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Summary sheet: Amphetamine
Chemical Nomenclature
Common names Amphetamine, Speed, Adderall, Pep
Substitutive name α-Methylphenethylamine
Systematic name (RS)-1-Phenylpropan-2-amine
Class Membership
Psychoactive class Stimulant
Chemical class Phenethylamine
Routes of Administration

WARNING: Always start with lower doses due to differences between individual body weight, tolerance, metabolism, and personal sensitivity. See responsible use section.

Threshold Common Heavy
5 - 5 - 15 - 30 - 50 mg
Light Strong
Threshold 5 mg
Light 5 - 15 mg
Common 15 - 30 mg
Strong 30 - 50 mg
Heavy 50 mg +
Total 6 - 8 hours
Onset 15 - 30 minutes
Peak 2.5 - 4 hours
Offset 2 - 3 hours
After effects 5 - 10 hours

Threshold Common Heavy
5 - 15 - 25 - 40 - 75 mg
Light Strong
Threshold 5 - 15 mg
Light 15 - 25 mg
Common 25 - 40 mg
Strong 40 - 75 mg
Heavy 75 mg +
Total 3 - 6 hours
Onset 1 - 5 minutes
Peak 1 - 2 hours

DISCLAIMER: PW's dosage information is gathered from users and resources for educational purposes only. It is not a recommendation and should be verified with other sources for accuracy.

Amphetamine (also known as speed and pep) is a widely used stimulant substance of the phenethylamine class. Amphetamine is the parent compound of a group known as substituted amphetamines, which includes bupropion, phenmetrazine, MDMA, and DOx. Its primary mechanism of action is to increase the activity of dopamine and norepinephrine in the brain.

Amphetamine was discovered in 1887. It saw widespread medical and non-medical use in the 1930s as an over-the-counter medication and became regulated as a prescription drug in the mid-1960s.[1] Today, amphetamine is used throughout the world for the treatment of attention deficit hyperactivity disorder (ADHD) and narcolepsy, popularly known by the trademark "Adderall".[2][3] It is also used illictly as a an athletic performance and cognitive enhancer.

Typical effects include enhanced focus, increased libido, suppressed appetite, and euphoria. It is usually taken orally, but can also be insufflated, injected, or administered rectally. Recreational use of amphetamines is associated with dependence and abuse.

History and culture

Amphetamine was first synthesized in Germany in 1887 by the Romanian chemist Lazăr Edeleanu, who named it phenylisopropylamine.[4] However, its pharmacological effects remained unknown until 1927, when it was independently re-synthesized by Gordon Alles and discovered to have sympathomimetic properties.[5]

Amphetamine had no medical use until late 1933, when Smith, Kline and French began selling it as a decongestant inhaler under the name Benzedrine.[6] Benzedrine sulfate was introduced 3 years later and was used to treat a wide variety of medical conditions, including narcolepsy, obesity, low blood pressure, low libido, and chronic pain, among others.[7]

During World War II, amphetamine and methamphetamine were used extensively by both the Allied and Axis forces for their stimulant and performance-enhancing effects.[8][9] As its addictive properties became known, governments began to place strict controls on its sale.[10]

Amphetamine is still illegally synthesized and sold on the black market, primarily in European countries.[11] Among European Union (EU) member states, 1.2 million young adults used illicit amphetamine or methamphetamine in 2013. During 2012, approximately 5.9 metric tons of illicit amphetamine were seized within EU member states;[11] the "street price" of illicit amphetamine within the EU ranged from €6–38 per gram during the same period.[11] Outside Europe, the illicit market for amphetamine is much smaller than the market for methamphetamine and MDMA.[11]



This chemistry section is incomplete.

You can help by adding to it.

Amphetamine is composed of a phenethylamine core featuring a phenyl ring bound to an amino (NH2) group through an ethyl chain with an additional methyl substitution at Rα. It can be referred to as a methyl homolog of phenethylamine as it has the same general formula, differing only in the addition of one methyl group. The name 'amphetamine' is a contraction from αlphamethylphenethylamine

In its free base form and at room temperature, amphetamine is a colorless oil.[12]


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This pharmacology section is incomplete.

You can help by adding to it.

