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For the racemic compound, see Amphetamine.
Systematic (IUPAC) name
Clinical data
Trade names Dexedrine, Dextrostat
AHFS/ monograph
MedlinePlus a605027
Licence data US Daily Med:link
Pregnancy cat.
Legal status
Moderate to High
Routes Medical (oral) non medical (Oral, IV, IM, intranasal)
Pharmacokinetic data
Bioavailability Oral 75–100%[1]
Metabolism CYP2D6,[2] DBH,[3] FMO3,[4] XM-ligase,[5] and ACGNAT[6]
Half-life 10-12 hours[7][8]
Excretion Renal (45%);[9] urinary pH-dependent
CAS number 51-64-9 YesY
ATC code N06BA02
PubChem CID 5826
DrugBank DB01576
ChemSpider 5621 YesY
KEGG D03740 YesY
Chemical data
Formula C9H13N 
Mol. mass 135.20622
Physical data
Density 0.913 g/cm³
Boiling point 201.5 °C (395 °F)
Solubility in water 20 mg/mL (20 °C)
 YesY (what is this?)  (verify)

Dextroamphetamine[note 1] is a potent psychostimulant and amphetamine stereoisomer prescribed for the treatment of attention deficit hyperactivity disorder (ADHD) in children and adults and the rare sleep disorder, narcolepsy. Dextroamphetamine is also widely used by military air forces as a 'go-pill' during fatigue-inducing mission profiles such as night-time bombing missions. Preparations containing dextroamphetamine were also used in World War II as a treatment against fatigue.

The amphetamine molecule has two stereoisomers:[note 2] levoamphetamine and dextroamphetamine. Dextroamphetamine is the more active 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. Dextroamphetamine is also the active metabolite of the prodrug[note 3] lisdexamfetamine.

Dextroamphetamine, like other amphetamines, elicits its stimulating effects via two distinct actions: first, it inhibits the transporter proteins for the monoamine neurotransmitters (namely the serotonin, norepinephrine and dopamine transporters) via trace amine-associated receptor 1 (TAAR1); and second, it releases these neurotransmitters from synaptic vesicles via vesicular monoamine transporter 2. It also shares many chemical and pharmacological properties with the human trace amine neurotransmiters, especially phenethylamine and N-methylphenethylamine, the latter being an isomer of amphetamine that is produced within the human body.




Dexedrine Spansule 5, 10 and 15 mg capsules

Dextroamphetamine is used to treat attention deficit hyperactivity disorder (ADHD) and narcolepsy, an excessive tendency to fall asleep. It is sometimes prescribed off-label for its past medical indications, such as depression, obesity, and nasal congestion.[10][11] Long-term amphetamine exposure in some animal species is known to produce abnormal dopamine system development or nerve damage,[12][13] but, in humans with ADHD, amphetamines appear to improve brain development and nerve growth.[14][15][16] Magnetic resonance imaging (MRI) studies suggest that long-term treatment with amphetamine decreases abnormalities in brain structure and function found in subjects with ADHD, and improves function in several parts of the brain, such as the right caudate nucleus of the basal ganglia.[14][15][16]

Reviews of clinical stimulant research have established the safety and effectiveness of long-term amphetamine use for ADHD.[17][18] Controlled trials spanning two years have demonstrated treatment effectiveness and safety.[18][19] One review highlighted a nine-month randomized controlled trial in children with ADHD that found an average increase of 4.5 IQ points and continued improvements in attention, disruptive behaviors, and hyperactivity.[19]

Current models of ADHD suggest that it is associated with functional impairments in some of the brain's neurotransmitter systems;[20] these functional impairments involve impaired dopamine neurotransmission in the mesocorticolimbic projection and norepinephrine neurotransmission in the locus coeruleus and prefrontal cortex.[20] Psychostimulants like methylphenidate and amphetamine are effective in treating ADHD because they increase neurotransmitter activity in these systems.[21][20][22] Approximately 70% of those who use these stimulants see improvements in ADHD symptoms.[23][24] Children with ADHD who use stimulant medications generally have better relationships with peers and family members, perform better in school, are less distractible and impulsive, and have longer attention spans.[17][23] The Cochrane Collaboration's review[note 4] on the treatment of adult ADHD with amphetamines stated that while amphetamines improve short-term symptoms, they have higher discontinuation rates than non-stimulant medications due to their adverse side effects.[26]

