generation run 2026-05-03
282 min completedmodel pipeline-v5plan not recordedrun/206ee86e…Selection
Verification
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- seen / partial
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The model's own caveats
- sparse_evidence
Reproduce
- inputs
- 46 source keys (listed under Sources)
- plan
- not recorded — template version, prompt hash and git SHA are written from 2026-09 onward
- model
- pipeline-v5
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- none — agent transcripts are persisted from 2026-09 onward
24 searches — query, source, results, what was kept and why
| # | source | query | seen | kept | rationale |
|---|---|---|---|---|---|
| 1 | PubChem | lisdexamfetamine | 1 | 1 | Core chemical identity data needed to verify and expand seed data |
| 2 | PubMed | lisdexamfetamine pharmacokinetics human bioavailability half-life | 1 | 1 | Key human PK bioavailability study |
| 3 | PubMed | lisdexamfetamine ADHD clinical trial efficacy placebo controlled | 12 | 6 | High-quality efficacy evidence: Cochrane review, network meta-analysis, pivotal RCTs across populations |
| 4 | ClinicalTrials.gov | lisdexamfetamine | 15 | 5 | Most relevant clinical development history and ongoing research |
| 5 | PubMed | lisdexamfetamine pharmacology mechanism action dopamine norepinephrine | 2 | 2 | Good mechanistic detail on DAT/NAT inhibition and prodrug conversion; selected both |
| 6 | OpenAlex | lisdexamfetamine dimesylate pharmacokinetics metabolism | 10 | 3 | Pennick 2010 is the foundational absorption/metabolism paper. McElroy 2015 is pivotal BED trial. Spiller 2013 covers ADHD drug overdose. |
| 7 | OpenAlex | lisdexamfetamine abuse potential dependence amphetamine prodrug | 10 | 2 | Pivotal trial and cardiovascular safety review are relevant |
| 8 | PubMed | PMID 21539403 - intranasal vs oral PK | 1 | 1 | Alternate ROA PK — relevant to abuse potential |
| 9 | PubMed | lisdexamfetamine growth height weight children long-term safety | 1 | 1 | Long-term growth and safety data in pediatric population |
| 10 | PubMed | lisdexamfetamine binge eating disorder FDA approval pivotal trial | 1 | 1 | Confirms LDX as only FDA-approved drug for BED in adults |
| 11 | PubMed | lisdexamfetamine dimesylate abuse Vyvanse human subjective effects | 4 | 2 | Jasinski 2009 is the definitive human IV abuse liability study. Kammerer 2024 is current comparative review. |
| 12 | WebSearch | lisdexamfetamine Vyvanse Elvanse legal status UK Canada Australia EU controlled substance scheduling | 10 | 2 | Key legal jurisdictions confirmed |
| 13 | PubMed | PMID 27935735 - PK/PD in ADHD adults | 1 | 1 | Duration data for adults |
| 14 | PubMed | lisdexamfetamine withdrawal tolerance ADHD discontinuation | 2 | 2 | Withdrawal and relapse data for LDX |
| 15 | PubMed | PMID 18991468 - metabolism distribution elimination | 1 | 1 | Foundational PK characterization |
| 16 | PubMed | lisdexamfetamine pediatric children ADHD phase 3 randomized | 4 | 3 | Core clinical efficacy evidence in pediatric population |
| 17 | WebSearch | lisdexamfetamine Vyvanse FDA approval history New River Pharmaceuticals 2007 scheduling DEA Schedule II | 10 | 2 | Confirms approval date, developer, and scheduling |
| 18 | PubMed | lisdexamfetamine depression major depressive disorder augmentation treatment | 6 | 3 | LDX studied for MDD augmentation in Phase 3 — relevant to off-label use and investigation history |
| 19 | WebSearch | lisdexamfetamine SMILES InChIKey CAS number PubChem 11597698 chemical structure | 10 | 3 | SMILES and CAS not returned by get_pubchem_compound call |
| 20 | OpenAlex | lisdexamfetamine binge eating disorder FDA approval 2015 efficacy safety | 8 | 1 | Molecular MOA of LDX specific to ADHD treatment |
| 21 | PubMed | PMID 35951288 - molecular characterization LDX/MPH mechanism ADHD | 1 | 1 | Specific LDX MOA review at molecular level |
| 22 | WebSearch | Vyvanse lisdexamfetamine FDA prescribing information half-life d-amphetamine Tmax pharmacokinetics | 8 | 2 | Foundational PK parameters from FDA prescribing information |
| 23 | WebSearch | lisdexamfetamine tramadol interaction serotonin syndrome risk contraindication amphetamine | 10 | 2 | Investigating the tramadol 'lethal' interaction flag in the seed data |
