||This article needs more medical references for verification or relies too heavily on primary sources. (December 2013)|
|Systematic (IUPAC) name|
|Trade names||Dexedrine, Dextrostat, Dexamphetamine|
|Licence data||US Daily Med:|
|Pregnancy cat.||B3 (AU) C (US)|
|Legal status||Controlled (S8) (AU) Schedule I (CA) Class B (UK) Schedule II (US)|
|Dependence liability||Moderate to High|
|Routes||Oral (only medically-utilized route)|
|Metabolism||Hepatic (CYP2D6-mediated hydroxylation) and FMO|
|Excretion||Renal (45%); urinary pH-dependent|
|Boiling point||201.5 °C (395 °F)|
|Solubility in water||20 mg/mL (20 °C)|
Dextroamphetamine (USAN) or Dexamfetamine (INN and BAN) is a potent psychostimulant and amphetamine stereoisomer clinically prescribed for the treatment of attention deficit-hyperactivity disorder (ADHD) in Children and Adults and for a sleep disorder in children and adults clinically known as narcolepsy.
The amphetamine molecule has two stereoisomers: levoamphetamine and dextroamphetamine. Dextroamphetamine is the dextrorotatory, or "right-handed", enantiomer of the amphetamine molecule. Dextroamphetamine is available as a generic drug or under several brand names, including Dexedrine and Dextrostat, Dexamphetamine.
Dextroamphetamine is also an active metabolite of the prodrug lisdexamfetamine (Vyvanse), . Common side effects include dry mouth, insomnia and headache. Temporary growth rate reduction is also a known side effect in paediatric use.
- 1 Uses
- 2 Side effects
- 3 Withdrawal
- 4 Contraindications
- 5 Pharmacology
- 6 History, society, and culture
- 7 Notes
- 8 References
- 9 External links
- For more information, see Amphetamine#Uses.
Though such use remains out of the mainstream, dextroamphetamine has been successfully applied in the treatment of certain categories of depression as well as other psychiatric syndromes. Such alternate uses include reduction of fatigue in cancer patients, antidepressant treatment for HIV patients with depression and debilitating fatigue, and early-stage physiotherapy for severe stroke victims. If physical therapy patients take dextroamphetamine while they practice their movements for rehabilitation, they may learn to move much faster than without dexamfetamine, and in practice sessions with shorter lengths.
The physical side effects of dextroamphetamine can include:
- Weight loss
- Dry mouth
- Decreased fatigue
- Appetite loss
- Abdominal pain
- Hypertension or hypotension
- Exacerbation of motor and phonic tics and Tourette’s syndrome
- Reduced seizure threshold
- Transient growth stunting
The psychological side effects of dextroamphetamine can include:
- Emotional lability
- Insomnia or wakefulness
- Increased initiative
- Increased self-confidence
- Euphoria, sometimes followed by transient dysphoria
- Changes in libido
- Raynaud’s phenomenon
- A psychosis which, very rarely, can occur during long-term treatment at therapeutic doses
Recent studies by the FDA indicate that, in children, young adults, and adults, there is no association between serious adverse cardiovascular events (sudden death, myocardial infarction, and stroke) and the use of dextroamphetamine or other ADHD stimulants. According to the USFDA, "there is no systematic evidence that stimulants cause aggressive behavior or hostility."
An overdose on amphetamine enantiomers is rarely fatal with appropriate care, but can lead to a number of different symptoms. A moderate overdose may induce symptoms including: arrhythmia, confusion, dysuria, hypertension or hypotension, hyperthermia, hyperreflexia, myalgia, severe agitation, tachypnea, tremor, urinary hesitancy, and urinary retention. An extremely large overdose may produce symptoms such as adrenergic storm, amphetamine psychosis, anuria, cardiogenic shock, cerebral hemorrhage, circulatory collapse, hyperpyrexia, pulmonary hypertension, renal failure, rhabdomyolysis, serotonin syndrome, and stereotypy.[ref-note 1] Fatal amphetamine poisoning usually also involves convulsions and coma.
Abuse of amphetamines can result in a stimulant psychosis which may present with a variety of symptoms (e.g. paranoia,hallucinations, delusions). A Cochrane Collaboration review on treatment for amphetamine, dextroamphetamine, and metamphetamine induced psychosis states that about 5-15% of users fail to recover completely. The same review asserts that, based upon at least one trial, antipsychotic medications effectively resolve the symptoms of acute amfetamine psychosis. An amphetamine psychosis may also develop occasionally as a treatment-emergent side effect.
