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Summary sheet: Lisdexamfetamine
Chemical Nomenclature
Common names Lisdexamfetamine, Vyvanse, Elvanse
Substitutive name L-lysine-dextroamphetamine
Systematic name (2S)-2,6-Diamino-N-[(2S)-1-phenylpropan-2-yl]hexanamide
Class Membership
Psychoactive class Stimulant
Chemical class Amphetamine
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.

Bioavailability >96.4%[1]
Threshold 10 mg
Light 20 - 30 mg
Common 30 - 60 mg
Strong 60 - 90 mg
Heavy 90 mg +
Total 10 - 14 hours
Onset 60 - 90 minutes
Come up 30 - 60 minutes
Peak 3 - 5 hours
Offset 4 - 6 hours
After effects 2 - 6 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.


Lisdexamfetamine (also known as lisdextroamphetamine, L-lysine-dextroamphetamine, or lisdexamfetamine dimesylate when under the brand names Elvanse, Tyvense, and Vyvanse) is a stimulant substance of the amphetamine class. It is a "mutual prodrug" (codrug) for d-amphetamine (dextroamphetamine) that is approved for the treatment of attention deficit hyperactivity disorder (ADHD) and moderate to severe binge-eating disorder.[2] Like amphetamine, lisdexamfetamine produces its effects by promoting the release of neurotransmitters dopamine and norepinephrine in the brain.

Subjective effects are essentially identical to that of dextroamphetamine except with a slower onset and a longer duration. These include stimulation (in a small percent of the population paradoxal sedation), focus enhancement, motivation enhancement, euphoria, and in a smaller population . However, unlike dextroamphetamine, lisdexamfetamine was specifically designed to prevent non-oral forms of administration (marketed as an anti-abuse design). This means that insufflation, smoking or injection do not provide faster absorption or onset. It is sometimes sold and used illicitly as a "study drug" as well as a recreational substance.

Despite the marketed anti-abuse design, many users report that lisdexamfetamine is capable of producing dependence and addiction like other euphoric stimulants, particularly when it is taken above the recommended dosage. As a result, it is highly advised to use harm reduction practices if using this substance.

History and culture

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Lisdexamfetamine was developed by New River Pharmaceuticals as a longer-lasting and less-easily abused version of d-amphetamine (dextroamphetamine). [3]

The FDA approved lisdexamfetamine for ADHD treatment in adults on the 23th of April 2008 [4], followed by an approval binge eating disorder in adults in January 2015. [5]


Lisdexamphetamine is a codrug composed of the amino acid L-lysine, covalently bonded to dextroamphetamine.[6] Amphetamine is comprised 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 homologue of phenethylamine as it has the same general formula, differing only in the addition of one methyl group.


Lisdexamfetamine was developed with the goal of providing a long duration of effect that remains consistent throughout the day as well as reduced potential for abuse. The attachment of the amino acid lysine slows down the relative amount of dextroamphetamine that is released into the bloodstream. Because no free dextroamphetamine is present in lisdexamfetamine capsules, dextroamphetamine does not become available through mechanical manipulation, such as crushing or simple extraction. There is, therefore, no way to speed up absorption via alternate routes of administration, such as via insufflation, vaporization, or injection, making the drug theoretically less abusable.


As a prodrug, lisdexamfetamine is inactive in the form administered. Once ingested, it is enzymatically cleaved into two parts: L-lysine, a naturally occurring essential amino acid, and d-amphetamine, a central nervous system stimulant. Thus lisdexamfetamine functions as an extended release version of dexamphetamine. Because d-amphetamine needs to be liberated from lysine via contact with red blood cells, effects are independent of route of administration. Conversion of lisdexamfetamine into active d-amphetamine is enzymatically rate-limited, slowing down the time to achieve peak concentrations and decreasing its magnitude and dampening consequent striatal dopamine release, which is thought to be responsible for its euphoric and compulsive redosing effects.


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.[7][8][9] 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.

d-amphetamine's affinity for the TAAR1 receptor is twice that of l-amphetamine.[10] As a result, d-amphetamine produces three to four times as much central nervous system (CNS) stimulation as l-amphetamine. l-amphetamine, on the other hand, has stronger cardiovascular and peripheral effects.

Conversion rate

29.7% of the weight of lisdexamfetamine dimesylate (the usual prescribed form) is dexamphetamine: 30 mg lisdexamfetamine dimesylate is equivalent to 8.9 mg of dexamfetamine.[11][12]

The subjective experience will differ due to the slower, more steady release of active substance in the prodrug. An equivalent dose of dexamphetamine will have a higher peak plasma concentration and shorter duration.

Subjective effects

While the subjective effects are almost identical to that of amphetamine, lisdexamfetamine is significantly longer in its duration and more consistent in its intensity due to the slow release metabolism. Although this drug is rate-limited in its metabolism, sufficiently high doses are comparable to its instant release counterparts once the peak has been reached.

Peripheral effects (such as increased heart rate and higher body temperature) are reported to be less prominent than formulations that partly contain l-amphetamine, such as Adderall or the racemic amphetamine sulphate sold illicitly.

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

Visual effects

Cognitive effects

Auditory effects

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

In rodents and primates, sufficiently high doses of amphetamine cause dopaminergic neurotoxicity, or damage to dopamine neurons, which is characterized by reduced transporter and receptor function. There is no evidence that amphetamine is directly neurotoxic in humans. However, large doses of amphetamine may cause indirect neurotoxicity as a result of increased oxidative stress from reactive oxygen species and autoxidation of dopamine.