| 24 | Multiple | Verify DOIs for key citations | 3 | 0 | DOI verification for high-priority citations |
83 claims by section — every cited sentence, checked against its source
pharmacology19 · 17 ok
Claim in pharmacology — inconclusiveinconclusiveworking →
Following oral administration, the prodrug undergoes enzymatic hydrolysis — primarily in red blood cells — releasing d-amphetamine (the active moiety) and L-lysine.supported
Metabolism to d-amphetamine occurs primarily in red blood cells (not liver/kidney). pmid:20628632
Claim in pharmacology — inconclusiveinconclusiveworking →
Monoamine transporter reversal (carrier-mediated release): d-Amphetamine enters presynaptic terminals via dopamine-transporter and norepinephrine-transporter. Inside the neuron, it drives reversal of these transporters, causing non-exocytotic efflux of dopamine and norepinephrine into the synapse.supported
d-Amphetamine enhances DA and NE efflux; mechanism independent of neuronal firing rate, displacing intraneuronal catecholamines. j.neuropharm.2009.08.020
Monoamine transporter reversal (carrier-mediated release): d-Amphetamine enters presynaptic terminals via dopamine-transporter and norepinephrine-transporter. Inside the neuron, it drives reversal of these transporters, causing non-exocytotic efflux of dopamine and norepinephrine into the synapse.supported
Covers DAT/NET substrate activity, VMAT2, catecholamine release. s40120-022-00392-2
VMAT2 disruption: d-Amphetamine disrupts vmat2 function, depleting monoamine storage vesicles and increasing the cytoplasmic pool of DA and NE available for transporter-mediated release.supported
Also promotes release via VMAT. fpj.20033
VMAT2 disruption: d-Amphetamine disrupts vmat2 function, depleting monoamine storage vesicles and increasing the cytoplasmic pool of DA and NE available for transporter-mediated release.supported
Covers DAT/NET substrate activity, VMAT2, catecholamine release. s40120-022-00392-2
Reuptake inhibition: d-Amphetamine competitively inhibits DAT and NET, slowing clearance of released DA and NE from the synapse.supported
d-Amphetamine competitively inhibits DAT and NAT, increasing DA and NA in synaptic cleft. fpj.20033
d-Amphetamine is additionally an agonist at taar1 (TAAR1), which modulates dopaminergic, serotonergic, and glutamatergic neurotransmission and may contribute to regulatory effects on monoamine release.supported
TAAR1 acts as rheostat of dopaminergic, glutamatergic, and serotonergic neurotransmission. Amphetamine-class compounds are TAAR1 agonists. pr.117.015305
LDX is absorbed from the small intestine (not the colon) via the high-capacity peptide transporter PEPT1, a carrier-mediated process analogous to the absorption of di- and tri-peptidessupported
LDX absorbed via PEPT1 transporter in small intestine. pmid:20628632
Food delays the Tmax of both LDX and d-amphetamine by approximately 1 hour but does not significantly affect d-amphetamine AUC or Cmax, permitting administration with or without food.supported
Food does not significantly affect d-amphetamine bioavailability. t(max) of d-amphetamine delayed ~1 hour with food. 0091270007310381
Hydrolytic cleavage of LDX to d-amphetamine and L-lysine occurs primarily in red blood cells via an unidentified high-capacity enzymatic system — not in the liver or kidneysupported
Metabolism to d-amphetamine occurs primarily in red blood cells (not liver/kidney). pmid:20628632
This RBC-mediated hydrolysis produces a lower Cmax and extended Tmax for d-amphetamine compared to equivalent doses of immediate-release d-amphetamine, contributing to the consistent, reproducible pharmacokinetic profile of LDX.supported
d-amphetamine has lower Cmax, extended Tmax, lower PK variability vs IR d-amphetamine. s40261-015-0354-y
This RBC-mediated hydrolysis produces a lower Cmax and extended Tmax for d-amphetamine compared to equivalent doses of immediate-release d-amphetamine, contributing to the consistent, reproducible pharmacokinetic profile of LDX.supported
LDX shows low inter/intraindividual PK variability vs other long-acting stimulants. Systemic d-amphetamine exposure largely unaffected by food/GI factors due to RBC enzymatic cleavage. 11539410-000000000-00000
