Talk:Dextroamphetamine - PsychonautWiki

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Summary sheet: Dextroamphetamine
Dextroamphetamine
Dextroamphetamine.svg
Chemical Nomenclature
Common names Dextroamphetamine, Dexamphetamine, D-amphetamine, Dexedrine, Dex
Substitutive name D-Amphetamine
Systematic name (2S)-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 20-25[1]-75%+[2]
Threshold 3.75 mg
Light 3.75 - 10 mg
Common 10 - 16 mg
Strong 16 - 30 mg
Heavy 30 mg +
Duration
Total 6 - 8 hours
Onset 15 - 30 minutes
Peak 2.5 - 4 hours
Offset 2 - 3 hours
After effects 3 - 6 hours



Insufflated
Dosage
Threshold 3 mg
Light 3 - 7.5 mg
Common 7.5 - 12 mg
Strong 12 - 21.5 mg
Heavy 21.5 mg +
Duration
Total 3 - 6 hours
Onset 1 - 5 minutes
Peak 1 - 2 hours
Offset 1.5 - 3 hours
After effects 2 - 4 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


Dextroamphetamine (also known as Dexamphetamine, D-Amphetamine, Dex, or by brand names including Adderall, Dexedrine) is a stimulant substance and the right-handed enantiomer of amphetamine.

Dextroamphetamine is the more potent isomer of the two, but the effects are also slightly different in character. The small difference in affinity affects the mechanism resulting in a more mentally focused stimulation rather than physical, thus creating a stimulant that is more fit as a therapeutic drug rather than a recreational one. Therefore, the dextrorotatory enantiomer is preferred in treatment of attention deficit hyperactivity disorder, whereas a racemic mixture like amphetamine is found when sold on the streets.

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

Chemistry

With regular synthesis, the resulting product will always be a racemic mixture. An enantiopure can be obtained through a biological synthesis route, where certain proteins form only one of the two isomers or through isolation of one isomer from a previously racemic mixture. Financially it would be beneficial to use the biological process, since it requires only little materials, but instead can be performed by bacteria that can be genetically altered to perform the synthesis for you. Those bacteria multiply by themselves, thus automatically creating a long-term production solution. [citation needed]

History and culture

In 1935, 3 years after amphetamine became widely marketed, the medical community became aware of the stimulant properties of amphetamine, specifically dextroamphetamine, and in 1937 Smith, Kline, and French introduced tablets under the tradename Dexedrine. Dexedrine is used to treat narcolepsy, attention disorders, and obesity. Additionally, it is used as an athletic performance and cognitive enhancer, and recreationally as an aphrodisiac and euphoriant.

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.[3][4]
  • 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.[5]
  • 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.

Legal status

Internationally, amphetamine (and its isomers dextroamphetamine and levoamphetamine) are Schedule II controlled substances under the United Nations 1971 Convention on Psychotropic Substances.[6]

  • Australia: Dextroamphetamine is a Schedule 8 controlled substance.[7]
  • Austria: Dextroamphetamine is illegal to possess, produce and sell under the SMG (Suchtmittelgesetz Österreich).[8]
  • Brazil: Dextroamphetamine is a Class A3 psychoactice substance.[9]
  • Canada: Dextroamphetamine is a Schedule I drug in Canada.[10]
  • Germany: Dextroamphetamine is controlled under Anlage III BtMG (Narcotics Act, Schedule III).[11] It can only be prescribed on a narcotic prescription form.
  • The Netherlands: Dextroamphetamine is a List I controlled substance.[12]
  • South Korea: Dextromphetamine is prohibited even for medical use in South Korea in compliance with the United Nations Convention on Psychotropic Substances.[13]
  • United Kingdom: Amphetamine is a Class B drug in the United Kingdom, without any clarification about isomers.[14]
  • United States: Amphetamine is a Schedule IIN controlled substance in the United States, citing several dextroamphetamine prescription drugs as examples.[15]

See also

External links

References

  1. "chemeurope.com - Amphetamine 
  2. "Drugbank - Amphetamine 
  3. Greenwald, M. K., Lundahl, L. H., Steinmiller, C. L. (December 2010). "Sustained Release d-Amphetamine Reduces Cocaine but not 'Speedball'-Seeking in Buprenorphine-Maintained Volunteers: A Test of Dual-Agonist Pharmacotherapy for Cocaine/Heroin Polydrug Abusers". Neuropsychopharmacology. 35 (13): 2624–2637. doi:10.1038/npp.2010.175. ISSN 0893-133X. 
  4. Siciliano, C. A., Saha, K., Calipari, E. S., Fordahl, S. C., Chen, R., Khoshbouei, H., Jones, S. R. (10 January 2018). "Amphetamine Reverses Escalated Cocaine Intake via Restoration of Dopamine Transporter Conformation". The Journal of Neuroscience. 38 (2): 484–497. doi:10.1523/JNEUROSCI.2604-17.2017. ISSN 0270-6474. 
  5. Krystal, J. H., Perry, E. B., Gueorguieva, R., Belger, A., Madonick, S. H., Abi-Dargham, A., Cooper, T. B., MacDougall, L., Abi-Saab, W., D’Souza, D. C. (1 September 2005). "Comparative and Interactive Human Psychopharmacologic Effects of Ketamine and Amphetamine: Implications for Glutamatergic and Dopaminergic Model Psychoses and Cognitive Function". Archives of General Psychiatry. 62 (9): 985. doi:10.1001/archpsyc.62.9.985. ISSN 0003-990X. 
  6. "CONVENTION ON PSYCHOTROPIC SUBSTANCES 1971" (PDF). United Nations. Retrieved December 19, 2019. 
  7. "POISONS STANDARD DECEMBER 2019". Office of Parliamentary Counsel. Retrieved December 19, 2019. 
  8. https://www.ris.bka.gv.at/GeltendeFassung.wxe?Abfrage=Bundesnormen&Gesetzesnummer=10011053
  9. https://www.in.gov.br/en/web/dou/-/resolucao-rdc-n-784-de-31-de-marco-de-2023-474904992
  10. Controlled Drugs and Substances Act | http://laws-lois.justice.gc.ca/eng/acts/C-38.8/page-24.html#h-28
  11. "Anlage III BtMG" (in German). Bundesministerium der Justiz und für Verbraucherschutz. Retrieved December 19, 2019. 
  12. https://wetten.overheid.nl/BWBR0001941/2009-07-01
  13. https://web.archive.org/web/20160331074842/https://treaties.un.org/pages/ViewDetails.aspx?src=TREATY&mtdsg_no=VI-16&chapter=6&lang=en
  14. Misuse of Drugs Act 1971 
  15. https://www.deadiversion.usdoj.gov/schedules/
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