotective effect under normal or pathological conditions. Pharmacol. it was demonstrated that CART. Hutson PH.05642. doi:10. little is known about the way in which CART peptide interacts with its receptors. "Targets". that may be involved in the cerebroprotection afforded by CART 158. 159.1440-1681.157. Patkar AA (September 2014).x. Amphetamine. First. "Monoamine oxidase (Homo sapiens)". T3DB.. Nat. Monogr.1038/nrn2493. "CART peptide stimulation of G protein-mediated signaling in differentiated PC12 cells: identification of PACAP 6–38 as a CART receptor antagonist". "CART peptides: regulators of body weight. Polgar WE. Lin Y. 161. Several studies on CART (cocaine. such as regulation of the immunological system and protection against energy failure. Rodriguez L. Retrieved24 February 2015. Hubert GW. doi:10. Physiol.and amphetamine-regulated transcript in the central nervous system". which focused attention on the role of CART in the central nervous system (CNS) and neurological diseases. 39 (6): 586– 592. In fact. 3.PMID 18802445. Han L. Retrieved 4 May 2014. PMID 9686407. Toll L. Neurosci. Clin.006. 162. PMC 3170513..178: 440–466. had a cerebroprotective against focal ischaemic stroke and inhibited the neurotoxicity of β-amyloid protein. Auh JS (March 1998). Slawecki C. Exp. PMC 4418456.1016/j. "Preclinical pharmacology of amphetamine: implications for the treatment of neuropsychiatric . O'Brien A. Haggart D. 1 January 2014. The literature indicates that there are many factors. Brandt SR. Kennedy JM. CART 55–102 inhibited voltage-gated L-type Ca2+ channels . Zhang M.1111/j. PMID 2185513 8.07. doi:10. Hall RA. Rogge G. as a neurotrophic peptide. Madhoo M. "Roles of cocaine. 163. Schwartz RW. Kuhar MJ (October 2011). Recen tly. BRENDA.and amphetamine-regulated transcript)peptide-induced cell signalling have demonstrated that CART peptides activate at least three signalling mechanisms. Kuhar MJ (October 2008). Adapa ID. University of Alberta.PMID 22077697.2011. 160. Jones D.2011. Berzetei-Gurske IP. 9 (10): 747– 758. Xu Y (June 2012). Farrington L. Rev.npep. Craymer K. White A. "Standard binding and functional assays related to medications development division testing for potential cocaine and opiate narcotic treatment medications". Tarazi FI. Neuropeptides 45 (5): 351– 358. Technische Universität Braunschweig. Lin Y. reward and other functions". NIDA Res.

pp.1300667. cortisol secretion. Biol. Edwards RH. 19 (23): . Britt JP. Miller GM. Gilmour B (December 2011). Schruers KR. Dickson SL. Pharmacol.2010. Landgren S. Engel JA. Hnasko TS. Ellingsen DM. 166. PMID 22386378. "Effects of Amphetamines in Humans". Zhou Y.02. Drug Addiction II: Amphetamine. Matthews PM..2012. Lingford-Hughes AR. Psychotogen. Mol. Bonci A (June 2010). 143 (3): 253– 264. PMID 25565999.1038/sj. PMC 2918390. "Trace amine-associated receptor 1 is a stereoselective binding site for compounds in the amphetamine class". Endocrinol. 2009) and following amphetamine administration in humans (Colasanti et al. 8: 1– 15.1754-10. McCaul M. Oswald LM. J. Lewin AH. Wong DF. Behav. Stuber GD. Neurosci.doi:10.doi:10.1016/j. Ther. Heidelberg. 340 (1): 80– 87. Long CJ. Rabiner EA (September 2012). 170. Leknes S (December 2014). Chem.Neuropsychopharmacology 30 (4): 821– 832. 30 (24): 8229–8233.doi:10.2014. 