Data from published human PK studies.supported
Pharmacokinetics of d-amphetamine derived from lisdexamfetamine in healthy adults. 0091270007310381
Data from published human PK studies.supported
Phase I absorption, metabolism, elimination study. Foundational PK characterization of LDX in healthy adults. 0044011-200828120-00002
Data from published human PK studies.supported
LDX hydrolysed in blood to yield d-amphetamine; d-amphetamine has lower Cmax, extended Tmax, lower PK variability vs IR d-amphetamine. s40261-015-0354-y
Therapeutic effects persist for at least 13 hours post-dose in children and at least 14 hours post-dose in adults — longer than any other published long-acting amphetamine formulation.partially supported
Duration: ≥13 h children, ≥14 h adults. s40261-015-0354-y
Therapeutic effects persist for at least 13 hours post-dose in children and at least 14 hours post-dose in adults — longer than any other published long-acting amphetamine formulation.partially supported
Clinical effects of LDX persist up to 14 hours in ADHD adults. cap.2016.0121
clinical-evidence13 · 12 ok
The pivotal multicenter, randomised, double-blind, forced-dose, parallel-group trial in children aged 6–12 years established efficacy and tolerability of LDX at 30, 50, and 70 mg/daysupported
Pivotal Phase 3 trial establishing efficacy. LDX described as therapeutically inactive prodrug with gradual release of d-amphetamine, extended duration, reduced abuse potential. pmid:17577466
A randomised withdrawal study design confirmed maintenance of efficacy in children and adolescents: patients stabilised on LDX who were randomised to placebo showed significant symptom recurrence compared to those continuing active treatment.supported
Phase 3 extension, randomized-withdrawal design confirming long-term maintenance of LDX efficacy in pediatric ADHD. j.jaac.2014.01.017
The dose range (30–70 mg) and adverse event profile were consistent with Western trial data.supported
LDX 30/50/70 mg all significantly superior to placebo on ADHD-RS-IV. Most common AEs: decreased appetite, headache, initial insomnia. cap.2019.0076
A double-blind, placebo-controlled study in adults demonstrated significant improvement on ADHD-RS-IV at doses of 30, 50, and 70 mg/daysupported
Pivotal adult ADHD trial evaluating LDX 30, 50, 70 mg/day vs placebo. pmid:19012818
Two pivotal Phase 3 randomised controlled trials in adults with moderate-to-severe BED established efficacy at 50 and 70 mg/daysupported
Two Phase 3 RCTs, n=383 and 390 adults. LDX 50-70 mg/day significantly reduced binge eating days/week vs placebo (p<0.001). npp.2015.275
A randomised 26-week withdrawal phase within a Phase 3 BED trial demonstrated that discontinuation of LDX markedly increased risk of BED relapse relative to continued treatment.supported
Long-term studies including 26-week randomized withdrawal showed LDX markedly reduced BED relapse. s40263-017-0477-1
A Phase IV, 2-year, open-label study in European children and adolescents demonstrated sustained efficacy with an acceptable safety profilesupported
Phase IV, 2-year open-label European study of LDX safety and efficacy in pediatric ADHD. s40263-017-0443-y
LDX efficacy and safety were evaluated in preschool children (ages 4–5) with ADHD, extending the evidence base to a younger population.supported
Preschool ADHD RCT. j.jaac.2022.03.034
A Cochrane systematic review confirmed amphetamine efficacy and safety in adult ADHD populations.supported
Cochrane review of amphetamines (including LDX) for adult ADHD. Efficacy and safety data. 14651858.cd007813.pub3
Neuroimaging revealed reduced thalamic activation during food cue processingsupported
Reduced thalamic activity during food pictures. s41398-021-01770-4
The most recent systematic review and meta-analysis confirmed LDX efficacy and acceptable safety/tolerability in BED across pooled trial data.supported
Systematic review and meta-analysis of LDX RCTs in BED. LDX enhances impulse control and targets reward pathways. erv.70070
Claim in clinical-evidence — inconclusiveinconclusiveworking →
A 12-month open-label extension provided additional safety data in this population.supported