A Cochrane Collaboration review on the treatment of ADHD in children with tic disorders such as Tourette syndrome indicated that stimulants in general do not make tics worse, but high doses of dextroamphetamine could exacerbate tics in some individuals.[27] Other Cochrane reviews on the use of amphetamine following stroke or acute brain injury indicated that it may improve recovery, but further research is needed to confirm this.[28][29][30]


Therapeutic doses of amphetamine improve cortical network efficiency, resulting in higher performance on working memory tests in all individuals.[21][31] Amphetamine and other ADHD stimulants also improve task saliency (motivation to perform a task) and increase arousal (wakefulness), in turn promoting goal-directed behavior.[21][32][33] Stimulants such as amphetamine can improve performance on difficult and boring tasks[21][32] and are used by some students as a study and test-taking aid.[34] Based upon studies of self-reported illicit stimulant use, students primarily use stimulants such as amphetamine for performance enhancement rather than abusing them as recreational drugs.[35] However, high amphetamine doses that are above the therapeutic range can interfere with working memory and cognitive control.[21][32]

Amphetamine is used by some athletes for its psychological and performance-enhancing effects, such as increased stamina and alertness;[36][37] however, its use is prohibited at sporting events regulated by collegiate, national, and international anti-doping agencies.[38][39] In healthy people at oral therapeutic doses, amphetamine has been shown to increase physical strength, acceleration, stamina, and endurance, while reducing reaction time.[36][40][41] Amphetamine improves stamina, endurance, and reaction time primarily through reuptake inhibition and effluxion of dopamine in the central nervous system.[40][41][42] At therapeutic doses, the adverse effects of amphetamine do not impede athletic performance;[36][40][41] however, at much higher doses, amphetamine can induce effects that severely impair performance, such as rapid muscle breakdown and elevated body temperature.[43][44][40]


This section is transcluded from Amphetamine. (edit | history)

According to the International Programme on Chemical Safety (IPCS) and United States Food and Drug Administration (USFDA),[note 5] amphetamine is contraindicated in people with a history of drug abuse, heart disease, severe agitation, or severe anxiety.[45][46] It is also contraindicated in people currently experiencing arteriosclerosis (hardening of the arteries), glaucoma (increased eye pressure), hyperthyroidism (excessive production of thyroid hormone), or hypertension (high blood pressure).[45][46] People who have experienced allergic reactions to other stimulants in the past or who are taking monoamine oxidase inhibitors (MAOIs) are advised not to take amphetamine.[45][46] These agencies also state that anyone with anorexia nervosa, bipolar disorder, depression, elevated blood pressure, liver or kidney problems, mania, psychosis, Raynaud's phenomenon, seizures, thyroid problems, tics, or Tourette syndrome should monitor their symptoms while taking amphetamine.[45][46] Evidence from human studies indicates that therapeutic amphetamine use does not cause developmental abnormalities in the fetus or newborns (i.e., it is not a human teratogen), but amphetamine abuse does pose risks to the fetus.[46] Amphetamine has also been shown to pass into breast milk, so the IPCS and USFDA advise mothers to avoid breastfeeding when using it.[45][46] Due to the potential for reversible growth impairments,[note 6] the USFDA advises monitoring the height and weight of children and adolescents prescribed amphetamines.[45]

Side effects[edit]

This section is transcluded from Amphetamine. (edit | history)


