Dextroamphetamine
Viewing r1 — May 3, 2026 — CURRENT
Back to HistoryInteractions, related substances, and reports reflect the current entry and are not shown for historical revisions.
Dextroamphetamine is a synthetic stimulant of the phenethylamine class. It is the more potent enantiomer of amphetamine, carrying 3–5× greater central nervous system activity than levoamphetamine.[1] Dextroamphetamine is a monoamine releasing agent, producing its effects by forcing dopamine and norepinephrine out of nerve terminals into the synapse.[2]
Psychedex is in open beta. We are still fine-tuning the generation and review process. Please double-check sources.
methamphetamine, lisdexamfetamine, mixed amphetamine salts +1 moremethamphetamine, lisdexamfetamine, mixed amphetamine salts, methylphenidate show less
First synthesized as racemic mixture amphetamine in 1887 and pharmacologically characterized by Gordon Alles in 1927,[3] dextroamphetamine became one of the most prescribed stimulants in medicine — a 2018 network meta-analysis of 133 RCTs identified amphetamines as the most effective pharmacological treatment for ADHD in children and adolescents.[4] It remains FDA-approved for ADHD and narcolepsy, available as immediate-release tablets and through the prodrug lisdexamfetamine.
Subjective effects include cognitive enhancement, psychomotor activation, euphoria, increased motivation, and appetite suppression. The experience is one of focused drive — a sustained mental acceleration with heightened confidence and goal-directed energy, shaped substantially by individual genetic variation in DAT expression.[5] Insomnia, jaw tension, anxiety, and a depressive rebound effect upon wearing off are characteristic unsought effects.
Dextroamphetamine carries high psychological dependence liability and cardiovascular toxicity that intensifies with chronic use[6] — an FDA black box warning notes sudden cardiac death risk in patients with structural heart abnormalities.[1] Tolerance develops through receptor adaptation and neurotransmitter store depletion, while intermittent dosing paradoxically sensitizes the reward system — a pattern that can drive compulsive escalation.[7][8] Nine decades of clinical use make dextroamphetamine one of the best-characterized stimulants in medicine.
History[edit]
Discovery
Racemic amphetamine was first synthesized in 1887 by Romanian chemist Lazăr Edeleanu at the University of Berlin, though no pharmacological activity was recognized at the time.[3] Four decades later, American pharmacologist Gordon Alles independently resynthesized the compound while searching for an ephedrine substitute for asthma, tested it on himself, and characterized its stimulant properties — filing a US patent for amphetamine sulfate in 1932.[3] The dextro-enantiomer was subsequently identified as substantially more potent for CNS effects, leading to the development of Dexedrine (dextroamphetamine sulfate) as a more targeted clinical formulation.
Clinical and military significance
Smith, Kline & French launched the Benzedrine inhaler in 1934 for nasal congestion, and oral tablet formulations followed rapidly for narcolepsy and depression. Amphetamines saw massive military deployment during World War II — the Royal Air Force officially approved Benzedrine for operational use in November 1942, and an estimated 72 million tablets were distributed to British armed forces during the conflict.[9] The 2018 Cortese network meta-analysis subsequently confirmed amphetamines as the most efficacious pharmacological treatment for ADHD in children and adolescents,[4] cementing their position in modern psychiatry.
Regulation and modern use
Widespread non-medical use through the 1950s–1970s — including over-the-counter diet pills and recreational abuse — drove increasing regulatory control, culminating in Schedule II classification under the US Controlled Substances Act in 1970. Dexedrine remains FDA-approved for ADHD and narcolepsy as of 2026, though lisdexamfetamine (Vyvanse), a prodrug that releases d-amphetamine after enzymatic hydrolysis, has largely supplanted immediate-release formulations in many markets due to its abuse-deterrent pharmacokinetic profile.
The name amphetamine derives from the compound's chemical name alpha-methylphenethylamine. Dextroamphetamine takes its prefix from the Latin dexter ("right"), referring to the direction the molecule rotates plane-polarized light. Widely prescribed formulations include Dexedrine (US/UK), Dextrostat (US), Attentin (Spain), and Procentra (oral solution, US). The mixed amphetamine salt formulation Adderall — containing a 75:25 ratio of dextro- to levo-amphetamine — became one of the most recognized prescription stimulant brand names in American popular culture.