167. Nutt DJ. Findings from several prior investigations have shown that plasma levels of glucocorticoids and ACTH are increased by acute administration of AMPH in both rodents and humans 169. Egecioglu E. and Marihuana Dependence. Choi L. Jerlhag E (June 2011). Cell.3389/fnbeh. Gunn RN. Tziortzi AC. Kuwabara H. Psychiatry 72 (5): 371– 377. Neurosci. Quelch D. S imilar MOR activation patterns were reported during positive mood induced by an amusing video clip (Koepp et al. "Statedependent μ-opioid modulation of social motivation".mce.005. Reed LJ. PMC 4264475. Bioorg.1523/JNEUROSCI..pharmthera.disorders". doi:10.biopsych.2011.2014. Berlin. PMID 24657455. "Relationships among ventral striatal dopamine release. 165.00430. 247–260. Reiley RR. Front. Wand GS (April 2005). Waldman AD. 164. Erritzoe D. doi:10."Dopaminergic terminals in the nucleus accumbens but not the dorsal striatum corelease glutamate". PMID 21354264.doi:10. Skibicka KP. Colasanti A.017. and subjective responses to amphetamine". Germany: Springer. 168.ISBN 9783642667091. Loseth GE.npp.1016/j.PMID 15702139.03. Searle GE. Gunne LM (2013). Germany. Med. Retrieved 4 December 2015. Brasic J. Hill SP. "The role of the central ghrelin system in reward from food and chemical drugs".027. "Endogenous opioid release in the human brain reward system induced by acute amphetamine administration". 2012). P MID 20554874.01.1016/j.

A. PMC 2830119. Retrieved 7 May 2014. Proc.S. Wettstein JG. p-Hydroxynorephedrine. Technische Universität Braunschweig. Ozmen L. Hoener MC (May 2005). Hoener MC (May 2011). Chapter 5— Medical Aspects of Stimulant Use Disorders.1073/pnas. Shire US Inc. . "Route of Administration". Trube G. Natl.007. Richard RA (1999). BRENDA. PMC 3101002. Davenport AP (March 2009). "International Union of Pharmacology.1124/pr. Phenylpropanolamine. Gainetdinov RR.10.1016/j.2011. January 2015. Sotnikova TD. Retrieved 15 October 2013. butyrate-CoA ligase. PMC 3236098. Bonner TI. "Vyvanse Prescribing Information" (PDF). BRENDA. Neubig RR.7044–7048. "TAAR1 activation modulates monoaminergic neurotransmission. Pharmacol. 108 (20): 8485– 8490. PubChem Compound. Bradaia A. Acad. 176. "Substrate/Product". 12–16. 173. doi:10. 177. 178. Trends Pharmacol.61 (1): 1– 8. Chaboz S. p-Hydroxyamphetamine. Mory R. Recommendations for trace amine receptor nomenclature". Lindemann L. National Center for Biotechnology Information. National Center for Biotechnology Information. Zbinden KG. Pouzet B. Treatment Improvement Protocol 33. Retrieved 15 October 2013. National Center for Biotechnology Information Bookshelf. "Compound Summary". PubChem Compound. Foord SM.109. 171. preventing hyperdopaminergic and hypoglutamatergic activity". United States Food and Drug Administration. 174. Maguire JJ. Revel FG. PMID 19325074. National Center for Biotechnology Information. Substance Abuse and Mental Health Services Administration. 179. Caron MG. Metzler V. pp.bmc. Rev. U. PubChem Compound. PMID 22 037049. Retrieved 7 May 2014. Norcross R. 172. Durkin S. Parker WA. Technische Universität Braunschweig.doi:10. "Substrate/Product". Bettler B. glycine N-acyltransferase. LXXII. Meyer CA.1103029108. "A renaissance in trace amines inspired by a novel GPCR family".doi:10. Retrieved 15 October 2013. 180. "Compound Summary". Retrieved24 February 2015.001107. Sci. Moreau JL. 175. PMID 21525407 . "Compound Summary".

