Amphetamine

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Summary sheet: Amphetamine
Amphetamine
Amphetamine.svg
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.



Oral
Dosage
Bioavailability 75%+[1]
Threshold 2.5 mg
Light 5 - 10 mg
Common 10 - 25 mg
Strong 25 - 50 mg
Heavy 50 mg +
Duration
Total 6 - 8 hours
Onset 30 - 45 minutes
Come up 30 - 135 minutes
Peak 2.5 - 4 hours
Offset 2 - 3 hours
After effects 3 - 6 hours



Insufflated
Dosage
Threshold 4 mg
Light 6 - 15 mg
Common 15 - 30 mg
Strong 30 - 50 mg
Heavy 50 mg +
Duration
Total 3 - 6 hours
Onset 1 - 5 minutes
Come up 30 - 90 minutes
Peak 1 - 2 hours
Offset 1.5 - 3 hours
After effects 2 - 4 hours





Intravenous
Dosage
Threshold 4 mg
Light 6 - 15 mg
Common 15 - 30 mg
Strong 30 - 50 mg
Heavy 50 mg +
Duration
Total 3 - 6 hours
Onset 2 - 10 seconds
Come up 2 - 10 seconds
Peak 2 - 4 hours
Offset 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.

Interactions
Alcohol
GHB
GBL
Opioids
Cocaine
Cannabis
Caffeine
Ketamine
Methoxetamine
Psychedelics
DXM
PCP
25x-NBOMe
2C-T-x
5-MeO-xxT
DOx
Tramadol
aMT
MAOIs

Amphetamine (also known as alpha-methylphenethylamine, amfetamine, and speed) is a classical stimulant substance of the phenethylamine class. It is the parent compound of the substituted amphetamines, a diverse group that includes methamphetamine, MDMA, cathinone, and bupropion. The mechanism of action involves promoting release of the neurotransmitters dopamine and norepinephrine.[2]

It was first synthesized in 1887, but its psychostimulant effects were not discovered until 1929.[3] In the 1930s, it was sold over-the-counter under the name "Benzedrine" as a decongestant.[4] It became widely used to treat a range of ailments such as alcohol hangover, narcolepsy, depression, and obesity.[5] Due to issues with addiction and abuse, it was eventually listed as a controlled substance under the United Nations 1971 "Convention on Psychotropic Substances".[6]

Amphetamine is now primarily a prescription drug used to treat attention deficit hyperactivity disorder (ADHD), narcolepsy, and obesity.[7][8] Additionally, it sees widespread illicit use as a performance enhancing agent and recreational substance.

Subjective effects include stimulation, focus enhancement, motivation enhancement, increased libido, appetite suppression, and euphoria. It is usually taken orally, but can also be insufflated, injected, or administered rectally. Lower doses tend to increase focus and productivity while higher doses tend to increase sociability, sexual desire, and euphoria.

Amphetamine has high abuse potential. Chronic use (i.e. high dose, repeat administration) is associated with compulsive redosing, escalating tolerance, and psychological dependence. Additionally, abuse has been linked to a number of health conditions, especially cardiovascular issues such as high blood pressure and increased risk of stroke.[9]

It is highly advised to use harm reduction practices if using this substance.

History and culture

Amphetamine was first synthesized in Germany in 1887 by the Romanian chemist Lazăr Edeleanu, who named it phenylisopropylamine.[10] However, its stimulant effects remained unknown until 1927, when it was independently re-synthesized by Gordon Alles and discovered to have sympathomimetic properties.[11]

In late 1933, Smith, Kline and French began selling amphetamine in the form of a decongestant inhaler under the name Benzedrine.[4] 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.[12]

During World War II, amphetamine and methamphetamine were used extensively by both the Allied and Axis forces for their stimulant and performance-enhancing effects.[13][14] As its addictive properties became known, governments began to place strict controls on its sale.[15]

Amphetamine is still illegally synthesized and sold on the black market, primarily in European countries.[16] 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;[16] the "street price" of illicit amphetamine within the EU ranged from €6–38 per gram during the same period.[16]

Outside Europe, the illicit market for amphetamine is much smaller than the market for methamphetamine and MDMA.[16]

Chemistry

Amphetamine, also known as alpha-methylphenethylamine, is a synthetic substance of the phenethylamine family. The chemical structure of amphetamine consists of phenethylamine, a phenyl ring bound to an amino (NH2) group through an ethyl chain, with an additional methyl substitution at Rα. The name 'amphetamine' is a contraction from αlphamethylphenethylamine

It is the parent compound of the substituted amphetamines, a highly diverse group that includes such substances as bupropion, phenmetrazine, methamphetamine, MDMA, and the DOx series.