Chemistry[edit]
Structural class
Dextroamphetamine belongs to the phenethylamine structural class — specifically, it is the alpha-methyl homolog of phenethylamine. The amphetamine scaffold serves as the parent structure for a large family of psychoactive substances including methamphetamine, MDMA, and numerous substituted amphetamine research chemicals. The alpha-methyl group at C-2 confers resistance to monoamine oxidase degradation, substantially prolonging duration of action compared to unsubstituted phenethylamine.
Molecular properties
| Molecular formula | C₉H₁₃N |
| Molecular weight | 135.21 g/mol |
The molecule comprises a phenyl ring connected via a methylene bridge to a chirality amine-bearing carbon. The alpha-methyl substitution at C-2 creates the stereocenter that distinguishes the two enantiomers and provides the metabolic stability characteristic of the amphetamine class.
Stereochemistry
Dextroamphetamine is the (2S)-(+)-enantiomer of amphetamine. The S-configuration confers dextrorotatory optical activity and approximately 3–5× greater potency than levoamphetamine for CNS stimulant effects, owing to stronger activity at dopamine and norepinephrine transporters.[1] The widely prescribed mixed salt formulation Adderall contains a 75:25 d:l enantiomer ratio.
Physical properties
The free base is a colourless to pale yellow volatile oil at room temperature. The sulfate salt is a white crystalline powder (melting point ~300°C with decomposition), highly water-soluble and suitable for oral administration. The free base is moderately lipophilic, conferring good blood-brain barrier penetration.
Pharmacology[edit]
Mechanism of action
Dextroamphetamine enters nerve terminals through the DAT (DAT) and NET (NET), then forces stored neurotransmitters out into the synapse through a process called reverse transport.[10][11] This non-exocytotic release of dopamine and norepinephrine — mechanistically distinct from the reuptake blockade produced by drugs like cocaine — is the principal driver of its stimulant and reinforcement.[12]
Inside the neuron, dextroamphetamine disrupts vesicular storage by interfering with VMAT2 (vesicular monoamine transporter-2), causing dopamine to leak from storage vesicles into the cell interior.[13] A 2024 structural study confirmed that amphetamine binds the same pocket as dopamine within the vesicular transporter.[13] This cytoplasmic pool of displaced dopamine provides the substrate for reverse transport at the cell surface — a process that does not require calcium signaling.[14]
Dextroamphetamine also activates TAAR1 (trace amine-associated receptor 1), an intracellular receptor that triggers removal of dopamine and norepinephrine transporters from the cell surface.[15][16][17] This transporter internalization further reduces the neuron's ability to clear monoamines from the synapse, amplifying the overall effect.
Additional actions include stimulation of adrenergic receptors via elevated synaptic norepinephrine,[1] weak inhibition of monoamine oxidase at high concentrations,[1] and progressive depletion of monoamine stores with repeated dosing.[7]
Pharmacokinetics
Oral bioavailability is approximately 90%, with peak plasma levels reached around 3 hours after an immediate-release dose.[1] The drug distributes extensively into tissues including the brain, with low protein binding (<20%).
Elimination half-life is 9–11 hours in adults at normal urinary pH. Metabolism occurs primarily through liver enzymes, producing active metabolites. Approximately 30–40% of a dose is excreted unchanged in urine. Renal clearance is markedly pH-dependent: alkaline urine prolongs the drug's effects, while acidic urine accelerates elimination.[1]
Food delays peak levels by approximately 2.5 hours without affecting total absorption. Elimination half-life is approximately 1 hour shorter in children than adults. Intranasal administration produces onset within 1–5 minutes and substantially earlier peak levels than oral dosing.[18]
Neuroscience[edit]
Where it acts
Dextroamphetamine's reinforcing and euphoric effects arise from enhanced dopamine release in the mesolimbic pathway — specifically, projections from the ventral tegmental area to the nucleus accumbens. The magnitude of dopamine surge in this region correlates directly with subjective euphoria in human studies.[19] Even strong dopamine receptor blockade fails to completely abolish amphetamine euphoria, suggesting additional receptor systems contribute to the rewarding experience.[19]
The therapeutic benefit in ADHD operates through a different circuit: norepinephrine and dopamine enhancement in the prefrontal cortex strengthens sustained attention, working memory, and impulse control — executive functions impaired in ADHD.[20] This prefrontal mechanism activates at lower doses than mesolimbic reward, creating the therapeutic window between cognitive enhancement and euphoria.
