Does Vyvanse (lisdexamfetamine) increase the release of dopamine or block its reuptake in patients with Attention Deficit Hyperactivity Disorder (ADHD)?

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Vyvanse's Mechanism of Action: Both Dopamine Release and Reuptake Blockade

Vyvanse (lisdexamfetamine) works through a dual mechanism: it both blocks the reuptake of dopamine AND increases the release of dopamine into the synaptic cleft. 1

Primary Mechanism of Action

Lisdexamfetamine is a prodrug that is enzymatically hydrolyzed to its active form, dextroamphetamine, after oral administration. 1 The active metabolite dextroamphetamine then exerts its therapeutic effects through two complementary pathways:

Reuptake Inhibition

  • Amphetamines block the reuptake of both norepinephrine and dopamine into the presynaptic neuron, preventing these neurotransmitters from being cleared from the synaptic cleft. 1
  • Dextroamphetamine competitively inhibits the dopamine transporter (DAT) and noradrenaline transporter (NAT), increasing dopamine and noradrenaline concentrations in the synaptic space. 2
  • The parent drug lisdexamfetamine itself does not bind to dopamine or norepinephrine reuptake sites in vitro—only the active metabolite dextroamphetamine has this effect. 1, 3

Enhanced Neurotransmitter Release

  • Amphetamines increase the release of dopamine and norepinephrine into the extraneuronal space, providing an additional mechanism beyond reuptake blockade alone. 1
  • Dextroamphetamine is taken up into neuronal cells where it acts on the vesicular monoamine transporter, promoting the release of dopamine and noradrenaline from presynaptic neurons. 2
  • This dual action—blocking reuptake while simultaneously promoting release—distinguishes amphetamines from medications like bupropion, which only block reuptake without enhancing neurotransmitter release. 4

Clinical Implications

The combination of reuptake inhibition and enhanced release results in a substantial increase in synaptic dopamine and norepinephrine concentrations. 4 This enhanced monoamine signaling in the prefrontal cortex and striatum is thought to improve executive function, impulse control, and working memory deficits characteristic of ADHD. 4

The prodrug design of lisdexamfetamine provides rate-limited conversion to active dextroamphetamine, resulting in a gradual release of the active compound with reduced abuse potential compared to immediate-release amphetamine formulations. 5, 6

References

Research

Lisdexamfetamine dimesylate for childhood ADHD.

Drugs of today (Barcelona, Spain : 1998), 2008

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Research

Lisdexamfetamine.

Paediatric drugs, 2007

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Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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