Amphetamine is a full agonist of the trace amine-associated receptor 1 (TAAR1), which is a key regulator of common and trace brain monoamines such as dopamine, serotonin and noradrenaline.[13][14][15] The agonism of this set of receptors results in the release of increased concentrations of dopamine, serotonin and noradrenaline in the synaptic cleft. This leads to cognitive and physical stimulation within the user.

Subjective effects

The effects listed below are based upon the subjective effects index and personal experiences of PsychonautWiki contributors. These effects should be taken with a grain of salt and will rarely (if ever) occur all at once, but heavier doses will increase the chances of inducing a full range of effects. Likewise, adverse effects become much more likely on higher doses and may include serious injury or death.

Physical effects

Visual effects

Cognitive effects

After effects
Aftereffects (3).svg

Experience reports

There are currently no anecdotal reports which describe the effects of this compound within our experience index. Additional experience reports can be found here:

Toxicity and harm potential


This toxicity and harm potential section is a stub.

As such, it may contain incomplete or even dangerously wrong information. You can help by expanding or correcting it.
We also recommend that you conduct independent research and use harm reduction practices when using this substance.

This radar plot shows therelative physical harm, social harm, and dependence of amphetamine.[16]

In rodents and primates, sufficiently high doses of amphetamine causes damage to dopamine neurons, characterized as reduced transporter and receptor function.[17] As of March 2014, there is no evidence that amphetamine is directly neurotoxic in humans.[18] However, high-dose amphetamine can cause indirect neurotoxicity as a result of increased oxidative stress from reactive oxygen species and autoxidation of dopamine.[19][20][21] Animal models of neurotoxicity from high-dose amphetamine exposure indicate that the occurrence of hyperpyrexia (i.e., core body temperature ≥ 40 °C) is necessary for the development of amphetamine-induced neurotoxicity. [22]

Lethal dosage

The LD50 (the dosage required to kill 50% of the test subjects) of amphetamine in rats has been found to be between roughly 15mg and 180mg per kilogram depending on the study.[23] No formal studies in humans have been carried out and the exact toxic dosage is unknown.

It is strongly recommended that one use harm reduction practices when using this substance.

Tolerance and addiction potential

As with other stimulants, the chronic use of amphetamine can be considered moderately addictive with a high potential for abuse and is capable of causing psychological dependence among certain users. When addiction has developed, cravings and withdrawal effects may occur if a person suddenly stops their usage.[24][25] Addiction is a serious risk with heavy recreational amphetamine use, but is unlikely to arise from typical medical use.[26][27][28]

Tolerance to many of the effects of amphetamine develops with prolonged and repeated use. This results in users having to administer increasingly large doses to achieve the same effects. Upon single administration, it takes about 3 - 7 days for the tolerance to be reduced to half and 1 - 2 weeks to be back at baseline (in the absence of further consumption). Amphetamine presents cross-tolerance with all dopaminergic stimulants, meaning that after the consumption of amphetamine all stimulants will have a reduced effect.

Withdrawal symptoms

After taking amphetamine on a regular basis, some users will become addicted. When the drug is discontinued immediately, the user will experience what has come to be known as a "crash" along with a number of other amphetamine withdrawal symptoms including paranoia, depression, dream potentiation, anxiety, itching, mood swings, irritability, fatigue, insomnia, an intense craving for more amphetamine or other stimulants, and, in some cases, nausea and vomiting.


Main article: Stimulant psychosis

Abuse of amphetamine can result in a stimulant psychosis that may present with a variety of symptoms (e.g., paranoia, hallucinations, delusions).[29] A review on treatment for amphetamine, dextroamphetamine, and methamphetamine abuse-induced psychosis states that about 5–15% of users fail to recover completely.[30][31] The same review asserts that, based upon at least one trial, antipsychotic medications effectively resolve the symptoms of acute amphetamine psychosis.[32] Psychosis very rarely arises from therapeutic use.[33][34]

Dangerous interactions

Although many psychoactive substances are safe to use on their own, they can become dangerous or even life-threatening when taken with other substances. The list below contains some potentially dangerous combinations, but may not include all of them. Certain combinations may be safe in low doses but still increase the possibility of injury of death. Independent research should always be conducted to ensure that a combination of two or more substances is safe before consumption.