Why it matters
Two opposing neuroadaptations define long-term amphetamine use. Daily dosing produces tolerance through downregulation and neurotransmitter depletion.[8] Intermittent dosing produces behavioral sensitization — progressive amplification of rewarding and locomotor effects — through redistribution of vesicular dopamine stores.[7]
This sensitization may persist for months to years after cessation and is thought to underlie the chronic relapsing nature of amphetamine addiction.[8] Separately, dextroamphetamine paired with rehabilitation has been shown to enhance neural recovery in post-stroke aphasia, suggesting its noradrenergic actions can facilitate structural brain plasticity beyond acute cognitive effects.[21]
Key unresolved questions include the dose and duration threshold at which d-amphetamine causes measurable dopamine terminal damage in humans — most neurotoxicity data extrapolate from methamphetamine or animal models.[22] Whether prescribed daily amphetamine produces behavioral sensitization or whether continuous dosing prevents it through tolerance mechanisms remains unclear.
Subjective Effects[edit]
The subjective character of dextroamphetamine is defined by a clean catecholaminergic drive with minimal serotonergic color. The experience centers on heightened focus, mental clarity, and a sense of motivated purpose — a state closer to an idealized concentration than to intoxication. At lower doses the effect is primarily cognitive: sharper attention, faster processing, reduced fatigue. At higher doses euphoria and physical energy dominate, with a pronounced sense of confidence and social fluency. Individual response varies dramatically with genetic differences in DAT expression — identical doses produce primarily cognitive enhancement in some users and pronounced euphoria in others.[5]
Compared to cocaine, dextroamphetamine produces a longer, less compulsive stimulation with more sustained cognitive enhancement. Relative to MDMA, the experience is purely stimulant — absent the empathogenic warmth, prosocial openness, and serotonergic perceptual shifts that characterize entactogens. The subjective profile most closely resembles methamphetamine at equivalent doses, though with lower peak euphoria and reduced neurotoxic potential.
Effect Grid
At common doses (10–16 mg oral), the full stimulant profile manifests. Thought acceleration becomes prominent, accompanied by increased motivation, talkativeness, and a sense of confidence. Euphoria is present in most individuals, though its intensity varies substantially with DAT gene polymorphisms — some users experience pronounced mood elevation while others note primarily cognitive enhancement without hedonic effects.
Cardiovascular activation becomes measurable: systolic blood pressure rises 5–15 mmHg, heart rate increases 10–20 bpm, and appetite suppression is significant. Jaw clenching, increased sweating, and urinary retention may occur. Pupil dilation is noticeable.
Total subjective duration is 4–6 hours for immediate-release, with residual wakefulness extending several hours beyond. Sleep is impractical for 8+ hours post-dose.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Tinnitus · Auditory hallucinations · External hallucinations · Shadow people
Pupil dilation · Wakefulness · Dry mouth · Physical fatigue · Heart rate perception changes · Restlessness · Body high · Bruxism · Dehydration sensation · Excessive sweating · Muscle tension · Respiratory stimulation · Breathing alteration · Headache · Sexual arousal enhancement · Trembling · Bodily lightness · Nausea · Pain suppression · Spontaneous body sensations · Tactile euphoria · Tingling / electric sensations · Motor control enhancement · Constipation · Dizziness · Involuntary body movements · Sexual arousal suppression · Vomiting · Tactile hallucination
Heart rate perception changes · Restlessness · Body high · Bruxism · Dehydration sensation · Excessive sweating · Muscle tension · Respiratory stimulation · Breathing alteration · Headache · Sexual arousal enhancement · Trembling · Bodily lightness · Nausea · Pain suppression · Spontaneous body sensations · Tactile euphoria · Tingling / electric sensations · Motor control enhancement · Constipation · Dizziness · Involuntary body movements · Sexual arousal suppression · Vomiting · Tactile hallucination
Motivation enhancement · Immersion enhancement · Thought acceleration · Analysis enhancement · Information processing enhancement · Cognitive dysphoria · Cognitive flexibility · Conceptual thinking · Memory enhancement · Motivation suppression · Pattern recognition enhancement · Thought organization · Creativity enhancement · Language enhancement · Aesthetic enhancement · Introspection enhancement · Multiple thought streams · Openness enhancement · Thought loops · Humor enhancement · Cognitive impairment · Creativity suppression · Confusion · Thought disorganization · Delirium · Delusions
Analysis enhancement · Information processing enhancement · Cognitive dysphoria · Cognitive flexibility · Conceptual thinking · Memory enhancement · Motivation suppression · Pattern recognition enhancement · Thought organization · Creativity enhancement · Language enhancement · Aesthetic enhancement · Introspection enhancement · Multiple thought streams · Openness enhancement · Thought loops · Humor enhancement · Cognitive impairment · Creativity suppression · Confusion · Thought disorganization · Delusions
Irritability · Anhedonia · Emotional enhancement · Emotional lability · Anxiety suppression · Emotional suppression · Empathy enhancement · Empathy suppression · Mania
Emotional lability · Anxiety suppression · Emotional suppression · Empathy enhancement · Empathy suppression
Self-control enhancement · Sociability enhancement · Compulsive behavior reduction · Disinhibition · Ego inflation · Social connection · Sociability suppression · Social disconnection · Trust enhancement · Depersonalization · Derealization
Ego inflation · Social connection · Sociability suppression · Social disconnection · Trust enhancement · Depersonalization · Derealization
Mindfulness enhancement
Timeline
First alerts emerge as subtle wakefulness and slight mood brightening. Effects are sub-threshold and easily attributed to placebo.