At normal therapeutic doses, the physical side effects of amphetamine vary widely by age and from person to person.[44] Cardiovascular side effects can include cardiac dysrhythmia (abnormal heart rhythm), hypertension (high blood pressure) or hypotension (low blood pressure) from a vasovagal response, and Raynaud's phenomenon (reduced blood flow to extremities).[44][37][47] Sexual side effects in males may include erectile dysfunction, frequent erections, or prolonged erections.[44] Abdominal side effects may include stomach pain, loss of appetite, nausea, and weight loss.[44] Other potential side effects include dry mouth, excessive grinding of the teeth, acne, profuse sweating, blurred vision, reduced seizure threshold, and tics (a type of movement disorder).[44][37][47] Dangerous physical side effects are rare at typical pharmaceutical doses.[37]

Amphetamine stimulates the medullary respiratory centers, producing faster and deeper breaths.[37] In a normal person at therapeutic doses, this effect is usually not noticeable, but when respiration is already compromised, it may be evident.[37] Amphetamine also induces contraction in the urinary bladder sphincter, the muscle which controls urination, which can result in difficulty urinating. This effect can be useful in treating bed wetting and loss of bladder control.[37] The effects of amphetamine on the gastrointestinal tract are unpredictable.[37] If intestinal activity is high, amphetamine may reduce gastrointestinal motility (the rate at which content moves through the digestive system);[37] however, amphetamine may increase motility when the smooth muscle of the tract is relaxed.[37] Amphetamine also has a slight analgesic effect and can enhance the pain relieving effects of opiates.[37]



Common psychological effects of therapeutic doses can include increased alertness, apprehension, concentration, decreased sense of fatigue, mood swings (elated mood followed by mildly depressed mood), increased initiative, insomnia or wakefulness, self-confidence, and sociability.[44][37] Less common side effects include anxiety, change in libido, grandiosity, irritability, repetitive or obsessive behaviors, and restlessness;[sources 2] these effects depend on the user's personality and current mental state.[37] Amphetamine psychosis (e.g., delusions and paranoia) can occur in heavy users.[43][44][54] Although very rare, this psychosis can also occur at therapeutic doses during long-term therapy.[43][44][55] According to the USFDA, "there is no systematic evidence" that stimulants produce aggressive behavior or hostility.[44]


This section is transcluded from Amphetamine. (edit | history)

An amphetamine overdose can lead to many different symptoms, but is rarely fatal with appropriate care.[46][56] The severity of overdose symptoms increases with dosage and decreases with drug tolerance to amphetamine.[37][46] Tolerant individuals have been known to take as much as 5 grams of amphetamine in a day, which is roughly 100 times the maximum daily therapeutic dose.[46] Symptoms of a moderate and extremely large overdose are listed below; fatal amphetamine poisoning usually also involves convulsions and falling into a coma.[43][37] People who chronically overdose on amphetamine are at a high risk of becoming addicted to it since high doses result in increased expression of the addiction gene ΔFosB. While there are currently no effective drugs for treating amphetamine addiction, aerobic exercise appears to reduce the risk of developing such an addiction. Aerobic exercise also seems to work well as a secondary treatment for amphetamine addiction when used together with cognitive behavioral therapy, which is currently the best treatment available.[57]

Overdose symptoms by system
System Minor or moderate overdose[43][37][46] Severe overdose[sources 3]
Central nervous
  • Rapid breathing


Addiction glossary[60][61]
addictive drug – a drug that is both rewarding and reinforcing
addictive behavior – a behavior that is both rewarding and reinforcing
(edit | history)

Addiction is a serious risk with heavy recreational amphetamine use, but is unlikely to arise from typical medical use at therapeutic doses.[43][62][37] Tolerance develops rapidly in heavy amphetamine use, so periods of extended use require increasingly larger doses of the drug in order to achieve the same effect.[63][64]