assigned to Smith Kline French . "The Mechanism of the Leuckart Reaction". Ely R (April 2009). "Recommended methods of the identification and analysis of amphetamine. Int.and N-substituted amphetamines as heptafluorobutyryl derivatives". (Phila. Tetrahedron Lett. Retrieved 6 December 2014. Forensic Science International 42 (3): 183– 199. 9–12.1016/S0040-4039(00)88151-4. Vermont Department of Health. "Review: Synthetic Methods for Amphetamine" (PDF). Retrieved 8 November 2013. 2006. National Center for Biotechnology Information. and their ring-substituted analogues in seized materials"(PDF). Korte T (March 1991). 188.1021/jo01145a001. Retrieved 29 January 2012. 26 (5): 274– 281. Jansen ACA (May 1983). J. United Nations. Government of Vermont.516752. 186.doi:10.3109/15563650. 190.2005. Cantrell TS (August 1989).Sci. ISSN 1556-3650. Pubchem Compound.doi:10. PMID 1855720. 189. doi:10. Schep LJ. Lillsunde P.tips.007.2'-diol". PMID 15860375.) 48 (7): 675–694. Slaughter RJ. Pubchem Compound. "Amphetamine Hydrochloride". "Method for the separation of optically active alpha-methylphenethylamine". 191. US patent 2276508.1016/j. Nabenhauer FP. "Amphetamine Phosphate". Chem. "Synthetic reductions in clandestine amphetamine and methamphetamine laboratories: A review". Crime Scene (Northwest Association of Forensic Scientists) 37 (2): 15–25. pp. Retrieved 14 October 2013.2010.1'-binaphthalene]-2. Forensic Sci. "Historical overview of methamphetamine". doi:10. published 17 March 1942. 185. Org. methamphetamine. Clin. doi:10. 182. 49 (2): 205–213. United Nations Office on Drugs and Crime. 181. Beasley DM (August 2010).1016/03790738(91)90081-s. PMI D 20849327. Allen A.03. 187. Allen A. National Center for Biotechnology Information. Toxicol. 24 (31): 3261–3262. 16 (5): 661– 672. "Determination of ring.1016/0379-0738(89)90086-8. 184. "A highly stereoselective synthesis of s(−)-[1. Brussee J. Pollard CB. Retrieved 8 November 2013. "The clinical toxicology of metamfetamine". Young DC (May 1951). doi:10. 183.

Salouros H. "Determination of amphetamine. and Atomoxetine (Straterra)". "Bioanalytical procedures for determination of drugs of abuse in blood". J. 201. Collins M. PMID 9700558. Cota DJ (March 2011). Chromatogr.doi:10. "δ13C and δ2H isotope ratios in amphetamine synthesized from benzaldehyde and nitroethane". Chem. Robertson J. Am. Anal. Organic Reactions 17: 216. Chem. p. PMID 17468860. 388 (7): 1415–1435. USA: Wiley-Interscience. doi:10. In Johnson DS.4563. Kraemer T.or017. McBee ET. 200. 247. Appl. Hass HB (June 1946). Soc. doi:10. Goldberger BA. J.192. J.1021/ja01192a023. Retrieved 31 October 2013. PMID 8075776. 193. Kalish J (December 1948). Chromatogr. Leonard N. "Synthesis of isomer-free benzyl methyl acetoacetic methyl ester".1021/ja01210a032. 2012.03. J. United States Department of Health and Human Services. "Confirmatory tests for drugs in the workplace by gas chromatography-mass spectrometry". "A new reaction of nitriles.1016/00219673(94)85218-9. 198. ISBN 9780471752158. Arenas-Queralt A (June 2010). Substance Abuse and Mental Health Services Administration. Gray DL (2007). Flisik AC.doi:10. Cone EJ (July 1994). methamphetamine and amphetamine-derived designer drugs or medicaments in blood and urine". 195. Methylphenidate (Ritalin).1016/S03784347(97)00515-X. Rapid Commun. doi:10.1002/rcm. Technical Assistance Publication Series 32. New York. 24 (11): 1653– 1658. A674 (1–2): 73–86. PMID 18105933. "The Ritter Reaction". The Art of Drug Synthesis. Ritter JJ. 194.doi:10. Bioanal. Patrick TM. Heagney AC. Soc. 199. from allyl chloride". Li JJ. Cawley AT. published 31 December 1946. synthesis of t-carbinamines". doi:10. assigned to Kay Fries Chemicals Inc 197. PMID 20985610. PMID 20486262. "Clinical Drug Testing in Primary Care" (PDF). Paul LD (August 2007). Maurer HH (August 1998). Sci.1007/s00216-007-12716. "Synthesis of arylpropylamines. US patent 2413493. Mass Spectrom. 70 (12): 4048– 4050.1002/0471264180. 68: 1009– 1011. 196. Bitler WP. 713 (1): 163–187. "Approved Treatments for Attention Deficit Hyperactivity Disorder: Amphetamine (Adderall). B Biomed. Kraemer T. Am. . Krimen LI. Chem.