Stimulation builds progressively. Concentration sharpens, energy increases, and appetite begins to diminish. Heart rate elevation becomes perceptible.
Maximum cognitive enhancement, euphoria, and psychomotor activation. Cardiovascular effects plateau at their highest. Tmax reached approximately 3 hours post-ingestion.
Effects sustain at moderate intensity. Focus remains enhanced but euphoria diminishes. Appetite suppression continues.
Gradual return toward baseline. Residual stimulation persists due to the 9-11 hour half-life. Fatigue may emerge as catecholamine stores deplete.
Residual wakefulness and mild appetite suppression. Some individuals report irritability or low mood during this phase.
⚠ Do not drive or operate machinery during the comedown period, as fatigue and impaired concentration may develop abruptly as residual stimulation fades.
Safety[edit]
- Acute toxicity
- Moderate
- Chronic toxicity
- Moderate
- Withdrawal
- Moderate
- Tolerance buildup
- moderate
- Tolerance reset
- 14 days
- Physical
- Low
- Psychological
- High
- Compulsive redosing
- Moderate
- Dose escalation
- Moderate
- Cross-tol.
- methamphetamine · lisdexamfetamine · mixed amphetamine salts
Toxicity
Acute toxicity
Death has occurred at doses of 20–25 mg/kg in sensitive individuals, though chronic users with developed tolerance may survive far higher amounts.[1] No formal human lethal dose is established. The therapeutic dose range (5–60 mg/day) provides a substantial margin from lethal doses in stimulant-naive individuals, though this margin narrows considerably in people with heart conditions.
Overdose presents with agitation, dangerously elevated body temperature, rapid heart rate, high blood pressure, dilated pupils, tremors, seizures, muscle breakdown, and stroke.[1] No specific antidote exists. Treatment is supportive: activated charcoal if recently ingested, benzodiazepines for agitation and seizures, blood pressure medications for severe hypertension, active cooling for dangerously elevated temperature, and continuous heart monitoring.[1]
Heart and circulation
Chronic amphetamine use significantly raises blood pressure.[6] Cardiomyopathy, heart attack, and stroke are documented rare adverse events.[1] The FDA black box warning notes risk of sudden cardiac death in patients with structural heart abnormalities — this risk applies at both prescribed and misused doses.[1]
Research has shown that amphetamine's cardiovascular effects are partially mediated through the central melanocortin system, independent of appetite-suppressing effects.[23]
High-dose nerve damage
At high sustained doses, d-amphetamine causes damage to dopamine nerve terminals in the striatum through oxidative stress and inflammatory activation.[22][24] This neurotoxic process is pharmacologically distinct from therapeutic-dose effects and requires sustained high-dose exposure far exceeding normal clinical parameters.[22]
Pregnancy and breastfeeding
Amphetamine use during pregnancy is associated with increased risk of premature delivery, low birth weight, gastroschisis, and preeclampsia.[1] Amphetamines concentrate in breast milk at 3–7× higher than maternal blood levels; breastfeeding is contraindicated during use.[1]
Pediatric growth
Long-term stimulant use in children is associated with reduced weight and height gain; some evidence suggests growth normalizes after discontinuation.[25]
Psychological risks
Amphetamine psychosis is the most severe psychiatric adverse effect. Chronic high-dose use produces a paranoid psychotic state indistinguishable from paranoid schizophrenia — characterized by persecutory delusions, auditory hallucinations, and disordered thinking.[8] The condition is reversible upon cessation in most cases, though resolution may take weeks.
