Home
    Disclaimer
    Lisdexamfetamine molecular structure

    Lisdexamfetamine Stats & Data

    Vyvanse Elvanse Tyvense Lisdextroamphetamine lisdextroamfetamine lisdexamphetamine
    NPS DataHub
    MW263.38
    FormulaC15H25N3O
    CAS608137-32-2
    IUPAC(2S)-2,6-diamino-N-[(2S)-1-phenylpropan-2-yl]hexanamide
    SMILESNCCCCC(N)C(=O)NC(C)Cc1ccccc1
    InChIKeyVOBHXZCDAVEXEY-JSGCOSHPSA-N
    Phenethylamines; 2020/1. Von 2-Phenethylamin abgeleitete Verbindungen; 2021/1. Von 2-Phenethylamin abgeleitete Verbindungen; 2022/1. Von 2-Phenethylamin abgeleitete Verbindungen
    Chemical Class Amphetamine
    Psychoactive Class Stimulant
    Half-Life ~1 hour (LDX prodrug); active d‑amphetamine ~10–11.3 hours in adults (longer in urine alkalinization).

    Pharmacology

    DrugBank
    State Liquid

    Description

    Also known as _Vyvanse_, lisdexamfetamine (L-lysine-d-amphetamine) is a prodrug of the psychostimulant d-amphetamine . It is paired with the essential amino acid _L-lysine_. Lisdexamfetamine dimesylate increases attention span and decreases restlessness in children and adults who are overactive/hyperactive, cannot concentrate for long periods, or are easily distracted or impulsive . As a central nervous system stimulant, lisdexamfetamine is utilized as an adjunct therapy in the treatment of attention deficit hyperactivity disorder (ADHD). As a prodrug, lisdexamfetamine was specifically engineered as an abuse-resistant product . The mechanism by which this occurs is through delayed release after ingestion (unlike some other psychostimulant drugs, which may be abused). After oral administration and absorption, enzyme hydrolysis after contact with red blood cells metabolize lisdexamfetamine into L- lysine, a naturally occurring essential amino acid and active _d-amphetamine_, which is responsible for the drug’s pharmacological effects. Gastrointestinal pH does not affect this conversion, and the addition of the L-lysine slows the amount of d-amphetamine available in the circulation and central nervous system .

    Mechanism of Action

    Lisdexamfetamine is a prodrug of dextroamphetamine. The active form of this drug blocks the reuptake of norepinephrine and dopamine into the presynaptic neuron and increase the release of these monoamines into the extraneuronal space. The parent drug, lisdexamfetamine, does not bind to the sites for the reuptake of norepinephrine and dopamine in vitro . The mechanism of therapeutic action in attention deficit hyperactivity disorder (ADHD) is not fully understood , . Amphetamines have been recently found to target the trace amine-associated receptor 1 (TAAR1), which was recently discovered. This may explain some of its effects on the extraneuronal space , ,. Ultimately, the ability of this agent to increase synaptic concentrations of the catecholamine neurotransmitters noradrenaline and dopamine in the prefrontal cortex (PFC), and in the striatum, results in several behavioral changes , .

    Pharmacodynamics

    Lisdexamfetamine dimesylate is a prodrug of _d-amphetamine_. Amphetamines are non-catecholamine sympathomimetic amines with CNS stimulating properties . This agent works primarily by inducing the release of the neurotransmitters dopamine and norepinephrine from their storage areas in presynaptic nerve terminals . Both of these transmitters contribute to alertness, increased concentration, in addition to effort and motivation.

    Metabolism

    THe conversion of Lisdexamfetamine dimesylate (LDX) to the active metabolite d-amphetamine occurs primarily in the blood through enzymatic cleavage after active absorption of LDX from the gastrointestinal lumen . Lisdexamfetamine dimesylate is hydrolyzed in the blood to d-amphetamine, which is responsible for the drug’s therapeutic activity, as well as L-lysine. Amphetamine is reported to be oxidized at the 4 position of the benzene ring to form 4-hydroxyamphetamine, or on the side chain α or β carbons to form alpha-hydroxy-amphetamine or norephedrine, respectively. Norephedrine and 4-hydroxy-amphetamine are both active and each is subsequently oxidized to form 4-hydroxy-norephedrine. Alpha-hydroxy-amphetamine undergoes the process of deamination to form phenylacetone, which finally forms benzoic acid and its glucuronide and the glycine conjugate, _hippuric acid_. Although the enzymes involved in amphetamine metabolism have not been clearly identified, CYP2D6 is known to be involved with the formation of 4-hydroxy-amphetamine from amphetamine .