  • 25x-NBOMe/25x-NBOH - Members of the 25x family are highly stimulating and physically straining. Combinations with stimulants should be avoided due to the risk of excessive stimulation. This can result in panic attacks, thought loops, seizures, increased blood pressure, vasoconstriction, and heart failure in extreme cases.
  • Alcohol - Alcohol can be dangerous to combine with stimulants due to the risk of accidental over-intoxication. Stimulants mask the sedative effects of alcohol, which is the main factor people use to assess their degree of intoxication. Once the stimulant wears off, the depressant effects of alcohol are left unopposed, which can result in blackouts and respiratory depression. If combined, one should strictly limit themselves to only drinking a certain amount of alcohol per hour.
  • DXM - Combinations with DXM should be strictly avoided due to DXM's effects on serotonin and dopamine reuptake. This can lead to panic attacks, hypertensive crisis, or serotonin syndrome.
  • MXE - Combinations with MXE may dangerously elevate blood pressure and increase the risk of psychosis.
  • Tramadol - Tramadol lowers the seizure threshold.[36] Combinations with stimulants may further increase this risk.
  • MDMA - The neurotoxic effects of MDMA may be increased when combined with amphetamines.
  • MAOIs - This combination may increase the amount of neurotransmitters such as dopamine to dangerous or even fatal levels. Examples include syrian rue, banisteriopsis caapi, 2C-T-2, 2C-T-7, αMT, and some antidepressants.[37]

Legal status

Internationally, amphetamine is a schedule II controlled substance under the United Nations 1971 Convention on Psychotropic Substances.[citation needed] It is therefore illegal to sell and possess without a prescription.

  • Austria: Amphetamine is illegal to possess, produce and sell under the SMG (Suchtmittelgesetz Österreich).[citation needed]
  • Canada: Amphetamine is a Schedule I drug in Canada.[38]
  • Germany: Amphetamine is a controlled substance under Anlage 3 of the BtMG.[citation needed]
  • Japan: Amphetamine is prohibited even for medical use in Japan.[39]
  • South Korea: Amphetamine is prohibited even for medical use in South Korea.[citation needed]
  • Thailand: Amphetamine is classified as a category 1 narcotic in the Thai Narcotic Act of 2012.[40]
  • United Kingdom: Amphetamine is a Class B drug in the United Kingdom.[41]
  • United States: Amphetamine is a Schedule II controlled substance in the United States.[42]

See also

External links


  • Galli, A., Poulsen, N.W., Sulzer, D., & Sonders, M.S. (2005). Mechanisms of neurotransmitter release by amphetamines: a review. Progress in Neurobiology, 75 6, 406-33.
  • Berman, S. M., Kuczenski, R., McCracken, J. T., & London, E. D. (2009). Potential adverse effects of amphetamine treatment on brain and behavior: a review. Molecular Psychiatry, 14(2), 123.
  • Baumann, M., Carroll, F.I., Dersch, C.M., Partilla, J.S., Rothman, R.B., Romero, D., & Rice, K. (2001). Amphetamine-type central nervous system stimulants release norepinephrine more potently than they release dopamine and serotonin. Synapse, 39 1, 32-41. doi: 10.1002/1098-2396(20010101)39:1<32::AID-SYN5>3.0.CO;2-3