Biomolecular mechanisms

Current models of addiction from chronic drug use involve alterations in gene expression in certain parts of the brain, particularly the nucleus accumbens.[65][66][67] The most important transcription factors[note 7] that produce these alterations are ΔFosB, cyclic adenosine monophosphate (cAMP) response element binding protein (CREB), and nuclear factor kappa B (NFκB).[66] ΔFosB is the most significant transcription factor in drug addiction, since its overexpression in the nucleus accumbens is necessary and sufficient for many of the associated neural adaptations that occur; that is, ΔFosB overexpression always occurs together with the changes in the brain seen in drug addiction.[66] It has been implicated in addictions to alcohol, cannabinoids, cocaine, nicotine, opiates, phencyclidine, and substituted amphetamines.[66][69][70]

ΔJunD is the transcription factor which directly opposes ΔFosB.[66] Increases in nucleus accumbens ΔJunD expression using viral vectors can reduce or, with a large increase, even block many of the neural and behavioral alterations seen in chronic drug abuse (i.e., the alterations mediated by ΔFosB).[66] ΔFosB also plays an important role in regulating behavioral responses to natural rewards, such as palatable food, sex, and exercise.[66][69][71] Since both natural rewards and drugs of abuse induce expression of ΔFosB (i.e., they cause the brain to make more of it), chronic acquisition of these rewards can result in a similar pathological state of addiction.[69][66] Consequently, ΔFosB is the key transcription factor involved in amphetamine addiction and amphetamine-induced sex addictions, which are compulsive sexual behaviors that result from amphetamine use. These sex addictions are caused by dopamine dysregulation syndrome, which has been observed in some patients taking dopaminergic medications like amphetamine.[69][71][72]

The effects of amphetamine on gene regulation are both dose- and route-dependent.[67] Most of the research on gene regulation and addiction is based upon animal studies with intravenous amphetamine administration at very high doses.[67] The few studies that have used equivalent (weight-adjusted) human therapeutic doses and oral administration show that these changes, if they occur, are relatively minor.[67]

Pharmacological treatments

A Cochrane Collaboration review on amphetamine and methamphetamine addiction and abuse indicates that the current evidence on effective treatments is extremely limited.[73] The review indicated that fluoxetine[note 8] and imipramine[note 9] have some limited benefits in treating abuse and addiction, but concluded that there is currently no effective pharmacological treatment for amphetamine addiction or abuse.[73] A corroborating review indicated that amphetamine addiction is mediated through increased activation of dopamine receptors and co-localized NMDA receptors in the mesolimbic dopamine pathway (a pathway in the brain that connects the ventral tegmental area to the nucleus accumbens).[74] This review also noted that magnesium ions and serotonin inhibit NMDA receptors and that the magnesium ions do so by blocking the receptor's calcium channels.[74] It also suggested that, based upon animal testing, pathological (addiction-inducing) amphetamine use significantly reduces the level of intracellular magnesium throughout the brain.[74] Supplemental magnesium,[note 10] like fluoxetine treatment, has been shown to reduce amphetamine self-administration (doses given to oneself) in both humans and lab animals.[73][74]

Behavioral treatments

Cognitive behavioral therapy is currently the most effective clinical treatment for psychostimulant addiction.[75] Additionally, research on the neurobiological effects of physical exercise suggests that consistent aerobic exercise, especially endurance exercise (e.g., marathon running), prevents the development of drug addiction and is an effective adjunct (supplemental) treatment for amphetamine addiction.[57][69] Exercise leads to better treatment outcomes when used as an adjunct treatment, particularly for psychostimulant addictions.[57] In particular, aerobic exercise decreases psychostimulant self-administration, reduces the reinstatement (i.e., relapse) of drug-seeking, and induces opposite effects on striatal dopamine receptor D2 (DRD2) signaling (increased DRD2 density) to those induced by pathological stimulant use (decreased DRD2 density).[69]


According to another Cochrane Collaboration review on withdrawal in highly addicted 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."[76] This review noted that withdrawal symptoms in chronic, high-dose users are frequent, occurring in up to 87.6% of cases, and persist for three to four weeks with a marked "crash" phase occurring during the first week.[76] Amphetamine withdrawal symptoms can include anxiety, drug craving, depressed mood, fatigue, increased appetite, increased movement or decreased movement, lack of motivation, sleeplessness or sleepiness, and lucid dreams.[76] The review indicated that withdrawal symptoms are associated with the degree of dependence, suggesting that therapeutic use would result in far milder discontinuation symptoms.[76] Manufacturer prescribing information does not indicate the presence of withdrawal symptoms following discontinuation of amphetamine use after an extended period at therapeutic doses.[77][78][79]

Psychosis and toxicity

For more information on amphetamine psychosis, see Stimulant psychosis#Substituted amphetamines.