Cody JT (May 2002). bronchodilator. Environ. 210. PMID 12024689. "Illegal or legitimate use? Precursor compounds to amphetamine and methamphetamine".5. doi:10. 85– 88. (±)-MDMA. Verstraete AG. doi:10. Topical nasal decongestants --(i) For products containing levmetamfetamine identified in 341. PMID 15516295. "Precursor medications as a source of methamphetamine and/or amphetamine positive drug testing results".20(b)(1) when used in an inhalant dosage form. (±)-MDA. 205. and antiasthmatic drug products for over-the-counter human use". 207. Retrieved 27 August2015.359. (±)-methamphetamine. doi:10. cough. Jacobs A. and (±)-MDEA in urine specimens by GC-EI-MS after derivatization with (R)-(−). 29 (5): 359– 364. Alcohol and Drug Misuse: A Handbook for Students and Health Professionals. April 2015. United States Food and Drug Administration. Occup. "Comparison of the sensitivity and specificity of six immunoassays for the detection of amphetamines in urine". 32(1): 15– 44.1081/DMR-100100562. Retrieved 7 March 2016. Anal.1093/jat/28. United Nations Office on Drugs and Crime. Jemionek J. June 2015. PMID 10711406. Musshoff F (February 2000). Sulzer D. J.ISBN 9780203871171. 209. "Part 341 – cold.). 211. Toxicol. England: Routledge. Retrieved 2 January 2014. p. allergy. 203.449. Searles DA (September 2004). Pubchem Compound. "Mechanisms of neurotransmitter release by amphetamines: a . Code of Federal Regulations Title 21: Subchapter D – Drugs for human use. Toxicol. Seal Beach.or (S)-(+)-α-methoxy-α-(trifluoromethyl)phenylacetyl chloride (MTPA)". Sonders MS. USA: Biomedical Publications. London.PMID 16105261. Med. 204. Anal.6. doi:10.1097/00043764-200205000-00012. "Identification". J. Paul BD. Rev. "Enantiomeric separation and quantitation of (±)-amphetamine. Heyden FV (August 2005). 208. "Annual prevalence of drug use by regions and globally by drug types". Galli A (April 2005). Rassool GH (2009).150 milligrams of levmetamfetamine. Levomethamphetamine.1093/jat/29. Baselt RC (2011). 113.04 to 0.202. 44 (5): 435– 450. Drug Metab. National Center for Biotechnology Information. 28 (6): 449– 455. Lesser D. Poulsen NW. pp. The product delivers in each 800 milliliters of air 0. J. Disposition of Toxic Drugs and Chemicals in Man (9th ed. 206.ISBN 9780962652387.