  1. Angrist, B., & Sudilovsky, A. (1978). Central nervous system stimulants: historical aspects and clinical effects. In Stimulants (pp. 99-165). Springer, Boston, MA.
  2. The pharmacology and clinical outcomes of amphetamines to treat ADHD: does composition matter? ( / NCBI) |
  3. Narcolepsy: current treatment options and future approaches |
  4. Lazăr Edeleano: Über einige Derivate der Phenylmethacrylsäure und der Phenylisobuttersäure. In: Berichte der Deutschen chemischen Gesellschaft zu Berlin; 20. Jg. (1887), Band 3, S. 616–622.
  5. Sulzer D, Sonders MS, Poulsen NW, Galli A (April 2005). "Mechanisms of neurotransmitter release by amphetamines: a review". Prog. Neurobiol. 75 (6): 406–433. doi:10.1016/j.pneurobio.2005.04.003. PMID 15955613.
  6. Rasmussen N (July 2006). "Making the first anti-depressant: amphetamine in American medicine, 1929–1950". J. Hist. Med. Allied Sci. 61 (3): 288–323. PMID 16492800.
  7. Bett WR (August 1946). "Benzedrine sulphate in clinical medicine; a survey of the literature". Postgrad. Med. J. 22 (250): 205–218. doi:10.1136/pgmj.22.250.205. PMC 2478360  Freely accessible. PMID 20997404.
  8. Rasmussen N (2011). "Medical science and the military: the Allies' use of amphetamine during World War II". J. Interdiscip. Hist. 42 (2): 205–233. PMID 22073434.
  9. Defalque RJ, Wright AJ (April 2011). "Methamphetamine for Hitler's Germany: 1937 to 1945". Bull. Anesth. Hist. 29 (2): 21–4, 32. PMID 22849208.
  10. "Historical overview of methamphetamine". Vermont Department of Health. Government of Vermont. Archived from the original on 5 October 2012. Retrieved 29 January 2012.
  11. 11.0 11.1 11.2 11.3 Mohan J, ed. (June 2014). "World Drug Report 2014" (PDF). United Nations Office on Drugs and Crime. p. 3. Retrieved 18 August 2014.
  13. The Emerging Role of Trace Amine Associated Receptor 1 in the Functional Regulation of Monoamine Transporters and Dopaminergic Activity ( / NCBI) |
  14. Drug banks amphetamine targets |
  15. TA1 receptor |
  16. Development of a rational scale to assess the harm of d rugs of potential misuse (ScienceDirect) |
  17. Update on Amphetamine Neurotoxicity and Its Relevance to the Treatment of ADHD |
  18. Human health effects - Amphetamine |
  19. Malenka RC, Nestler EJ, Hyman SE (2009). "15". In Sydor A, Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. p. 370. ISBN 9780071481274. "Unlike cocaine and amphetamine, methamphetamine is directly toxic to midbrain dopamine neurons."
  20. Toxicity of amphetamines: an update |
  21. Dopaminergic neuron-specific oxidative stress caused by dopamine itself. ( / NCBI) |
  22. Bowyer JF, Hanig JP (November 2014). "Amphetamine- and methamphetamine-induced hyperthermia: Implications of the effects produced in brain vasculature and peripheral organs to forebrain neurotoxicity". Temperature (Austin). 1 (3): 172–182. "Hyperthermia alone does not produce amphetamine-like neurotoxicity but AMPH and METH exposures that do not produce hyperthermia (≥40°C) are minimally neurotoxic. Hyperthermia likely enhances AMPH and METH neurotoxicity directly through disruption of protein function, ion channels and enhanced ROS production. ... The hyperthermia and the hypertension produced by high doses amphetamines are a primary cause of transient breakdowns in the blood-brain barrier (BBB) resulting in concomitant regional neurodegeneration and neuroinflammation in laboratory animals. ... In animal models that evaluate the neurotoxicity of AMPH and METH, it is quite clear that hyperthermia is one of the essential components necessary for the production of histological signs of dopamine terminal damage and neurodegeneration in cortex, striatum, thalamus and hippocampus." |
  23. Amphetamine - human health effects |
  24. "Amphetamines: Drug Use and Abuse" |
  25. Efficacy of psychostimulant drugs for amphetamine abuse or dependence | [1]
  26. "Adderall XR Prescribing Information" |
  27. Stolerman IP (2010). Stolerman IP, ed. Encyclopedia of Psychopharmacology. Berlin; London: Springer. p. 78. ISBN 9783540686989.
  28. "Miscellaneous Sympathomimetic Agonists" |
  29. Treatment for amphetamine psychosis | [2]
  30. Treatment for amphetamine psychosis | [3]
  31. Hofmann FG (1983). A Handbook on Drug and Alcohol Abuse: The Biomedical Aspects (2nd ed.). New York: Oxford University Press. p. 329. ISBN 9780195030570.
  32. Treatment for amphetamine psychosis | [4]
  33. Stimulant Misuse: Strategies to Manage a Growing Problem |
  35. Adderall Prescription info |
  36. Talaie, H., Panahandeh, R., Fayaznouri, M. R., Asadi, Z., & Abdollahi, M. (2009). Dose-independent occurrence of seizure with tramadol. Journal of Medical Toxicology, 5(2), 63-67.
  37. Gillman, P. K. (2005). Monoamine oxidase inhibitors, opioid analgesics and serotonin toxicity. British Journal of Anaesthesia, 95(4), 434-441.
  38. Controlled Drugs and Substances Act |
  39. The problem of the abuse of amphetamines in Japan |
  40. Thai Narcotic Act of 2012 |
  41. Misuse of Drugs Act of 1971 |
  42. Controlled Drugs and Substances Act |