Lisdexamfetamine
![](/Images/godic/202501/24/Lisdexamfetamine_ball-and-stick_model5043.png")
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![Pharmacodynamics of amphetamine in a dopamine neuron
via AADC
Amphetamine enters the presynaptic neuron across the neuronal membrane or through DAT. Once inside, it binds to TAAR1 or enters synaptic vesicles through VMAT2. When amphetamine enters the synaptic vesicles through VMAT2, dopamine is released into the cytosol (yellow-orange area). When amphetamine binds to TAAR1, it reduces postsynaptic neuron firing rate via potassium channels and triggers protein kinase A (PKA) and protein kinase C (PKC) signaling, resulting in DAT phosphorylation. PKA-phosphorylation causes DAT to withdraw into the presynaptic neuron (internalize) and cease transport. PKC-phosphorylated DAT may either operate in reverse or, like PKA-phosphorylated DAT, internalize and cease transport. Amphetamine is also known to increase intracellular calcium, an effect which is associated with DAT phosphorylation through a CAMKIIα-dependent pathway, in turn producing dopamine efflux.](/Images/godic/202501/24/TAAR1_Dopamine.svg5043.png")
Lisdexamfetamine (contracted from L-lysine-dextroamphetamine) is a central nervous system (CNS) stimulant and dextroamphetamine prodrug of the phenethylamine class and amphetamine class that is used in the treatment of attention deficit hyperactivity disorder (ADHD) and binge eating disorder. Its chemical structure consists of dextroamphetamine coupled with the essential amino acid L-lysine. Lisdexamfetamine itself is inactive and acts as a prodrug to dextroamphetamine upon cleavage of the lysine portion of the molecule.