Additional psychological risks include anxiety worsening, depressive "crashes" following use (from temporary neurotransmitter depletion), mania induction in people with bipolar vulnerability, and paranoia even at therapeutic doses in sensitive individuals.[1]
Tolerance and dependence
Tolerance to mood, appetite, and cardiovascular effects develops with repeated use through downregulation and progressive neurotransmitter store depletion.[8][7] Appetite suppression tolerance typically precedes tolerance to cognitive and mood effects. Cross-tolerance exists with other catecholamine-releasing agents.
Paradoxically, intermittent use patterns can produce behavioral sensitization — progressive strengthening of rewarding effects — rather than tolerance.[7] Dextroamphetamine is classified Schedule II (US) due to high abuse potential and capacity for severe psychological dependence.[1]
Withdrawal following chronic use involves marked fatigue, excessive sleep, depressed mood, anhedonia, appetite enhancement, irritability, and dysphoria lasting days to weeks.[25] Physical withdrawal is generally less severe than with depressants such as alcohol or benzodiazepines.
Non-medical stimulant use is common in academic settings — one US study found 6.9% lifetime prevalence among college students, with higher rates in fraternities and competitive academic environments.[26]
Drug interactions
Serotonergic combinations
Although dextroamphetamine has low serotonin activity on its own, combining it with serotonergic drugs (SSRIs, SNRIs, triptans, linezolid, St. John's Wort) can create enough combined serotonin load to cause serotonin syndrome.[1] Risk increases further when CYP2D6 inhibitors (fluoxetine, paroxetine) simultaneously elevate amphetamine blood levels.[1]
MAO inhibitors
Combination with monoamine oxidase inhibitors is contraindicated — it produces massive norepinephrine buildup resulting in life-threatening blood pressure crisis. A minimum 14-day MAOI washout is required before starting dextroamphetamine.[1] This applies to phenelzine, tranylcypromine, selegiline, linezolid, and methylene blue.
Metabolic interactions
CYP2D6 inhibitors (fluoxetine, paroxetine, bupropion) slow amphetamine metabolism, raising blood levels and adverse event risk. Urinary pH modifiers alter elimination: alkalinizing agents (antacids, thiazide diuretics) prolong effects, while acidifying agents (vitamin C) reduce them.[1][27]
Stimulant stacking
Combining with other stimulants (cocaine, high-dose caffeine) produces additive cardiovascular stress — elevated blood pressure and heart rate with increased risk of irregular heartbeat and stroke.[25]
Alcohol
Stimulants mask perceived alcohol intoxication, leading to overconsumption and delayed recognition of dangerous blood alcohol levels. Cardiovascular strain is additive.[25]
Contraindications
Absolute contraindications:
- Hypersensitivity to amphetamine or any formulation component
- Concurrent or recent (within 14 days) MAOI use
- Advanced hardening of the arteries
- Symptomatic heart disease
- Moderate-to-severe high blood pressure
- Overactive thyroid
- Narrow-angle glaucoma
- Agitated states
Relative contraindications:
- History of substance use disorder
- Bipolar disorder (risk of triggering mania)
- Psychotic disorders or family history of psychosis
- Pregnancy and breastfeeding
- Structural heart abnormalities (FDA black box warning — sudden cardiac death risk)
- Tourette syndrome or tic disorders
All contraindications derived from FDA prescribing information.[1]
Harm Reduction[edit]
Forms & Identification
Dextroamphetamine circulates primarily as pharmaceutical tablets and capsules, where identity is typically confirmed by imprint codes. In non-medical contexts, tablets may be crushed for insufflation or dissolved for injection — both routes carry substantially higher cardiovascular risk and reinforcement potential than oral administration. Reagent testing is most relevant when tablets lack identifiable imprints or when powder is obtained outside pharmaceutical supply chains, where substitution with methamphetamine or other stimulants is possible.
