|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)|
The amfetamine molecule has two stereoisomers: levamfetamine and dexamfetamine. Dexamfetamine is the dextrorotatory, or "right-handed", enantiomer of the amfetamine molecule. Dexamfetamine is available as a generic drug or under several brand names, including Dexedrine and Dextrostat.
Dexamfetamine is also an active metabolite of the prodrug lisdexamfetamine (Vyvanse), as well as of several older N-substituted amfetamine prodrugs used as anorectics, such as clobenzorex (Asenlix), benzphetamine (Didrex), and amphetaminil (Aponeuron). Common side effects include dry mouth, insomnia and headache. Temporary growth rate reduction is also a known side effect in paediatric use.
- 1 Medical use
- 2 Adverse effects
- 3 Chemistry
- 4 Mechanism of action
- 5 Pharmacokinetics
- 6 History
- 7 Society and culture
- 8 References
- 9 Notes
- 10 Further reading
- 11 External links
Though such use remains out of the mainstream, dexamfetamine 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 dexamfetamine while they practice their movements for rehabilitation, they may learn to move much faster than without dexamfetamine, and in practice sessions with shorter lengths.
Very common (>10% incidence)
- Appetite loss
- Abdominal pain
Common (1-10% incidence)
- Weight loss
- Dry mouth
- Dyspepsia (indigestion)
- Emotional lability
Unknown frequency adverse effects
- Sexual dysfunction
- Exacerbation of motor and phonic tics and Tourette’s syndrome
Serious adverse effects
- Growth stunting
- Myocardial infarction (heart attack)
- Psychosis which can occur at therapeutic doses after chronic treatment.
- Drug dependence
- Raynaud’s phenomenon
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 dexamfetamine or other ADHD stimulants.
A study on comparative effects between amfetamine mixed salts (commonly known as adderall) and dexamfetamine in children who have been treated for a year or more have shown a temporary decrease in growth rate that does not affect final adult height. Change in weight was reported as slightly greater for amfetamine mixed salts and authors concluded that the result may be clinically insignificant.
Studies on rats show long-term neurological and behavioural changes resulting from prenatal and early postnatal exposure to amfetamines. Warnings from the Patient Medication Guide for Adderall include emergence of new psychotic or manic symptoms, aggression and blurred vision.
Abuse of amfetamines 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 amfetamine, dexamfetamine, and metamfetamine 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 amfetamine psychosis may also develop occasionally as a treatment-emergent side effect.
Withdrawal symptoms of dexamfetamine primarily consist of fatigue, depression and an increased appetite. Symptoms may last for days with occasional use and weeks or months with chronic use, with severity dependent on the length of time and the amount of dexamfetamine used. Withdrawal symptoms may also include anxiety, irritability,headaches, agitation, seizures, vomiting, akathisia, hypersomnia (excessive sleeping),vivid or lucid dreams, deep REM sleep and suicidal ideation.
- 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)
The Physician's 1991 Drug Handbook reports: "Symptoms of overdose include restlessness, tremor, hyperreflexia, tachypnea, confusion, aggressiveness, hallucinations, and panic." Dilated pupils are common with high doses. Repeated high doses may lead to manifestations of acute psychosis. Additionally at least one case report identifies rhabdomyolysis as an associated side effect of dexamfetamine in the presence of other risk factors.
The fatal dose in humans is not precisely known, but in various species of rat generally ranges between 50 and 100 mg/kg, or a factor of 100 over what is required to produce noticeable psychological effects. Although the symptoms seen in a fatal overdose are similar to those of metamfetamine, their mechanisms are not identical, as some substances which inhibit dexamfetamine toxicity do not do so for metamfetamine.
An extreme symptom of overdose is amfetamine psychosis, characterized by vivid visual, auditory, and sometimes tactile hallucinations. Many of its symptoms are identical to the psychosis-like state which follows long-term sleep deprivation, so it remains unclear whether these are solely the effects of the drug, or due to the long periods of sleep deprivation which are often undergone by the chronic user. Amfetamine psychosis, however, is extremely rare in individuals taking oral amfetamines at therapeutic doses; it is usually seen in cases of prolonged or high-dose intravenous (IV) for non-medicinal uses.