12-month open-label extension evaluating LDX safety as MDD augmentation. jcp.0000000000000897
safety13 · 10 ok
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Clinical trials across ADHD and BED populations document modest, generally well-tolerated cardiovascular changes at therapeutic doses: mean heart rate increases of 4.41–6.31 BPM and systolic blood pressure increases of 0.2–1.45 mmHgsupported
Pulse increase 4-6 bpm; BP increases ~1-2 mmHg systolic/diastolic. npp.2015.275
Clinical trials across ADHD and BED populations document modest, generally well-tolerated cardiovascular changes at therapeutic doses: mean heart rate increases of 4.41–6.31 BPM and systolic blood pressure increases of 0.2–1.45 mmHgpartially supported
Review: stimulants cause modest HR increase (~11 BPM initially), minor BP changes. cap.1992.2.279
The 2-year Phase IV European study confirmed this pattern in LDX-treated children and adolescents; ongoing growth monitoring is recommended for pediatric patients on long-term therapy.supported
Phase IV, 2-year open-label European study of LDX safety and efficacy in pediatric ADHD. s40263-017-0443-y
Clinical tolerance to the cardiovascular effects of stimulants (heart rate, blood pressure) develops with continued use and is considered a safety featuresupported
Tolerance develops to cardiovascular effects. cap.1992.2.279
Therapeutic efficacy in ADHD is generally maintained during long-term treatment — the 2-year European Phase IV study demonstrated sustained symptom improvement without evidence of tolerance to cognitive effects.supported
Phase IV, 2-year open-label European study of LDX safety and efficacy in pediatric ADHD. s40263-017-0443-y
The prodrug design substantially reduces the rate of euphoria onset that drives addictive behaviour: IV LDX produces significantly lower drug-liking scores than IV d-amphetamine despite delivering the same active moleculesupported
IV LDX did not produce significant abuse-related liking vs placebo; IV d-amp 20 mg did (p<0.05). 0269881108093841
A comprehensive literature review confirmed reduced abuse potential for oral LDX compared to oral dexamphetamine.supported
Review comparing pharmacology and abuse potential of oral dexamphetamine vs lisdexamfetamine (prodrug). LDX has lower abuse potential due to prodrug design. hup.2910
Claim in safety — inconclusiveinconclusiveworking →
A case report documented stimulant withdrawal with rebound-effect hyperactivity and emotional dysregulation in a child with ASD/ADHD upon discontinuation.supported
Case report examining tolerance and withdrawal concepts for stimulant medications in a child with ASD and ADHD. pmid:29662527
In the BED indication, a randomised 26-week withdrawal phase demonstrated that LDX discontinuation markedly increased the risk of binge eating relapse relative to continued treatment, raising questions about psychological-dependence on the appetite-suppressive effects in this population.supported
Long-term studies including 26-week randomized withdrawal showed LDX markedly reduced BED relapse. s40263-017-0477-1
A case report documented hypertensive emergency with ST-elevation myocardial infarction from combined MAOI, extended-release amphetamine, and psilocybin.partially supported
Case report: severe hypertension/MI following combination of psilocybin mushrooms, dextroamphetamine, and tranylcypromine (MAOI). 02791072.2024.2368617
summary9 · 7 ok
Cardiovascular activation — heart rate increase of 4–6 BPM, systolic blood pressure rise of 1–2 mmHg — occurs reliably at clinical dosessupported
Pulse increase 4-6 bpm; BP increases ~1-2 mmHg systolic/diastolic. npp.2015.275
It simultaneously disrupts vmat2 (VMAT2), increasing cytoplasmic monoamine pools. serotonin release via serotonin-transporter occurs with substantially lower potency (DA >> NE >> 5-HT).partially supported
d-Amphetamine enhances DA and NE efflux; mechanism independent of neuronal firing rate, displacing intraneuronal catecholamines. j.neuropharm.2009.08.020
The compound is pharmacologically inactive until enzymatic hydrolysis in red blood cells liberates d-amphetamine, producing a sustained therapeutic duration of ≥13 hours in children and ≥14 hours in adults — the longest published duration among amphetamine formulations.partially supported