Guidelines
- Test any non-pharmaceutical material with appropriate reagent kits before use
- Start with the lowest effective dose and wait for full onset before considering redosing
- Set a firm time limit — stimulant-driven productivity loops easily extend into sleep deprivation
- Eat a meal before dosing; appetite suppression makes it easy to go 8+ hours without food
- Keep water accessible and drink regularly — stimulants mask dehydration signals
- Avoid redosing in the afternoon or evening to protect sleep
- Have a sleep aid plan: a dark, cool room, no screens, and if needed, a non-stimulant sleep support
Set & Setting
The stimulant effect profile makes environmental context especially important. A calm, organized setting supports the focused cognitive enhancement that characterizes lower doses, while chaotic or high-stimulation environments can amplify anxiety, paranoia, and cardiovascular stress. Adequate hydration, food availability, and a defined end-time help prevent the common pattern of redosing through fatigue signals. Individuals with anxiety disorders or cardiovascular vulnerability should approach with particular caution.
Aftercare & integration. The stimulant comedown — fatigue, low mood, irritability, appetite enhancement — reflects temporary neurotransmitter depletion and resolves within 1–3 days. Prioritize sleep, even if it requires a full day of rest. Eat nutrient-dense meals to replenish depleted stores. Avoid the temptation to redose through the comedown, as this extends the depletion cycle and accelerates tolerance.
If use was for productivity or academic performance, reflect honestly on whether the output justified the recovery cost. Stimulant-assisted work often feels more productive than it is, and the pattern of reliance can develop quickly.
Recovery & Support
Amphetamine dependence is primarily psychological — the compulsion to use often centers on productivity, weight management, or euphoria rather than physical withdrawal avoidance. Professional support is particularly important for people who began using to manage ADHD symptoms, as untreated ADHD persists after stimulant cessation and requires alternative management.
SMART Recovery and similar programs offer structured support for stimulant dependence. Medical consultation can help manage the withdrawal period and assess whether underlying ADHD or other conditions require treatment. Tapering under medical supervision, rather than abrupt cessation, reduces withdrawal severity.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: chest pain, seizure, loss of consciousness, body temperature hot enough to feel through clothing, severe confusion, or stroke symptoms (sudden weakness on one side, slurred speech, facial drooping) require immediate medical attention. These are not normal stimulant side effects.
Immediate steps:
- 1. Call emergency services if any of the above signs are present
- 2. Move the person to a cool, quiet environment
- 3. Remove excess clothing and apply cool water if body temperature is dangerously elevated
- 4. Do not restrain the person unless they are in immediate danger of self-harm
- 5. Do not induce vomiting
- 6. If the person is unconscious, place them in the recovery position
What to tell the dispatcher: Name the substance (dextroamphetamine or amphetamine), estimated amount, time taken, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug emergency.
Legal Status[edit]
Dextroamphetamine is internationally controlled as a substance with recognized medical utility but high abuse potential. It is legal by prescription for approved indications (ADHD, narcolepsy) in most jurisdictions, while non-medical possession and supply are criminalized under controlled substance scheduling.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Schedule II (Controlled Substances Act, 1970) | FDA-approved for ADHD and narcolepsy; no refills permitted; 90-day maximum prescription[1] |
| United Kingdom | Class B, Schedule 2 (Misuse of Drugs Act 1971) | Class A if prepared for injection; possession up to 5 years imprisonment; supply up to 14 years[28] |
| Australia | Schedule 8 (Controlled Drugs) | Prescription-only under Poisons Standard; state-level permit requirements for prescribing[25] |
| Canada | Schedule III (CDSA) | Prescription required; possession offence up to 3 years imprisonment[29] |
| European Union | Varies by member state | Generally classified as prescription-only controlled substance; specific scheduling differs nationally |
The UK classification introduces a notable severity escalation: amphetamines prepared for injection are reclassified from Class B to Class A, carrying maximum penalties equivalent to heroin or cocaine possession (7 years imprisonment) and supply (life imprisonment).[28]
references
- [1]
- [2]
- [3]
- [4] ^abCortese S, Adamo N, Del Giovane C, et al. (2018) Comparative efficacy and tolerability of medications for ADHD in children, adolescents, and adults: a systematic review and network meta-analysis — The Lancet Psychiatry doi:10.1016/s2215-0366(18)30269-4
- [5] ^abcHamidovic A, Dlugos A, Palmer AA, de Wit H (2010) Polymorphisms in dopamine transporter (SLC6A3) are associated with stimulant effects of D-amphetamine: an exploratory pharmacogenetic study using healthy volunteers — Behavior Genetics doi:10.1007/s10519-009-9331-7
- [6] ^abChan M, Chan JJ, Wright JM (2025) Effect of amphetamines on blood pressure — Cochrane Database of Systematic Reviews doi:10.1002/14651858.cd007896.pub4