Mechanism of action
Scientific findings have established that dexamfetamine administration increases the activity of the phosphoinositol cycle via an indirect release of dopamine and Norepinephrine. These results are the first time that this has been confirmed in humans. Because dexamfetamine is a substrate at monoamine transporters, at all doses, dexamfetamine prevents the re-uptake of these neurotransmitters by competing with endogenous monoamines for uptake. At higher doses, when the concentration of dexamfetamine is sufficient, the drug can trigger direct release of norepinephrine and dopamine from the cytoplasmic transmitter pool, that is, dexamfetamine will cause norepinephrine and dopamine efflux via transporter proteins, functionally reversing transporter action, which triggers a cascading release of catecholamines.
Dexamfetamine's binding profile
On average, about one half of a given dose is eliminated unchanged in the urine, while the other half is broken down into various metabolites (mostly benzoic acid). However, the drug's half-life is highly variable because the rate of excretion is very sensitive to urinary pH. Under alkaline conditions, direct excretion is negligible and 95%+ of the dose is metabolized. Having an alkaline stomach will cause the drug to be absorbed faster through the stomach resulting in a higher blood level concentration of amfetamine. Having an alkaline bladder causes dexamfetamine to be excreted more slowly from the blood and into the urine. Alkalinization of the urine can decrease the renal elimination of amfetamines, both potentiating the strength and prolonging the mechanism of action, especially when ingested with sodium bicarbonate.
The main metabolic pathway is:
Another pathway, mediated by enzyme CYP2D6, is:
dexamfetamine p-hydroxyamfetamine p-hydroxynorephedrine.
Subjective effects are increased by larger doses, however, over the course of a given dose there is a noticeable divergence between such effects and drug concentration in the blood. In particular, mental effects peak before maximal blood levels are reached, and decline as blood levels remain stable or even continue to increase. This indicates a mechanism for development of acute tolerance, perhaps distinct from that seen in chronic use. The long-term effects of amphetamines use on neural development in children has not been well established.
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).
Society and culture
In the United States, an instant-release (IR) tablet preparation of the salt dexamfetamine sulfate is available[clarification needed] 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 under the generic name dexamphetamine [sic] as 5 mg instant release sulfate tablets., 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 [sic] 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-amfetamine), available by the brand name Vyvanse. Lisdexamfetamine is metabolised in the gastrointestinal tract, while dexamfetamine's metabolism is hepatic. Lisdexamfetamine is therefore an inactive compound until it is converted into an active compound by the digestive system. Although still rated as a Schedule II drug by the U.S. Drug Enforcement Administration, lisdexamfetamine has a slower onset and its route of administration is limited to being taken orally, unlike dexamfetamine, Adderall, and methylphenidate, which can be insufflated to achieve a faster onset with a higher bioavailability. 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 dexamfetamine base is 0.2948, thus a 30 mg-strength Vyvanse capsule is molecularly equivalent to 8.844 mg dexamfetamine base.
Mixed amfetamine salts
Another pharmaceutical that contains dexamfetamine is Adderall. The drug formulation of Adderall (both controlled and instant release forms) is:
Adderall is roughly three-quarters dexamfetamine, with it accounting for 72.7% of the amfetamine base in Adderall (the remaining percentage is levoamfetamine).
An experiment with rats suggested Adderall's inclusion of levoamfetamine provides the pharmaceutical with a quicker onset and longer clinical effect compared to pharmaceuticals exclusively formulated of dexamfetamine. One study has shown that although the human brain usually has a preference for dexamfetamine over levoamfetamine, certain children have a better clinical response to levoamfetamine.
Amfetamine exists as two stereoisomers that differ in effects. The l- enantiomer (levoamfetamine) produces more cardiovascular and peripheral effects than the d- enantiomer (dexamfetamine). At low doses, levoamfetamine produces greater arousal than dexamfetamine, acting primarily on norepinephrine. At higher doses, dexamfetamine has stimulant properties that are three to four times as potent as those of levoamfetamine, and acts primarily on dopamine, although few clinical studies of ADHD have documented differences among d-, l- and racemic amfetamine.
Just as dexamfetamine has greater central effects and fewer peripheral effects than levoamfetamine, metamfetamine, which is equipotent to deamfetamine in producing behavioral stimulant effects, has even fewer peripheral effects and greater central effects than dexamfetamine.
In relation to other over-the-counter ADD/ADHD pharmaceuticals, the d- isomer of racemic amfetamine is superior in bioavailibility and CNS stimulation.
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.
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