Abuse of amphetamine can result in a stimulant psychosis that may present with a variety of symptoms (e.g., paranoia and delusions).[54] A Cochrane Collaboration review on treatment for amphetamine, dextroamphetamine, and methamphetamine abuse-induced psychosis states that about 5–15% of users fail to recover completely.[54][80] According to the same review, there is at least one trial that shows antipsychotic medications effectively resolve the symptoms of acute amphetamine psychosis.[54] Psychosis very rarely arises from therapeutic use.[55][45]

In rodents and primates, sufficiently high doses of amphetamine cause dopaminergic neurotoxicity, or damage to dopamine neurons, which is characterized by reduced transporter and receptor function.[81] There is no evidence that amphetamine is directly neurotoxic in humans.[82][83] High-dose amphetamine can cause indirect neurotoxicity as a result of increased oxidative stress from reactive oxygen species and autoxidation of dopamine.[12][84][85]




Pharmacodynamics of amphetamine enantiomers in a dopamine neuron

A pharmacodynamic model of amphetamine and TAAR1
via AADC

Amphetamine and its enantiomers have been identified as potent full agonists of trace amine-associated receptor 1 (TAAR1), a GPCR, discovered in 2001, that is important for regulation of monoaminergic systems in the brain.[86][87] 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 inducing the release of these monoamine neurotransmitters (effluxion).[86][88][89] Amphetamine enantiomers are also substrates for a specific neuronal synaptic vesicle uptake transporter called VMAT2.[90] When amphetamine is taken up by VMAT2, the vesicle releases (effluxes) dopamine, norepinephrine, and serotonin, among other monoamines, into the cytosol in exchange.[90]

Dextroamphetamine (the dextrorotary enantiomer) and levoamphetamine (the levorotary enantiomer) have identical pharmacodynamics, but their binding affinities to their biomolecular targets vary.[87][37] Dextroamphetamine is a more potent agonist of TAAR1 than levoamphetamine.[87] Consequently, dextroamphetamine produces roughly three to four times more central nervous system (CNS) stimulation than levoamphetamine;[87][37] however, levoamphetamine has slightly greater cardiovascular and peripheral effects.[37]

Related endogenous compounds[edit]

For more details on related compounds, see Trace amines.

Amphetamine has a very similar structure and function to the endogenous trace amines, which are naturally occurring neurotransmitter molecules produced in the human body and brain.[89][91] Among this group, the most closely related compounds are phenethylamine, the parent compound of amphetamine, and N-methylphenethylamine, an isomer of amphetamine (i.e., it has an identical molecular formula).[89][91][92] In humans, phenethylamine is produced directly from L-phenylalanine by the aromatic amino acid decarboxylase (AADC) enzyme, which converts L-DOPA into dopamine as well.[91][92] In turn, N‑methylphenethylamine is metabolized from phenethylamine by phenylethanolamine N-methyltransferase, the same enzyme that metabolizes norepinephrine into epinephrine.[91][92] Like amphetamine, both phenethylamine and N‑methylphenethylamine regulate monoamine neurotransmission via TAAR1;[89][92] unlike amphetamine, both of these substances are broken down by monoamine oxidase B, and therefore have a shorter half-life than amphetamine.[91][92]