At room temperature, the pure freebase is a mobile, colorless, and volatile liquid with a characteristically strong amine odor, and acrid, burning taste.[17]

Enantiomers

Amphetamine is a chiral compound. Racemic amphetamine (dl-amphetamine) contains two optical isomers, or enantiomers:

  • l-amphetamine (l-amph, l-AMP), levamfetamine (INN), levoamphetamine, levorotatory amphetamine, l-isomer amphetamine, (R)-(−)-amphetamine, (R)-amphetamine, (−)-amphetamine, or (2R)-1-Phenylpropan-2-amine (IUPAC name), is the 'left-handed' enantiomer form of amphetamine.
  • d-amphetamine (d-amph, d-AMP), dexamphetamine (INN), dextroamphetamine, dextrorotatory amphetamine, d-isomer amphetamine, or (S)-(+)-amphetamine, (S)-amphetamine, (+)-amphetamine, (2S)-1-phenylpropan-2-amine (IUPAC name), or "Dexedrine" (trade name amongst others), is the 'right-handed' enantiomer form of amphetamine.

Adderall and many other formulations of mixed amphetamine salts contain the enantiomers in a 3:1 ratio of d to l. This is achieved by mixing one part racemic amphetamine and one part d-amphetamine.

Pharmacology

Amphetamine exerts its behavioural effects by increasing the signaling activity of neurotransmitters norepinephrine and dopamine in the reward and executive function pathways of the brain. The reinforcing and motivational effects of amphetamine are mostly due to enhanced dopaminergic activity in the mesolimbic pathway.[18]

The euphoric and locomotor-stimulating effects of amphetamine are dependent upon the magnitude and speed by which it increases synaptic dopamine and norepinephrine concentrations in the striatum.[3]

It is a potent full agonist of the trace amine-associated receptor 1 (TAAR1) and interacts with vesicular monoamine transporter 2 (VMAT2).[19][20][21] Combined action on TAAR1 and VMAT2 results in increased concentrations of dopamine and norepinephrine in the synapses, which stimulates neuronal activity.

Dextroamphetamine is a more potent agonist of TAAR1 than levoamphetamine.[22] Consequently, dextroamphetamine produces greater CNS stimulation than levoamphetamine, roughly three to four times more, but levoamphetamine has slightly stronger cardiovascular and peripheral effects.[23][24]

The exact bioavailability of amphetamine is not known, but it is believed to be over 75% by mouth, and higher by injection or intranasal administration[25]. Its absorption and excretion may be pH dependent. The basic form is more readily absorbed in the intestine and less readily removed by the kidneys, potentially increasing its half life [25]. It is removed by the kidneys via excretion and a small amount is removed by hepatic enzymes.

Subjective effects

Disclaimer: The effects listed below cite the Subjective Effect Index (SEI), an open research literature based on anecdotal user reports and the personal analyses of PsychonautWiki contributors. As a result, they should be viewed with a healthy degree of skepticism.

It is also worth noting that these effects will not necessarily occur in a predictable or reliable manner, although higher doses are more liable to induce the full spectrum of effects. Likewise, adverse effects become increasingly likely with higher doses and may include addiction, severe injury, or death ☠.


Physical effects
Child.svg

Cognitive effects
User.svg

After effects
Aftereffects (3).svg

Experience reports

Anecdotal reports which describe the effects of this compound within our experience index include:

Additional experience reports can be found here:

Toxicity and harm potential

Ambulance2.png

This toxicity and harm potential section is a stub.

As a result, it may contain incomplete or even dangerously wrong information! You can help by expanding upon or correcting it.
Note: Always conduct independent research and use harm reduction practices if using this substance.