While addiction is a serious risk with heavy recreational amphetamine use, it is unlikely to arise from typical medical use. Tolerance is developed rapidly in amphetamine abuse; therefore, periods of extended use require increasing amounts of the drug in order to achieve the same effect. According to a Cochrane Collaboration review on withdrawal in highly dependent amphetamine and methamphetamine abusers, "when chronic heavy users abruptly discontinue amphetamine use, many report a time-limited withdrawal syndrome that occurs within 24 hours of their last dose." This review noted that withdrawal symptoms in chronic, high-dose users are frequent, occurring in up to 87.6% of cases, and persist for 3–4 weeks with a marked "crash" phase occurring during the first week. Amphetamine withdrawal symptoms can include fatigue, dysphoric mood, increased appetite, vivid or lucid dreams, hypersomnia or insomnia, increased movement or decreased movement, anxiety, and drug craving. The review suggested that withdrawal symptoms are associated with the degree of dependence, suggesting that therapeutic use would result in far milder discontinuation symptoms. The USFDA does not indicate the presence of withdrawal symptoms following discontinuation of pharmaceutical amphetamine use after an extended period at therapeutic doses.
- Moderate-severe hypertension
- Tourette syndrome
- Psychomotor agitation
- Advanced arteriosclerosis
- Ischaemic heart disease
- Angina pectoris
- Hypersensitivity or idiosyncrasy to the sympathomimetic amines
- During or within 14 days following the administration of monoamine oxidase inhibitors (MAOIs) (hypertensive crisis may occur)
- For more information, see Amphetamine#Pharmacodynamics.
Amphetamine and its enantiomers have been identified as potent full agonists of trace amine-associated receptor 1 (TAAR1) (aka "TAAR1"), a GPCR, discovered in 2001, that is important for regulation of monoaminergic systems in the brain. Activation of TAAR1 increases cAMP production via adenylyl cyclase activation and inhibits the function of the dopamine transporter, norepinephrine transporter, and serotonin transporter, as well as induce effluxion of these neurotransmitters. Amphetamine enantiomers are also substrates for a specific neuronal synaptic vesicle uptake transporter called VMAT2. When amphetamine is taken up by VMAT2, the vesicle releases (effluxes) dopamine, norepinephrine, and serotonin, among other monoamines, into the cytosol in exchange.
Dextroamphetamine (the dextrorotary enantiomer) and levoamphetamine (the levorotary enantiomer) have identical pharmacodynamics, but their binding affinities to their biomolecular targets vary. Dextroamphetamine is a more potent agonist of TAAR1 than levoamphetamine. Consequently, dextroamphetamine produces roughly three to four times more CNS stimulation than levoamphetamine; however, levoamphetamine has slightly greater cardiovascular and peripheral effects.
Related endogenous compounds
- For more information, see Trace amines.
Amphetamine has a very similar structure and function to the endogenous trace amines, which are naturally occurring molecules produced in the human body and brain. Among this group, the most closely related compounds are phenethylamine, the parent compound of amphetamine, and N-methylphenethylamine, an isomer of amphetamine (i.e., identical molecular formula). In humans, phenethylamine is produced in the body directly from phenylalanine by the same enzyme that converts L-DOPA into dopamine, aromatic amino acid decarboxylase. In turn, N‑methylphenethylamine is metabolized from phenethylamine by phenylethanolamine N-methyltransferase, which the same enzyme that metabolizes norepinephrine into adrenaline. Like amphetamine, both phenethylamine and N‑methylphenethylamine regulate monoamine neurotransmission via TAAR1; however, unlike amphetamine, both of these substances are broken down by monoamine oxidase, and therefore have a shorter half-life than amphetamine.
The half-life of amphetamine enantiomers differ and vary with age. The half life for dextroamphetamine is 9 hours for children of ages 6–12, 11 hours in adolescents aged 13–17, and 10 hours in adults. For levoamphetamine, the half-life is 11 hours for children of ages 6–12, 13–14 hours in adolescents aged 13–17, and 13 hours in adults. The immediate-release and extended release variants of salts of both isomers reach peak plasma concentrations at 3 hours and 7 hours post-dose respectively. Amphetamine is eliminated renally with 30–40% of the drug being excreted unchanged at normal urinary pH. Amphetamine is a weak base with a pKa of 9–10; consequently, when the urinary pH is basic, more of the drug is in its free base form and less is excreted. When urine pH is abnormal, the urinary recovery of amphetamine may range from a low of 1% to as much as 75%, depending mostly upon whether urine is too alkaline or acidic respectively. Amphetamine is usually eliminated within two days of the last oral dose. Apparent half-life and duration of effect increase with repeated use and accumulation of drug.
Metabolism occurs mostly in the liver by the cytochrome P450 (CYP) detoxification system. CYP2D6 and flavin-containing monooxygenase are the only enzymes currently known to metabolize amphetamine in humans. Amphetamine has a variety of excreted metabolic products, including 4-hydroxyamfetamine, 4-hydroxynorephedrine, 4-hydroxyphenylacetone, benzoic acid, hippuric acid, norephedrine, and phenylacetone. Among these metabolites, the active sympathomimetics are 4‑hydroxyamphetamine, 4‑hydroxynorephedrine, and norephedrine.