Duration: ≥13 h children, ≥14 h adults. s40261-015-0354-y
The indication expanded to adult ADHD (2008) and moderate-to-severe binge eating disorder in January 2015, making LDX the only FDA-approved pharmacotherapy for BED as of 2026partially supported
LDX 50-70 mg/day significantly reduced binge eating days/week vs placebo (p<0.001). npp.2015.275
d-Amphetamine released from LDX reverses the dopamine-transporter (DAT) and norepinephrine-transporter (NET), driving non-exocytotic efflux of dopamine and norepinephrine into the synapsesupported
Covers DAT/NET substrate activity, VMAT2, catecholamine release. s40120-022-00392-2
It simultaneously disrupts vmat2 (VMAT2), increasing cytoplasmic monoamine pools. serotonin release via serotonin-transporter occurs with substantially lower potency (DA >> NE >> 5-HT).partially supported
Also promotes release via VMAT. fpj.20033
Claim in summary — inconclusiveinconclusiveworking →
The prodrug design substantially reduces abuse-liability — intravenous LDX produces markedly lower peak euphoria than equivalent d-amphetamine — but does not eliminate itpartially supported
IV LDX did not produce significant abuse-related liking vs placebo; IV d-amp 20 mg did (p<0.05). 0269881108093841
Claim in summary — inconclusiveinconclusiveworking →
pharmacokinetic-detail7 · 6 ok
Following IV administration of LDX 50 mg, d-amphetamine Cmax was 38.9 ng/mL (Tmax 2.51 h), compared to 105 ng/mL (Tmax 0.82 h) after IV d-amphetamine 20 mgsupported
IV LDX 50 mg: Cmax d-amp 38.9 ng/ml, Tmax 2.51 h. IV d-amp 20 mg: Cmax 105 ng/ml, Tmax 0.82 h. 0269881108093841
Data compiled from FDA prescribing information, Krishnan et al., Ermer et al., and Adler et al..supported
PK data of LDX and d-amphetamine in ADHD adults. cap.2016.0121
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
Data compiled from FDA prescribing information, Krishnan et al., Ermer et al., and Adler et al..supported
Pharmacokinetics of d-amphetamine derived from lisdexamfetamine in healthy adults. 0091270007310381
Data compiled from FDA prescribing information, Krishnan et al., Ermer et al., and Adler et al..supported
Phase I absorption, metabolism, elimination study. Foundational PK characterization of LDX in healthy adults. 0044011-200828120-00002
Hydrolysis of LDX to d-amphetamine and L-lysine occurs primarily in red blood cells via an unidentified high-capacity enzymatic systemsupported
Metabolism to d-amphetamine occurs primarily in red blood cells (not liver/kidney). pmid:20628632
A randomised crossover study in healthy adult men demonstrated that intranasal LDX does not substantially increase d-amphetamine Cmax compared to oral administrationsupported
Intranasal route does not deliver meaningful lisdexamfetamine for abuse relative to oral; d-amphetamine systemic PK characterized. 11588190-000000000-00000
history6 · 3 ok
The pivotal human intravenous abuse-liability study demonstrated that IV LDX 50 mg produced d-amphetamine Cmax of 38.9 ng/mL (Tmax 2.51 h), compared to 105 ng/mL (Tmax 0.82 h) after IV d-amphetamine 20 mg — confirming that the prodrug structure substantially blunted the rate of rise even via parenteral routessupported
IV LDX 50 mg: Cmax d-amp 38.9 ng/ml, Tmax 2.51 h. IV d-amp 20 mg: Cmax 105 ng/ml, Tmax 0.82 h. 0269881108093841
Claim in history — inconclusiveinconclusiveworking →
Claim in history — inconclusiveinconclusiveworking →
On 30 January 2015, LDX received FDA approval for moderate-to-severe binge eating disorder in adults — the first and, as of 2026, still the only FDA-approved pharmacotherapy for BED.supported
Lisdexamfetamine dimesylate (LDX) is the ONLY drug approved by FDA for the treatment of BED in adults. s1092852915000759
Claim in history — inconclusiveinconclusiveworking →
A Phase 2 dose-ranging study yielded positive results, but two subsequent Phase 3 trials produced mixed results and the indication was not pursuedsupported
Meta-analysis of LDX as MDD augmentation. Mixed results on efficacy. j.jad.2017.09.041
neuroscience6 · 5 ok
The BED mechanism study demonstrated reduced thalamic activation during food cue processing at 50 mg, suggesting modulation of subcortical reward-salience circuits that drive compulsive eating behaviour.supported