This radar plot shows therelative physical harm, social harm, and dependence of amphetamine.[33]

As of March 2014, there is no evidence that amphetamine is directly neurotoxic in humans.[34] However, high-dose amphetamine can cause indirect neurotoxicity as a result of increased oxidative stress from reactive oxygen species and autoxidation of dopamine.[18][35][36]

In rodents and primates, sufficiently high doses of amphetamine causes damage to dopamine neurons, characterized as reduced transporter and receptor function.[37] 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. [38]

Melatonin has been shown to prevent (if used 30min+ before dosing) and reverse amphetamine induced neurotoxicity of TH-pSer40 and calpastatin levels in the Substantia Nigra of rats.[39][40]

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

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 15 mg and 180 mg per kilogram, depending on the study.[41] No formal studies in humans have been carried out and the exact toxic dosage is unknown.

Dependence and abuse potential

Amphetamine has high abuse potential and can cause psychological dependence with chronic use.

When dependence has developed, cravings and withdrawal effects may occur if use is suddenly discontinued.[42][43] Withdrawal symptoms include paranoia, depression, dream potentiation, anxiety, itching, mood swings, irritability, fatigue, insomnia, an intense craving for more amphetamine or other stimulants.

Addiction is a serious risk with chronic or heavy recreational amphetamine use, but is unlikely to arise from typical medical use.[44][45][46]

Tolerance to many of the effects of amphetamine develops with prolonged and repeated use. This results in the user 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 exhibits cross-tolerance with all dopaminergic stimulants, meaning that after the consumption of amphetamine most stimulants will have a reduced effect.

Psychosis

Main article: Stimulant psychosis

Severe amphetamine overdose can result in a stimulant psychosis that may present with a variety of symptoms (e.g., paranoia, hallucinations, delusions).[47] A review on treatment for amphetamine abuse-induced psychosis states that about 5–15% of users fail to recover completely.[47][48] The same review asserts that antipsychotic medications effectively resolve the symptoms of acute amphetamine psychosis.[47] Psychosis very rarely arises from therapeutic use.[49]

Dangerous interactions

Warning: Many psychoactive substances that are reasonably safe to use on their own can suddenly become dangerous and even life-threatening when combined with certain other substances. The following list provides some known dangerous interactions (although it is not guaranteed to include all of them).

Always conduct independent research (e.g. Google, DuckDuckGo, PubMed) to ensure that a combination of two or more substances is safe to consume. Some of the listed interactions have been sourced from TripSit.

  • Alcohol - Drinking alcohol on stimulants is considered risky because it reduces the sedative effects of the alcohol that the body uses to gauge drunkenness. This often leads to excessive drinking with greatly reduced inhibitions, increasing the risk of liver damage and increased dehydration. The effects of stimulants will also allow one to drink past a point where they might normally pass out, increasing the risk. If you do decide to do this then you should set a limit of how much you will drink each hour and stick to it, bearing in mind that you will feel the alcohol and the stimulant less.
  • GHB/GBL - Stimulants increase respiration rate allowing a higher dose of sedatives. If the stimulant wears off first then the depressant effects of the GHB/GBL may overcome the user and cause respiratory arrest.
  • Opioids - Stimulants increase respiration rate allowing a higher dose of opiates. If the stimulant wears off first then the opiate may overcome the patient and cause respiratory arrest.
  • Cocaine - The rewarding effects of cocaine are mediated by DAT inhibition, and an increase of exocytosis of dopamine through the cell membrane. Amphetamine reverses the direction of DAT and the direction vesicular transports within the cell by a pH mediated mechanism of displacement, thus excludes the regular mechanism of dopamine release through means of exocytosis because the effects Na+/K+ ATPase are inhibited. You will find cardiac effects with the combination of cocaine and amphetamine due to a SERT mediated mechanism from the subsequent activation of 5-HT2B, which is an effect of serotonin-related valvulopathy. Amphetamines generally cause hypertension in models of abuse, and this combination can increase the chances of syncope due to turbulent blood flow during valve operation. The rewarding mechanisms of cocaine are reversed by administration of amphetamine.[50][51]
  • Cannabis - Stimulants increase anxiety levels and the risk of thought loops and paranoia which can lead to negative experiences.
  • Caffeine - This combination of stimulants is generally considered unnecessary and may increase strain on the heart, as well as potentially causing anxiety and physical discomfort.
  • Tramadol - Tramadol and stimulants both increase the risk of seizures.
  • DXM - Both substances raise heart rate, in extreme cases, panic attacks caused by these substances have led to more serious heart issues.
  • Ketamine - Combining amphetamine and ketamine may result in psychoses that resemble schizophrenia, but not worse than the psychoses produced by either substance alone, but this is debatable. This is due to amphetamines ability to attenuated the disruption of working memory caused by ketamine. Amphetamine alone may result in grandiosity, paranoia, or somatic delusions with little to no effect on negative symptoms. Ketamine, however, will result in thought disorders, disruption of executive functioning, and delusions due to a modification of conception. These mechanisms are due to an increase of dopaminergic activity in the mesolimbic pathway caused by amphetamine due to its pharmacology effecting dopamine, and due to a disruption of dopaminergic functioning in the mesocortical pathways via NMDA antagonism effects of ketamine. Combining the two, you may expect mainly thought disorder along with positive symptoms.[52]
  • PCP - Increases risk of tachycardia, hypertension, and manic states.
  • Methoxetamine - Increases risk of tachycardia, hypertension, and manic states.
  • Psychedelics (e.g. LSD, mescaline, psilocybin) - Increases risk of anxiety, paranoia, and thought loops.
    • 25x-NBOMe - Amphetamines and NBOMes both provide considerable stimulation that when combined they can result in tachycardia, hypertension, vasoconstriction and, in extreme cases, heart failure. The anxiogenic and focusing effects of stimulants are also not good in combination with psychedelics as they can lead to unpleasant thought loops. NBOMes are known to cause seizures and stimulants can increase this risk.
    • 2C-T-x - Suspected of mild MAOI properties. May increase the risk of hypertensive crisis.
    • 5-MeO-xxT - Suspected of mild MAOI properties. May increase the risk of hypertensive crisis.
    • DOx
  • aMT - aMT has MAOI properties which may interact unfavorably with amphetamines.
  • MAOIs - MAO-B inhibitors can increase the potency and duration of phenethylamines unpredictably. MAO-A inhibitors with amphetamine can lead to hypertensive crises.