History, society, and culture
Racemic amfetamine was first synthesized under the chemical name "phenylisopropylamine" in Berlin, 1887 by the Romanian chemist Lazar Edeleanu. It was not widely marketed until 1932, when the pharmaceutical company Smith, Kline & French (now known as GlaxoSmithKline) introduced it in the form of the Benzedrine inhaler for use as a bronchodilator. Notably, the amfetamine contained in the Benzedrine inhaler was the liquid free-base,[n 1] not a chloride or sulfate salt.
Three years later, in 1935, the medical community became aware of the stimulant properties of amfetamine, specifically dexamfetamine, and in 1937 Smith, Kline, and French introduced tablets under the tradename Dexedrine. In the United States, Dexedrine was approved to treat narcolepsy, attention disorders, depression, and obesity. In Canada, epilepsy and parkinsonism were also approved indications. Dexamfetamine was marketed in various other forms in the following decades, primarily by Smith, Kline, and French, such as several combination medications including a mixture of dexamfetamine and amobarbital (a barbiturate) sold under the tradename Dexamyl and, in the 1950s, an extended release capsule (the "Spansule").
It quickly became apparent that dexamfetamine and other amfetamines had a high potential for misuse, although they were not heavily controlled until 1970, when the Comprehensive Drug Abuse Prevention and Control Act was passed by the United States Congress. Dexamfetamine, along with other sympathomimetics, was eventually classified as Schedule II, the most restrictive category possible for a drug with a government-sanctioned, recognized medical use. Internationally, it has been available under the names AmfeDyn (Italy), Curban (US), Obetrol (Switzerland), Simpamina (Italy), Dexedrine/GSK (US & Canada), Dexedrine/UCB (United Kingdom), Dextropa (Portugal), and Stild (Spain).
The U.S. Air Force uses dexamfetamine as one of its "go pills", given to pilots on long missions to help them remain focused and alert. Conversely, "no-go pills" are used after the mission is completed, to combat the affects of the mission and "go-pills". The Tarnak Farm incident was linked by media reports to the use of this drug on long term fatigued pilots. The military did not accept this explanation, citing the lack of similar incidents. Newer stimulant medications or awakeness promoting agents with different side effect profiles, such as modafinil, are being investigated and sometimes issued for this reason.
In the United States, an instant-release (IR) tablet preparation of the salt dexamfetamine sulfate is approved under the brand names Dexedrine and Dextrostat, in 5 mg and 10 mg strengths, and generic formulations from Teva Pharmaceutical Industries and recently Wilshire Pharmaceuticals. It is also available as a capsule preparation of controlled-release (CR) dexamfetamine sulfate, under the brand names Dexedrine SR and Dexedrine Spansule, in the strengths of 5 mg, 10 mg, and 15 mg. A bubblegum flavored oral solution is available under the brand name ProCentra, manufactured by FSC Pediatrics, which is designed to be an easier method of administration in children who have difficulty swallowing tablets, each 5 mL contains 5 mg dexamfetamine.
In Australia, dexamfetamine is available in bottles of 100 instant release 5 mg tablets as a generic drug. or slow release dexamfetamine preparations may be compounded by individual chemists. Similarly, in the United Kingdom it is only available in 5 mg instant release sulfate tablets under the generic name dexamfetamine sulphate having had been available under the brand name Dexedrine prior to UCB Pharma disinvesting the product to another pharmaceutical company (Auden Mckenzie).
Dexamfetamine is the active metabolite of the prodrug lisdexamfetamine (L-lysine-d-amphetamine), available by the brand name Vyvanse. Lisdexamfetamine is metabolised in the gastrointestinal tract, while dextroamphetamine's metabolism is hepatic. Lisdexamfetamine is therefore an inactive compound until it is converted into an active compound by the digestive system. Vyvanse is marketed as once-a-day dosing as it provides a slow release of dexamfetamine into the body. Vyvanse is available as capsules, and in six strengths; 20 mg, 30 mg, 40 mg, 50 mg, 60 mg, and 70 mg. The conversion rate of lisdexamfetamine to dextroamphetamine base is 0.2948, thus a 30 mg-strength Vyvanse capsule is molecularly equivalent to 8.844 mg dexamfetamine base.
Another pharmaceutical that contains dextroamphetamine is Adderall. The drug formulation of Adderall (both controlled and instant release forms) is:
Adderall is roughly three-quarters dextroamphetamine, with it accounting for 72.7% of the amphetamine base in Adderall (the remaining percentage is levoamphetamine).
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