Reduced thalamic activity during food pictures. s41398-021-01770-4
d-amphetamine released from LDX produces its primary central effects by dramatically increasing synaptic dopamine in the mesocorticolimbic pathway — specifically the ventral-tegmental-area (VTA) to nucleus-accumbens (NAc) projection (mesolimbic-pathway) and VTA to prefrontal-cortex projection (mesocortical pathway)supported
Comprehensive pharmacology review. Covers DAT/NET substrate activity, VMAT2, catecholamine release. s40120-022-00392-2
The therapeutic effects of LDX in ADHD are attributed primarily to enhanced catecholaminergic signalling in the prefrontal cortex (PFC)supported
Comprehensive pharmacology review. Covers DAT/NET substrate activity, VMAT2, catecholamine release. s40120-022-00392-2
In therapeutic ADHD populations, clinical efficacy is generally maintained during long-term treatment, suggesting that prefrontal cognitive enhancement does not undergo the same tolerance trajectory as euphorigenic effects.supported
Phase IV, 2-year open-label European study of LDX safety and efficacy in pediatric ADHD. s40263-017-0443-y
The gradual delivery curve of LDX may better approximate the optimal range across the dosing interval compared to IR formulations with sharp peak-trough kinetics.supported
d-amphetamine has lower Cmax, extended Tmax, lower PK variability vs IR d-amphetamine. s40261-015-0354-y
Claim in neuroscience — inconclusiveinconclusiveworking →
comparative-pharmacology4 · 4 ok
A comparative review of oral dexamphetamine and LDX confirmed that LDX produces lower peak subjective drug-liking and euphoria, consistent with the blunted Cmax and delayed Tmax. Abuse liability studies demonstrated that even IV LDX (50 mg) produced d-amphetamine Cmax of only 38.9 ng/mL (Tmax 2.51 h), compared to 105 ng/mL (Tmax 0.82 h) after IV d-amphetamine 20 mg.supported
Review comparing pharmacology and abuse potential of oral dexamphetamine vs lisdexamfetamine (prodrug). LDX has lower abuse potential due to prodrug design. hup.2910
A comparative review of oral dexamphetamine and LDX confirmed that LDX produces lower peak subjective drug-liking and euphoria, consistent with the blunted Cmax and delayed Tmax. Abuse liability studies demonstrated that even IV LDX (50 mg) produced d-amphetamine Cmax of only 38.9 ng/mL (Tmax 2.51 h), compared to 105 ng/mL (Tmax 0.82 h) after IV d-amphetamine 20 mg.supported
IV LDX 50 mg: Cmax d-amp 38.9 ng/ml, Tmax 2.51 h. IV d-amp 20 mg: Cmax 105 ng/ml, Tmax 0.82 h. IV LDX did not produce significant abuse-related liking vs placebo; IV d-amp 20 mg did (p<0.05). 0269881108093841
LDX produces a lower Cmax, extended Tmax (3.0–4.7 h vs. ~2 h for IR), and longer therapeutic duration (≥13–14 h vs. ~4–6 h for IR)supported
d-amphetamine has lower Cmax, extended Tmax, lower PK variability vs IR d-amphetamine. Duration: ≥13 h children, ≥14 h adults. s40261-015-0354-y
A double-blind, randomised, head-to-head study in children and adolescents demonstrated superior treatment response and remission rates for LDX compared to atomoxetine (a selective norepinephrine-transporter inhibitor)supported
Head-to-head RCT of LDX vs atomoxetine in pediatric ADHD inadequate MPH responders. s40263-014-0188-9
chemistry3 · 0 ok
receptor-pharmacology2 · 1 ok
d-amphetamine (the active metabolite of LDX) does not function as a conventional receptor ligand at monoamine transporters — it acts as a substrate that enters the presynaptic terminal via dopamine-transporter and norepinephrine-transporter and then drives transporter reversal, producing non-exocytotic neurotransmitter effluxsupported
d-Amphetamine enhances DA and NE efflux; mechanism independent of neuronal firing rate, displacing intraneuronal catecholamines. j.neuropharm.2009.08.020
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
effects-overview1 · 1 ok
Route of administration has minimal impact on the pharmacokinetic profile — intranasal and even intravenous LDX produce similarly blunted d-amphetamine peaks due to the obligatory RBC hydrolysis step.supported
IV LDX 50 mg: Cmax d-amp 38.9 ng/ml, Tmax 2.51 h. IV d-amp 20 mg: Cmax 105 ng/ml, Tmax 0.82 h. 0269881108093841