    Absorption

    After oral administration, lisdexamfetamine is rapidly absorbed from the gastrointestinal tract , . **Chewable tablet form:** After a single dose of 60 mg a chewable tablet in healthy subjects under fasted conditions, the Tmax of lisdexamfetamine and dextroamphetamine was reached at about 1 hour and 4.4 hour post administration, respectively . **Capsule form:** Following single-dose oral (30 mg, 50 mg, or 70 mg) in patients ages 6 to 12 years with ADHD under fasted conditions, Tmax of lisdexamfetamine and dextroamphetamine was reached at about 1 hour and 3.5 hours post administration, respectively .

    Toxicity

    **Acute toxicity**: Symptoms of acute overdosage with amphetamines include restlessness, tremor, hyperreflexia, rapid respiration, confusion, assaultiveness, hallucinations, panic states, hyperpyrexia, and rhabdomyolysis. Fatigue and depression generally follow the symptoms central nervous system stimulation. Cardiovascular effects include arrhythmias, hypertension or hypotension and/or circulatory collapse. Gastrointestinal symptoms include nausea, vomiting, diarrhea, and abdominal cramps. Lethal poisoning is usually preceded by convulsions and coma . Prescribers should consider that serious cardiovascular (CV) events have been reported with this class of drugs . **Long-term effects**: Acute administration of high doses of amphetamine (d- or d,l-) has been shown to produce long-term neurotoxic effects, which include irreversible nerve fiber damage, in rodents. The relevance of these findings to humans is currently unknown . **Oral LD50 (rat)**: 7,060 mg/kg **Oral LD50 (mouse)**: 3,450 mg/kg **Use in Pregnancy** This drug is categorized as a Pregnancy Category C: Animal studies have shown risk to the fetus, there are no controlled studies in women, or studies in women and animals are not available .

    Indication

    For the treatment of Attention-deficit/hyperactivity disorder (ADHD) and for moderate to severe binge eating disorder in adults , . This drug is not indicated for weight loss. Use of other sympathomimetic drugs for weight loss is associated with serious cardiovascular effects. The safety and effectiveness of this drug for the treatment of obesity have not yet been determined .

    Half-life

    The mean plasma elimination half-life of dextroamphetamine was about 12 hours after oral administration of lisdexamfetamine dimesylate . The plasma elimination half-life of lisdexamfetamine alone averaged less than one hour in studies of lisdexamfetamine dimesylate administered in volunteer subjects .

    Elimination

    After the oral administration of a 70mg dose of radiolabeled lisdexamfetamine dimesylate to six healthy subjects, about 96% of the oral dose radioactivity was recovered in the urine and only 0.3% recovered in the feces , .

    Volume of Distribution

    There is no accumulation of d-amphetamine (as measured by AUC) at steady state in healthy adults and no accumulation of lisdexamfetamine dimesylate after once-daily dosing for seven consecutive days , .

    Clearance

    In a study of 47 subjects aged 55 years of age or older, amphetamine clearance was approximately 0.7L/hr/kg for subjects 55-74 years of age and 0.55L/hr/kg for subjects ≥75 years of age. This is slightly reduced compared to younger adults (approximately 1L/hr/kg for subjects 18-45 years of age) .

