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Amphetamine

Amphetamine molecule structureAmphetamine molecule structure
α-Methylphenethylamine
Speed, Pep, Adderall, Dexedrine, Bennies
Psychoactive Class

Amphetamine is a central nervous system stimulantcitation needed of the substituted phenethylamine class, first discovered in 1887 by Lazăr Edeleanu. It exists as two enantiomers, levoamphetamine and dextroamphetamine, and serves as the parent compound of its own structural class. Prescribed clinically for ADHD and narcolepsy, it is also used recreationally for its euphoriant and wakefulness-promoting properties.

Dosage & Duration

Dosage

Doses are population estimates that vary widely between individuals.

Threshold~5 mg
Light5-15 mg
Moderate15-30 mg
Strong30-50 mg
Heavy50+ mg
Bioavailability
75-90%

Duration

Onset20-60 minutes
Come Up1-2 hours
Peak2-4 hours
Offset1-2 hours
After Effects2-24 hours
Total4-8 hours
Half-life
9-14 hours

Subjective Effects

Legacy content. A statistically backed ontology from Mindstate Design Labs is coming soon.

Effects vary widely by individual, dose, and context.

Physical

The physical effects of amphetamine can be broken down into several components which progressively intensify proportional to dosage.

Cognitive

The cognitive effects of amphetamine can be broken down into several components which progressively intensify proportional to dosage. The general head space of amphetamine is described by many as one of extreme mental stimulation, increased focus, and powerful euphoria. It contains a large number of typical stimulant cognitive effects. Although negative side effects are usually mild at low to moderate dosages, they become increasingly likely to manifest themselves with higher amounts or extended usage. This particularly holds true during the offset of the experience.

Forked from Subjective Effect Documentation byJosie Kins September 2015.

Reagent Testing

Expected colorimetric results for common reagent tests. Colors show reaction change over 1–2 minutes.

Marquis(MQ)
white → orange2
Mandelin(MD)
yellow2 → green2 → blue2
Robadope(RB)
orange1 → pink1 → pink2
Liebermann(LB)
white → orange2 → red2
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Pharmacology

Pharmacodynamics

Amphetamine exerts its primary pharmacological effects by promoting the release of dopamine and norepinephrine from presynaptic nerve terminals.citation needed It enters neurons via monoamine transporters (DAT, NET, and to a lesser extent SERT), where it acts as a competitive substrate that inhibits monoamine reuptake. Once inside the terminal, amphetamine displaces monoamines from vesicular storage by interacting with VMAT2, collapsing the vesicular pH gradient and expanding the cytosolic monoamine pool available for reverse transport. Amphetamine is also a potent full agonist at trace amine-associated receptor 1 (TAAR1), activation of which triggers intracellular kinase cascades (PKA, PKC, CaMKIIα) that phosphorylate monoamine transporters, further promoting neurotransmitter efflux into the synapse. At very high doses, amphetamine weakly inhibits monoamine oxidase. It also inhibits the neuronal glutamate transporter EAAT3 (SLC1A1), reducing glutamate clearance and potentiating excitatory neurotransmission.1 The only known post-synaptic receptor at which amphetamine binds in humans is the 5-HT1A receptor, where it acts as an agonist with low micromolar affinity.

Pharmacokinetics

Amphetamine is well absorbed from the gastrointestinal tract, with oral bioavailability typically around 90%.citation needed Absorption is favored in more basic intestinal environments, where the drug exists in a more lipid-soluble form. Peak plasma concentrations are reached approximately 1 to 3 hours after oral administration. Roughly 20% of circulating amphetamine is bound to plasma proteins, and the drug distributes readily into most tissues including brain and cerebrospinal fluid. Amphetamine is metabolized hepatically, primarily by CYP2D6, along with dopamine β-hydroxylase (DBH), flavin-containing monooxygenase 3 (FMO3), butyrate-CoA ligase (XM-ligase), and glycine N-acyltransferase (GLYAT). The major metabolic pathways include aromatic hydroxylation, aliphatic hydroxylation, and N-dealkylation, though a significant portion of the drug is excreted unchanged. Elimination half-life varies by enantiomer and is strongly influenced by urinary pH: at normal urine pH, the d-enantiomer has a half-life of approximately 9 to 11 hours and the l-enantiomer 11 to 14 hours, with highly acidic urine reducing these to around 7 hours and highly alkaline urine extending them up to 34 hours. Approximately 90% of an ingested dose is eliminated within 3 days.

Interactions

Dangerous

Highest risk

These combinations are considered extremely harmful and should always be avoided. Reactions to these drugs taken in combination are highly unpredictable and have a potential to cause death.