Retrieved19 November 2005.2 million or 0. Hill J (4 June 2004). "Medical science and the military: the Allies' use of amphetamine during World War II". J.wordsareimportant. doi:10. doi:10. 11 June 2009. August 2003. Preventing Amphetamine-type Stimulant Use Among Young People: A Policy and Programming Guide (PDF). Defalque RJ. 212. "Benzedrine sulphate in clinical medicine. 219. Bett WR (August 1946). Wright AJ (April 2011).2005. Gyenis A. Retrieved 25 May 2013.International Narcotics Control Board. United Nations Office on Drugs and Crime (2007).PMID 20997404. Retrieved 18 August2014. Mohan J. Med. 42 (2): 205– 233. 1. 22: 205– 218.review". 220. 32. 217. J. Mathematical Genius.ISBN 9789211482232. 24. doi:10. "World Drug Report 2014" (PDF).1162/JINH_a_00212. 218. a survey of the literature". 3. Wilson A (2008). 214. ISSN 2314-9086. "Controlled Substances Act". 75(6): 406– 433. 215.9% of young adults (15–34) used amphetamines in the last year 221. "List of psychotropic substances under international control" (PDF). Hist. Interdiscip.pneurobio. Portugal: European Monitoring Centre for Drugs and Drug Addiction. Hist. PMC 2478360.04. Retrieved 2 November 2013. (June 2014). 29 (2): 21–24. Lisbon. United Nations Office on Drugs and Crime.1016/s1522-8649(11)50016-2.com. May 2014: 13. Internet Journal of Criminology. PMID 22849208. PMID 15955613. . PMID 22073434. New York. Human (In That Order)" (PDF). Retrieved 11 November 2013. Rasmussen N (August 2011). "Methamphetamine for Hitler's Germany: 1937 to 1945".doi:10. Neurobiol. ed. "Forty Years of On the Road 1957– 1997". 216. Prog. Retrieved 18 March 2008. p.2810/32306. United States Food and Drug Administration. "Paul Erdos. "Mixing the Medicine: The unintended consequence of amphetamine control on the Northern Soul Scene" (PDF). Bull.003. Retrieved 18 August 2014. United Nations. 213.1016/j. 222. Archived from the original on 14 February 2008. Postgrad. Retrieved 4 November 2013. "European drug report 2014: Trends and developments" (PDF). USA: United Nations. DHARMA beat. Archived from the original (PDF) on 5 December 2005. Anesth.

Government of Canada. "Schedule 8". 2015. University of Alberta. 226. Australian Government Department of Health. Retrieved1 January 2016. Retrieved 19 August 2015. 228. March 2014. 231. social changes". "Class A. Retrieved7 March 2016. 234. 229. "Controlled Drugs and Substances Act". "Adzenys XR Prescribing Information" (PDF). . Park Jin-seng (25 May 2012). "Adzenys XR". Drugbank. Retrieved7 March 2016. 236. January 2016. Lisdexamfetamine. "Importing or Bringing Medication into Japan for Personal Use". "Moving to Korea brings medical. United States Food and Drug Administration. 237. Retrieved 19 August 2015. Archived from the original on 4 August 2007. Tocris. Retrieved 13 October 2013. 233. ADZENYS XR-ODT (amphetamine extended-release orally disintegrating tablet) contains a 3 to 1 ratio of d.to l-amphetamine. Retrieved 19 August 2015. Retrieved 14 November 2013. 22 May 2013. "Molecular Weight Calculator". 227. Government of the Netherlands. "Dextroamphetamine Sulfate USP". "Evekeo". United States Food and Drug Administration. a central nervous system stimulant. Government of the United Kingdom. Mallinckrodt Pharmaceuticals. United States Food and Drug Administration. Retrieved 11 November 2013. Retrieved 23 July2007. The Korean Times. Archived from the original (PDF) on 8 March 2014. 1 April 2004. Poisons Standard. 224. October 2015. Retrieved 3 April 2015. 235. Lenntech. Retrieved11 August 2015. Inc. Home Office. Retrieved 11 November 2013. "Dyanavel XR". Japanese Ministry of Health. 230.Thailand Food and Drug Administration. 225. "Table of controlled Narcotic Drugs under the Thai Narcotics Act" (PDF). Labour and Welfare.223. "D-amphetamine sulfate". Retrieved3 November 2013. "Opiumwet". p. Neos Therapeutics. 232. 15. B and C drugs". Canadian Justice Laws Website. 8 February 2013. Retrieved 15 December 2015. "Identification". United States Food and Drug Administration.

Mallinckrodt Pharmaceuticals. March 2014. March 2014. Mallinckrodt Pharmaceuticals. External links .238. "Dextroamphetamine Saccharate". "Amphetamine Sulfate USP". Retrieved 19 August 2015. March 2014. Retrieved 19 August 2015. "Amphetamine Aspartate". 239. Mallinckrodt Pharmaceuticals. 240. Retrieved 19 August 2015.