Amphetamine is well absorbed from the gut, and bioavailability is typically over 75% for dextroamphetamine.[93] However, oral availability varies with gastrointestinal pH.[94] Dextroamphetamine is a weak base with a pKa of 9–10;[2] consequently, when the pH is basic, more of the drug is in its lipid soluble free base form, and more is absorbed through the lipid-rich cell membranes of the gut epithelium.[2][94] Conversely, an acidic pH means the drug is predominantly in its water soluble cationic form, and less is absorbed.[2][94]

Approximately 15–40% of dextroamphetamine circulating in the bloodstream is bound to plasma proteins.[95]

The half-life of dextroamphetamine varies with urine pH.[2] At normal urine pH, the half-life of dextroamphetamine is 9–11 hours.[2] An acidic diet will reduce the half-life to 8–11 hours, while an alkaline diet will increase the range to 16–31 hours.[96][97] The immediate-release and extended release variants of dextroamphetamine salts reach peak plasma concentrations at 3 hours and 7 hours post-dose respectively.[2] Dextromphetamine is eliminated via the kidneys, with 30–40% of the drug being excreted unchanged at normal urinary pH.[2] When the urinary pH is basic, more of the drug is in its poorly water soluble free base form, and less is excreted.[2] 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 basic or acidic, respectively.[2] Amphetamine is usually eliminated within two days of the last oral dose.[96] Apparent half-life and duration of effect increase with repeated use and accumulation of the drug.[98]

CYP2D6, dopamine β-hydroxylase, flavin-containing monooxygenase, butyrate-CoA ligase, and glycine N-acyltransferase are the enzymes known to metabolize amphetamine or its metabolites in humans.[2][3][4][5][6][99] Amphetamine has a variety of excreted metabolic products, including 4-hydroxyamfetamine, 4-hydroxynorephedrine, 4-hydroxyphenylacetone, benzoic acid, hippuric acid, norephedrine, and phenylacetone.[2][96][100] Among these metabolites, the active sympathomimetics are 4‑hydroxyamphetamine,[101] 4‑hydroxynorephedrine,[102] and norephedrine.[103]

The main metabolic pathways involve aromatic para-hydroxylation, aliphatic alpha- and beta-hydroxylation, N-oxidation, N-dealkylation, and deamination.[2][96] The known pathways include:[2][4][100]

Metabolic pathways of amphetamine

Graphic of several routes of amphetamine metabolism
The primary active metabolites of amphetamine are 4-hydroxyamphetamine and norephedrine;[100] however, most of an administered dose is excreted as amphetamine itself and the inactive metabolites.[2] Benzoic acid is metabolized by butyrate-CoA ligase into an intermediate product, benzoyl-CoA,[5] which is then metabolized by glycine N-acyltransferase into hippuric acid.[6]

History, society, and culture[edit]

Racemic amphetamine was first synthesized under the chemical name "phenylisopropylamine" in Berlin, 1887 by the Romanian chemist Lazar Edeleanu.[104] 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 amphetamine contained in the Benzedrine inhaler was the liquid free-base,[note 11] not a chloride or sulfate salt.

Three years later, in 1935, the medical community became aware of the stimulant properties of amphetamine, specifically dexamfetamine, and in 1937 Smith, Kline, and French introduced tablets under the tradename Dexedrine.[105] In the United States, Dexedrine was approved to treat narcolepsy, attention disorders, depression, and obesity. In Canada, epilepsy and parkinsonism were also approved indications.[106] 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").[107] Preparations containing dextroamphetamine were also used in World War II as a treatment against fatigue.[108]

It quickly became apparent that dexamfetamine and other amphetamines 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.[109] 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).[110]


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 effects of the mission and "go-pills".[112][113][114][115] 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.[113]


United States
Adopted Name
(D:L) ratio
of salts
Adderall 3:1 tablet [116][117]
Adderall XR 3:1 capsule [116][117]
Dexedrine dextroamphetamine sulfate 1:0 capsule [116][117]
ProCentra dextroamphetamine sulfate 1:0 liquid [117]
Vyvanse lisdexamfetamine dimesylate 1:0 capsule [116][118]
Zenzedi dextroamphetamine sulfate 1:0 tablet [117]
An image of the lisdexamphetamine compound
The skeletal structure of lisdexamfetamine