Unsafe

Avoid

There is considerable risk of physical harm when taking these combinations, they should be avoided where possible.

2C-T-x compounds5-MeO-xxT tryptaminesDOx compoundsDXMNBOMe compoundsPCPPregabalin

Caution

Use caution

These combinations are not usually physically harmful, but may produce undesirable effects, such as physical discomfort or overstimulation. Extreme use may cause physical health issues. Synergistic effects may be unpredictable. Care should be taken when choosing to use this combination.

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Tolerance

Tolerance timelines are rules of thumb, not exact schedules, and vary widely between individuals and use patterns.

Full Tolerance
Prolonged repeated amphetamine use can reduce responsiveness to many effects, often rapidly when chronic high doses are involved. As tolerance rises, larger doses may be needed for comparable effects. Outside medical settings, tolerance usually develops quickly and can reduce many beneficial effects. Different effects may also show tolerance on different timelines.
Baseline Reset
1-2 weeks
Half Tolerance
3-7 days
Cross Tolerance

Dopaminergic stimulants

Harm Potential

Addiction & Dependence

Psychological

High

Amphetamine has high abuse potential and can cause psychological dependence with chronic use. Addiction is a serious risk with heavy recreational use but is unlikely to arise from typical medical use at therapeutic doses. Cravings and withdrawal effects occur if use is suddenly discontinued.citation needed

Physical

Moderate

Tolerance develops rapidly with recreational use, requiring increasingly larger doses. Withdrawal symptoms occur in roughly 88% of chronic high-dose users, persisting for 3-4 weeks with a marked crash phase during the first week.citation needed Symptoms include fatigue, depression, anxiety, irritability, intense hunger, disturbed sleep, and drug craving.

Toxicity

Cardiovascular

Cardiovascular effects including hypertension, tachycardia, and arrhythmias occur during intoxication; severe hypertensive crises, heart attacks, and circulatory collapse are primarily associated with high doses or pre-existing cardiovascular conditions.citation needed

Central Nervous System

No evidence of direct neurotoxicity in humans at typical doses; however, high-dose exposure may cause indirect neurotoxicity, particularly when hyperpyrexia occurs. Prolonged heavy use can lead to speech and thought disturbances.

Renal

Kidney damage is primarily associated with rhabdomyolysis from high-dose use, particularly when hyperthermia occurs; acute renal failure has been reported in overdose and fatality cases.citation needed

Hepatic

Hepatic injury has been reported in overdose contexts; liver damage and failure are possible with chronic high-dose use.citation needed

Dental and Oral

Long-term use is associated with dental caries, tooth loss, and gingivitis; jaw tension causes bruxism leading to permanent tooth wear and cracking.citation needed

Psychosis Risk

Stimulant psychosis can occur with severe overdose or chronic heavy use, presenting with paranoia, hallucinations, delusions, and bizarre or violent behavior.citation needed Symptoms usually disappear within weeks after cessation, but approximately 5-15% of users fail to recover completely. Psychosis rarely arises from therapeutic use. Risk increases with multi-day use, sleep deprivation, and high doses.

Seizure Risk

Amphetamine reduces seizure threshold and convulsions can occur at high doses.citation needed Fatal poisoning is usually preceded by convulsions and coma.3 Seizures are rare at typical doses but represent a serious risk in overdose situations.

History & Culture

Discovery and Early Synthesis

Amphetamine was first synthesized in 1887 by Romanian chemist Lazăr Edeleanu while working in Germany. Edeleanu originally named the compound phenylisopropylamine, though its central nervous system effects remained entirely unknown for the next four decades. The substance's stimulant properties

Legality

International

UN Convention on Psychotropic Substances 1971: scheduled

By Country

Illegal7
Finland flagFinlandIllegal
Israel flagIsraelIllegal
Japan flagJapanIllegal
Luxembourg flagLuxembourgIllegal
New Zealand flagNew ZealandIllegal
Singapore flagSingaporeIllegal
Thailand flagThailandIllegal
Controlled / restricted6
Australia flagAustraliaSchedule 8
India flagIndiaRestricted
Netherlands flagNetherlandsRestricted
Philippines flagPhilippinesRestricted
South Africa flagSouth AfricaRestricted
Ukraine flagUkraineRestricted
Prescription19
United States flagUnited StatesPrescription only
Austria flagAustriaPrescription only
Belgium flagBelgiumPrescription only
Brazil flagBrazilPrescription only
Canada flagCanadaPrescription only
China flagChinaPrescription only
Denmark flagDenmarkPrescription only
France flagFrancePrescription only
Germany flagGermanyPrescription only
Ireland flagIrelandPrescription only
Mexico flagMexicoPrescription only
Norway flagNorwayPrescription only
Poland flagPolandPrescription only
South Korea flagSouth KoreaPrescription only
Spain flagSpainPrescription only
Sweden flagSwedenPrescription only
Switzerland flagSwitzerlandPrescription only
United Arab Emirates flagUnited Arab EmiratesPrescription only
United Kingdom flagUnited KingdomPrescription only
Legal / decriminalized1
Portugal flagPortugalDecriminalized