    Receptor Profile

    Receptor Actions

    Agonists
    TAAR1 agonist
    Other
    Dopamine-norepinephrine releasing agent
    Serotonin releasing agent

    Receptor Binding

    Trace amine-associated receptor 1 agonist

    Effect Profile

    Curated + 51 Reports
    Stimulant 8.8

    Strong stimulation, euphoria, focus, and anxiety/jitters

    Stimulation / Energy×3
    1010
    Euphoria / Mood Lift×2
    107.9
    Focus / Productivity×2
    1010
    Anxiety / Jitters×1
    1010
    Catalog Erowid

    Tolerance & Pharmacokinetics

    drugs.wiki
    Half-Life
    ~1 hour (LDX prodrug); active d‑amphetamine ~10–11.3 hours in adults (longer in urine alkalinization).
    Addiction Potential
    Moderate to high. As a prodrug of dextroamphetamine, it carries a risk of psychological and physical dependence, especially with prolonged or high‑dose use.

    Tolerance Decay

    Full tolerance 7d Half tolerance 14d Baseline ~28d

    Clinical and community data indicate noticeable tolerance with repeated daily dosing within days, and partial reversal after several weeks of abstinence. Quantitative values are heuristic for harm‑reduction planning, not prescriptive dosing guidance.

    Cross-Tolerances

    Amphetamines
    80% ●●○
    Other stimulants
    30% ●○○

    Experience Report Analysis

    Erowid
    51 Reports
    2008–2025 Date Range
    40 With Age Data
    23 Effects Detected

    Demographics

    Gender Distribution

    Age Distribution

    Reports Over Time

    Effect Analysis

    Erowid

    Effects aggregated from 51 experience reports (51 Erowid)

    51 Reports
    23 Effects Detected
    9 Positive
    10 Adverse
    4 Neutral

    Effect Sentiment Distribution

    Confidence Distribution

    Positive Effects 9

    Stimulation 68.6% 70%
    Focus Enhancement 62.7% 70%
    Euphoria 52.9% 70%
    Music Enhancement 37.3% 70%
    Body High 27.5% 70%
    Empathy 19.6% 70%
    Tactile Enhancement 13.7% 70%
    Color Enhancement 11.8% 70%
    Creativity Enhancement 5.9% 70%

    Adverse Effects 10

    Anxiety 43.1% 70%
    Nausea 19.6% 70%
    Jaw Clenching 17.6% 70%
    Increased Heart Rate 17.6% 70%
    Confusion 17.6% 70%
    Sweating 15.7% 70%
    Headache 15.7% 70%
    Appetite Suppression 15.7% 70%
    Pupil Dilation 7.8% 70%
    Memory Suppression 5.9% 70%

    Dose-Response Correlation

    How effect frequency changes across dose levels

    View data table
    Effect Strong (n=19)
    Stimulation 68.4%
    Focus Enhancement 63.2%
    Euphoria 47.4%
    Music Enhancement 42.1%
    Anxiety 42.1%
    Nausea 36.8%
    Sedation 36.8%
    Body High 31.6%
    Jaw Clenching 26.3%
    Tactile Enhancement 26.3%
    Auditory Effects 26.3%
    Confusion 21.1%
    Increased Heart Rate 21.1%
    Empathy 15.8%
    Hospital 15.8%

    Dose–Effect Mapping

    Experience Reports

    How reported effects shift across dose tiers, based on 51 experience reports.

    Limited tier coverage — most reports fall within the Strong range. Effects at other dose levels may not be represented.

    Oral dose range: 40.0–80.0 mg (median 50.0 mg)
    Effect Strong (n=19)
    stimulation
    68%
    focus enhancement
    63%
    euphoria
    47%
    music enhancement
    42%
    anxiety
    42%
    nausea
    37%
    sedation
    37%
    body high
    32%
    jaw clenching
    26%
    tactile enhancement
    26%
    auditory effects
    26%
    confusion
    21%
    increased heart rate
    21%
    empathy
    16%
    hospital
    16%
    color enhancement
    16%
    headache
    16%
    appetite suppression
    16%
    visual distortions
    16%
    sweating
    10%

    Showing top 20 of 24 effects

    Dosage Distribution

    Dose distribution from experience reports

    Median: 50.0 mg IQR: 40.0–80.0 mg n=41

    Real-World Dose Distribution

    62K Doses

    From 96 individual dose entries

    Oral (n=86)

    Median: 50.0mg 25th: 30.0mg 75th: 60.0mg 90th: 70.0mg
    mg/kg median: 0.693 mg/kg 75th: 1.081