Dextroamphetamine sulfate[edit]

Dexamphetamine 5 mg generic name tablets

In the United States, an instant-release (IR) tablet preparation of dextroamphetamine sulfate is available under the brand name Dextrostat, in 5 mg and 10 mg strengths,[119] with generic versions marketed by Barr (Teva Pharmaceutical Industries), Mallinckrodt Pharmaceuticals and Wilshire Pharmaceuticals. Dextroamphetamine sulfate is also available as a controlled-release (CR) capsule preparation in strengths of 5 mg, 10 mg, and 15 mg under the brand name Dexedrine Spansule, with generic versions marketed by Barr and Mallinckrodt. 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.[120]

In Australia, dexamphetamine is available in bottles of 100 instant release 5 mg tablets as a generic drug.[121] or slow release dexamfetamine preparations may be compounded by individual chemists.[122] 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).[123]


Main article: Lisdexamfetamine

Dexamfetamine is the active metabolite of the prodrug lisdexamfetamine (L-lysine-dextroamphetamine), available by the brand name Vyvanse (Lisdexamfetamine dimesylate). Lisdexamfetamine is metabolised in the gastrointestinal tract, while dextroamphetamine's metabolism is hepatic.[124] 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 dimesylate to dextroamphetamine base is 0.2948,[125] thus a 30 mg-strength Vyvanse capsule is molecularly equivalent to 8.844 mg dexamfetamine base.

Amphetamine salts (Adderall)[edit]

Adderall tablets
Main article: Adderall

Another pharmaceutical that contains dextroamphetamine is commonly known by the brand name Adderall. The drug formulation of Adderall, including both the immediate release (IR) and extended release (XR) forms, is:

One-quarter dextroamphetamine saccharate
One-quarter dextroamphetamine sulfate
One-quarter racemic (d,l-)amphetamine sulfate

Adderall is roughly three-quarters dextroamphetamine, with it accounting for 72.7% of the amphetamine base in Adderall (the remaining percentage is levoamphetamine). The salt ratio, as noted above, is 75%:25% or 3:1 dextroamphetamine to levoamphetamine.


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    Physiologic and performance effects
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     • Improved reaction time
     • Increased muscle strength and delayed muscle fatigue
     • Increased acceleration
     • Increased alertness and attention to task
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  124. ^ FDA Approval of Vyvanse Pharmacological Reviews Pages 18 and 19
  125. ^ Mohammadi M, Akhondzadeh S (17 September 2011). "Advances and considerations in attention-deficit/hyperactivity disorder pharmacotherapy". Acta medica Iranica 49 (8): 491. PMID 22009816. Retrieved 12 March 2014. 


  1. ^ Synonyms and alternate spellings include dexamphetamine (AAN) and dexamfetamine (INN and BAN).
  2. ^ which are mirror images of the same molecule
  3. ^ that is, a drug that is metabolised in the body into another more biologically-active drug
  4. ^ Cochrane Collaboration reviews are high quality meta-analytic systematic reviews of randomized controlled trials.[25]
  6. ^ In individuals who experience sub-normal height and weight gains, a rebound to normal levels is expected to occur if stimulant therapy is briefly interrupted.[18][19][47] The average reduction in final adult height from continuous stimulant therapy over a 3 year period is 2 cm.[47]
  7. ^ Transcription factors are proteins that increase or decrease the expression of specific genes.[68]
  8. ^ During short-term treatment, fluoxetine may decrease drug craving.[73]
  10. ^ The review indicated that magnesium L-aspartate and magnesium chloride produce significant changes in addictive behavior;[74] other forms of magnesium were not mentioned.

Reference notes[edit]

  1. ^ [48][49][50][51]
  2. ^ [52][44][37][53]
  3. ^ [58][43][37][56][59]

External links[edit]