Reagent results

Exposing compounds to the reagents gives a colour change which is indicative of the compound under test.

Marquis Mecke Mandelin Liebermann Froehde Robadope
Orange - red No reaction slow (dark) green Orange - red No reaction Pink
Ehrlich Hofmann Simon’s Scott Folin
No reaction No reaction No reaction No reaction Light orange

Legal status

Internationally, amphetamine is a Schedule II controlled substance under the United Nations 1971 Convention on Psychotropic Substances.[53]

  • Australia: Amphetamine is a Schedule 8 controlled substance.[54]
  • Austria: Amphetamine is illegal to possess, produce and sell under the SMG (Suchtmittelgesetz Österreich).[citation needed]
  • Brazil: Amphetamine is a Class A3 psychoactice substance.[citation needed]
  • Canada: Amphetamine is a Schedule I drug in Canada.[55]
  • Germany: Amphetamine was added to the Opiumgesetz (Opium Act) in 1941.[56] In accordance to the Narcotics Act reform of 1981, it is controlled under Anlage III BtMG (Narcotics Act, Schedule III).[57] It can only be prescribed on a narcotic prescription form.
  • Japan: Amphetamine is prohibited even for medical use in Japan.[58]
  • Luxembourg: Amphetamine is a prohibited substance for recreational use. [59]
  • The Netherlands: Amphetamine is a List I controlled substance.[60]
  • New Zealand: Amphetamine is a Class B controlled substance.[61]
  • South Korea: Amphetamine is prohibited even for medical use in South Korea.[citation needed]
  • Sweden: Amphetamine is classified as a drug by the United Nations and is included in list P II in the 1971 Psychotropic Convention, as well as in list II in Sweden.[62]
  • Switzerland: Amphetamine is a controlled substance specifically named under Verzeichnis A. Medicinal use is permitted.[63]
  • Thailand: Amphetamine is classified as a category 1 narcotic under the Thai Narcotic Act of 2012.[64]
  • United Kingdom: Amphetamine is a Class B drug in the United Kingdom.[65]
  • United States: Amphetamine is a Schedule II controlled substance in the United States.[66]

See also

External links

Literature

  • 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. https://doi.org/10.1016/j.pneurobio.2005.04.003
  • 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. https://doi.org/10.1038/mp.2008.90.
  • 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

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