    Common Combinations

    Most co-occurring substances in experience reports

    Form / Preparation

    Most common forms and preparations reported

    Body-Weight Dosing

    Dose relative to body weight from reports with weight data

    Median: 0.76 mg/kg IQR: 0.504–1.16 mg/kg n=41

    Redose Patterns

    Redosing behavior across 42 reports

    19.0% Redosed
    1.2 Avg Doses
    120m Median Interval

    Legal Status

    Country Status Notes
    Australia It is a Schedule 8 drug.
    Canada Lisdexamfetamine, as well as other amphetamines, is a Schedule I drug.
    Germany Lisdexamfetamine is controlled under Anlage III BtMG ( Narcotics Act, Schedule III ) as of July 17, 2013. It can only be prescribed on a narcotic prescription form.
    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).
    Switzerland Lisdexamphetamine is a controlled substance as of October 1, 2014 specifically named under Verzeichnis A. Medicinal use is permitted.
    United Kingdom Lisdexamfetamine is a Schedule II, Class B controlled drug.
    United States Lisdexamfetamine is a Schedule II controlled drug.

    Harm Reduction

    drugs.wiki

    Evidence-based harm-reduction additions and clarifications: (1) Lisdexamfetamine (LDX) is a prodrug converted primarily by red blood cells to dextroamphetamine; manipulation of the dosage form or using non‑oral routes offers no pharmacological advantage and may increase harm. Red‑blood‑cell hydrolysis and PEPT1‑mediated intestinal transport underlie its smoother PK profile. (2) Food may delay Tmax by ~1 hour without meaningfully changing exposure; overall exposure and effect are more sensitive to urinary pH: acidification increases amphetamine elimination and weakens effects; alkalinization reduces elimination and can potentiate them (including with antacids). (3) Absolute contraindication with MAOIs and agents with MAOI activity (linezolid, methylene blue); risk includes hypertensive crisis and serotonin toxicity—observe 14‑day washout. (4) Concomitant SSRIs/SNRIs/TCAs are not automatically contraindicated but do raise serotonin‑toxicity and pressor risks; use of stimulants with potent CYP2D6 inhibitors (fluoxetine, paroxetine, bupropion) can elevate amphetamine exposure—monitor or avoid unsupervised combinations. (5) Additive sympathomimetic effects occur with OTC decongestants (pseudoephedrine/phenylephrine) and caffeine; even modest pseudoephedrine doses increase heart rate and slightly raise systolic BP. Avoid when possible. (6) Alcohol co‑use increases cardiovascular stress and impairs risk perception; stimulants are implicated in hypertensive crises and arrhythmias at high doses or with co‑ingestants—avoid mixing. (7) Peripheral vasculopathy (e.g., Raynaud phenomenon) has been reported during stimulant therapy; monitor for cold, numb, or discolored fingers/toes. (8) Psychiatric risks (anxiety, agitation, mania, psychosis) scale with dose/frequency; large cohort data suggest prescription stimulant–associated psychosis in ~1/660 adolescents/young adults, with amphetamines risk > methylphenidate. Stop escalation and seek care if hallucinations or delusions emerge. (9) Hydration, rest, and temperature management reduce hyperthermia and rhabdomyolysis risk during prolonged exertion on stimulants; urgent care is warranted for severe headache, chest pain, confusion, or overheating. (10) Pediatric users require growth monitoring; long‑term stimulant therapy is associated with small but measurable reductions in growth velocity. (11) Pregnancy/lactation: amphetamines cross into milk and have stimulant effects; discuss risks vs benefits with a clinician before use in these states. (12) Plan dosing timing to protect sleep (early morning dosing; avoid late‑day redosing). Insomnia worsens cardiovascular and anxiety risks. (13) Dry mouth and bruxism are common; frequent water, sugar‑free gum, and mouth care reduce dental risk. (14) Avoid polydrug stacks with additional stimulants or serotonergics; when on necessary interacting meds (e.g., SSRI), keep doses conservative and add BP/HR checks.

    ← Back to Lisdexamfetamine