References

Source Pages

  1. Drug Users Bible by Dominic Milton Trott
  2. DrugBank
  3. Erowid
  4. Erowid: Amphetamines Vault
  5. Isomer Design (TiHKAL/PiHKAL)
  6. PsychonautWiki
  7. The Drug Classroom
  8. TripSit Factsheets
  9. TripSit Wiki
  10. TripSit: Drug Combinations
  11. Wikipedia

Citations

  1. Suzanne M. Underhill, David S. Wheeler, Minghua Li, Spencer D. Watts, Susan L. Ingram, & Susan G. Amara. (July 2014). Amphetamine modulates excitatory neurotransmission through endocytosis of the glutamate transporter EAAT3 in dopamine neurons. Neuron, 83(2), 404–416. https://doi.org/10.1016/j.neuron.2014.05.0431
  2. Gregory M. Miller. (January 2011). The emerging role of trace amine-associated receptor 1 in the functional regulation of monoamine transporters and dopaminergic activity. Journal of Neurochemistry, 116(2), 164–176. https://doi.org/10.1111/j.1471-4159.2010.07109.x1
  3. Dextroamphetamine Sulfate Tablets, USP – Prescribing Information. U.S. Food and Drug Administration / DailyMed (n.d.). https://dailymed.nlm.nih.gov/dailymed/fda/fdaDrugXsl.cfm?setid=b2ad8d2b-ed94-43cd-95ea-85e91d997f261
  4. Bradley C. (2011). Bradley's Benzedrine Studies on Children with Behavioral Disorders. Journal of Attention Disorders. https://pmc.ncbi.nlm.nih.gov/articles/PMC3064242/1
  5. The ACT Drug Decriminalisation Laws: Here's What It Means — CODA Criminal Law. (n.d.). https://codalaw.com.au/the-act-drug-decriminalisation-laws-heres-what-it-means/1
  6. Suchtmittelgesetz (SMG); Suchtgiftverordnung, Anhang IV. ris.bka.gv.at (n.d.). https://www.ris.bka.gv.at/GeltendeFassung.wxe?Abfrage=Bundesnormen&Gesetzesnummer=100110401
  7. Suchtmittelgesetz (SMG); Suchtgiftverordnung, Anhang IV. ris.bka.gv.at (n.d.). https://ris.bka.gv.at/NormDokument.wxe?Abfrage=Bundesnormen&Anlage=4&Artikel=&Gesetzesnummer=10011053&Paragraf=&Uebergangsrecht=1
  8. Royal Decree of 6 September 2017 regulating narcotic and psychotropic substances. ejustice.just.fgov.be (n.d.). https://www.ejustice.just.fgov.be/eli/besluit/2017/09/06/2017031231/justel1
  9. Royal Decree of 6 September 2017 regulating narcotic and psychotropic substances. fagg-afmps.be (n.d.). https://www.fagg-afmps.be/sites/default/files/content/INSP/NARC/annex%20II_non%20official%20consolidated%20version.pdf1
  10. Royal Decree of 6 September 2017 regulating narcotic and psychotropic substances. fagg-afmps.be (n.d.). https://www.fagg-afmps.be/sites/default/files/content/INSP/NARC/kb-ar-20170906.pdf1

Further Reading

  1. DrugWise: Amphetamines
  2. EUDA: Amphetamine Drug Profile

Article Status

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Recent changes7 human edits · latest

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24 January 2026

  1. Josie Kins · Updated the article · also 1,4-Butanediol, 1B-LSD, 1cP-AL-LAD and 573 more

  2. Josie Kins · Updated the article · also 1,4-Butanediol, 1B-LSD, 1cP-AL-LAD and 573 more

  3. Josie Kins · Updated the article · also 1,4-Butanediol, 1B-LSD, 1cP-AL-LAD and 573 more

  4. Josie Kins · Updated the article · also 1,4-Butanediol, 1B-LSD, 1cP-AL-LAD and 573 more

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  6. Josie Kins · Updated the article · also 1,4-Butanediol, 1B-LSD, 1cP-AL-LAD and 573 more

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