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

Tolerance and addiction potential

Addiction is a serious risk with heavy recreational amphetamine use but is unlikely to arise from typical long-term medical use at therapeutic doses. Lisdexamfetamine has been posited to have less potential for abuse and addiction than other pharmaceutical amphetamines due to the slower onset and the self-limiting metabolism, which puts a cap on the maximum peak plasma concentration and consequent dopamine release. Caution is nonetheless advised, as with other drugs in the amphetamine class.

Tolerance develops rapidly in amphetamine abuse (i.e. a recreational amphetamine overdose), so periods of extended use require increasingly larger doses of the drug in order to achieve the same effect. Repeated use of lisdexamfetamine will result in a gradual tolerance proportional to the dosage taken. Patients prescribed this drug often must increase their dosage after a time to maintain its efficacy.


A severe amphetamine overdose can result in a stimulant psychosis that may involve a variety of symptoms, such as paranoia, delusions, and hallucinations, including the infamous Shadow people. A Cochrane Collaboration review on treatment for amphetamine, dextroamphetamine, and methamphetamine psychosis states that about 5–15% of users fail to recover completely. According to the same review, there is at least one trial that shows antipsychotic medications effectively resolve the symptoms of acute amphetamine psychosis. Psychosis very rarely arises from therapeutic use. The combination of prolonged use of high doses combined with sleep deprivation significantly increases the risk of stimulant psychosis.

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.[14][15]
  • 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.[16]
  • 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

Lisdexamphetamine is approved for medical use with a doctor's prescription, but in most countries it is illegal to sell or possess without a prescription.[citation needed]
It requires a special certificate while traveling within the Schengen Area, which covers most of Europe, but not the United Kingdom.[17][18]

  • Australia: It is a Schedule 8 drug.[citation needed]
  • Canada: Lisdexamfetamine, as well as other amphetamines, is a Schedule I drug.[19]
  • Germany: Lisdexamfetamine is controlled under Anlage III BtMG (Narcotics Act, Schedule III)[20] as of July 17, 2013.[21] It can only be prescribed on a narcotic prescription form.[22]
  • Norway: Lisdexamfetamine is a Class A drug under particularly strict control.
  • Sweden: Lisdexamfetamine is a Class II narcotic, with strict requirements for prescription. It has been placed under "utökad övervakning" (extended surveillance).[17]
  • Switzerland: Lisdexamphetamine is a controlled substance as of October 1, 2014 specifically named under Verzeichnis A. Medicinal use is permitted.[23]
  • United Kingdom: Lisdexamfetamine is a Schedule II, Class B controlled drug.[24]
  • United States: Lisdexamfetamine is a Schedule II controlled drug.[25]

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.


  3. Mattingly G (May 2010). "Lisdexamfetamine dimesylate: a prodrug stimulant for the treatment of ADHD in children and adults". CNS Spectrums. 15 (5): 315–325. doi:10.1017/S1092852900027541. PMID 20448522.  Unknown parameter |s2cid= ignored (help)
  4. "FDA Adult Approval of Vyvanse – FDA Label and Approval History" (PDF). Retrieved 12 March 2022. 
  5. "FDA expands uses of Vyvanse to treat binge-eating disorder". U.S. Food and Drug Administration (FDA) (Press release). 30 January 2015. Archived from the original on 26 January 2018. Retrieved 19 March 2023.  Unknown parameter |url-status= ignored (help)
  6. Blick SK, Keating GM (2007). "Lisdexamfetamine". Paediatric Drugs. 9 (2): 129–135; discussion 136–138. doi:10.2165/00148581-200709020-00007. PMID 17407369. 
  7. Miller, G. M. (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. doi:10.1111/j.1471-4159.2010.07109.x. ISSN 0022-3042. 
  8. Drug banks amphetamine targets 
  9. TA1 receptor |
  10. Lewin, A. H., Miller, G. M., Gilmour, B. (1 December 2011). "Trace amine-associated receptor 1 is a stereoselective binding site for compounds in the amphetamine class". Bioorganic & medicinal chemistry. 19 (23): 7044–7048. doi:10.1016/j.bmc.2011.10.007. ISSN 0968-0896. 
  11. Elvanse 20mg, 30mg, 40mg, 50mg, 60mg & 70mg Capsules, hard - Summary of Product Characteristics (SmPC) - (emc) 
  12. Stimulant Equivalency Table
  13. Huang, Y.-S., Tsai, M.-H. (July 2011). "Long-Term Outcomes with Medications for Attention-Deficit Hyperactivity Disorder: Current Status of Knowledge". CNS Drugs. 25 (7): 539–554. doi:10.2165/11589380-000000000-00000. ISSN 1172-7047. 
  14. 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. 
  15. 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. 
  16. 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. 
  17. 17.0 17.1 Elvanse - FASS Allmänhet 
  19. Consolidated federal laws of Canada, Controlled Drugs and Substances Act, 2022 
  20. "Anlage III BtMG" (in German). Bundesministerium der Justiz und für Verbraucherschutz. Retrieved December 19, 2019. 
  21. "Siebenundzwanzigste Verordnung zur Änderung betäubungsmittelrechtlicher Vorschriften" (in German). Bundesanzeiger Verlag. Retrieved December 19, 2019. 
  22. "§ 8 BtMVV" (in German). Bundesministerium der Justiz und für Verbraucherschutz. Retrieved December 19, 2019. 
  23. "Verordnung des EDI über die Verzeichnisse der Betäubungsmittel, psychotropen Stoffe, Vorläuferstoffe und Hilfschemikalien" (in German). Bundeskanzlei [Federal Chancellery of Switzerland]. Retrieved January 1, 2020. 
  25. 21 U.S. Code § 812 - Schedules of controlled substances