Atomoxetine classified as a selective norepinephrine reuptake inhibitor (SNRI) commonly used in the treatment of attention deficit hyperactivity disorder (ADHD) instead of stimulant medication such as methylphenidate, dextroamphetamine or lisdexamfetamine. Atomoxetine appears to only increase norepinephrine and dopamine levels within the prefrontal cortex without effecting concentration levels in the nucleus accumbens and or the striatum leading to little to no stimulant associated side effects with less abuse potential. It is a selective reuptake inhibitor of norepinephrine transporter (NET) leading to alleviating symptoms of ADHD. Recent studies have also shown that its binds to serotonin transporter (SERT) and also inhibits N-methyl-d-aspartate (NMDA) receptors, although further research is necessary to confirm these interactions. It is metabolized by cytochrome P450 2D6 into its metabolites of 4-hydroxy-atomoxetine which is equipotent as atomoxetine and its mechanism of action. If there is a lack of CYP2D6 enzymes then other cytochrome enzymes break down the drug and results in its minor metabolites being formed with less pharmacological activity. The metabolites are commonly glucuronidated and excreted as 4-hydroxyatomoxetine-O-glucuronide through the urine. During acute or chronic overdoses of atomoxetine, some symptoms observed is gastrointestinal symptoms, somnolence, dizziness, tremor and abnormal behavior. If these symptoms are seen poison control center should be phoned in order to plan a good course of action, as atomoxetine is protein bound and dialysis may not be effective treatment for an overdose.

Atomoxetine Pathway References