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A plain-language summary of the cited sources below. Informational only — not medical advice.
Atomoxetine works primarily by blocking the brain's reuptake of noradrenaline, a chemical messenger involved in attention and impulse control. It also has some effect on serotonin uptake and a weaker effect on dopamine. This mechanism is different from stimulant medications — atomoxetine doesn't directly increase dopamine in the same way. It's prescribed for attention deficit hyperactivity disorder in children aged six and over, adolescents, and adults, when the diagnosis meets the criteria set out in diagnostic manuals. How long it stays active in the body varies: in most people it clears within about four hours, but in a smaller group whose liver processes it differently, it can remain active for around 21 hours. This difference can affect how the medication is dosed.
Common side effects include reduced appetite, stomach pain or discomfort, nausea, and vomiting. Blood pressure can also increase. These effects are usually noticed early in treatment and may settle over time, though not always. Serious adverse effects, though less common, include suicidal thoughts or behaviour — this has been documented in clinical trials and post-market reports. Some people taking atomoxetine have experienced aggression, hostility, or symptoms of psychosis or mania. Seizures and changes to heart rhythm have also been reported.
There are several groups of people who should not take atomoxetine. It is contraindicated in anyone with known hypersensitivity to the medication, people with symptomatic cardiovascular disease such as moderate to severe high blood pressure or certain heart rhythm disorders, those with advanced hardening of the arteries, uncontrolled overactive thyroid, or phaeochromocytoma. It must not be taken at the same time as monoamine oxidase inhibitors, a class of antidepressant, or within two weeks of stopping an MAOI; similarly, an MAOI should not be started within two weeks of stopping atomoxetine. The combination can cause severe and sometimes fatal reactions including high fever, rigid muscles, unstable vital signs, and altered mental state. Atomoxetine is also not recommended for people with narrow angle glaucoma, as it has been associated with pupil dilation which can worsen that condition.
Attention deficit hyperactivity disorder Clinical criteria: Treatment Phase: Initial treatment Treatment criteria: Must be treated by a paediatrician or psychiatrist. The condition must be or have been diagnosed according to the DSM-5 criteria, AND Patient must have a contraindication to dexamfetamine, methylphenidate or lisdexamfetamine as specified in TGA-approved product information; OR Patient must have a comorbid mood disorder that has developed or worsened as a result of dexamfetamine, methylphenidate or lisdexamfetamine treatment and is of a severity necessitating treatment withdrawal; OR Patient must be at an unacceptable medical risk of a severity necessitating permanent stimulant treatment withdrawal if given a stimulant treatment with another agent; OR Patient must have experienced adverse reactions of a severity necessitating permanent treatment withdrawal following treatment with dexamfetamine, methylphenidate and lisdexamfetamine (not simultaneously). Population criteria: Patient must be or have been diagnosed between the ages of 6 and 18 years inclusive.
“Atomoxetine is a relatively potent inhibitor of the presynaptic noradrenaline transporter (Ki 4.5 nM), a moderate inhibitor of 5HT uptake (Ki 152 nM) and a weak inhibitor of dopamine uptake (Ki 658 nM), with minimal affinity for the other noradrenergic receptors.”
“The mean elimination half-life of atomoxetine after oral administration is 3.6 hours in extensive metabolisers and 21 hours in poor metabolisers.”
A plain-language summary of the cited sources below. Informational only — not medical advice.
Atomoxetine is a centrally acting sympathomimetic approved by the TGA for the treatment of Attention Deficit Hyperactivity Disorder in children aged six years and older, adolescents, and adults, when ADHD is defined by DSM-IV criteria. Its mechanism involves relatively potent inhibition of the presynaptic noradrenaline transporter (Ki 4.5 nM), moderate inhibition of serotonin uptake (Ki 152 nM), and weak inhibition of dopamine uptake (Ki 658 nM), with minimal affinity for other noradrenergic receptors.
Pharmacokinetically, atomoxetine exhibits bimodal elimination dependent on CYP2D6 metaboliser status: the mean half-life is 3.6 hours in extensive metabolisers and 21 hours in poor metabolisers. Atomoxetine does not cause clinically significant inhibition or induction of cytochrome P450 enzymes, including CYP1A2, CYP3A, CYP2D6, and CYP2C9. Common adverse effects include decreased appetite, abdominal pain, vomiting, nausea, and increased blood pressure. Serious adverse effects encompass suicidal ideation, completed suicide, suicide attempt, QT prolongation, seizures, and aggression, hostility, psychosis, or mania.
Atomoxetine is contraindicated in known hypersensitivity, symptomatic cardiovascular disease (including moderate to severe hypertension, atrial fibrillation, ventricular arrhythmias, and advanced arteriosclerosis), severe cardiovascular disorders that would be expected to deteriorate with clinically important increases in blood pressure or heart rate, uncontrolled hyperthyroidism, phaeochromocytoma or its history, and narrow-angle glaucoma. Concurrent use with monoamine oxidase inhibitors or within two weeks of MAOI discontinuation is contraindicated; a two-week washout is required before initiating MAOI therapy after atomoxetine cessation.
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Curated subset. The full adverse-effect list is in the TGA Product Information; click any citation above to open it.
“Atomoxetine did not cause clinically significant inhibition or induction of cytochrome P450 enzymes, including CYP1A2, CYP3A, CYP2D6 and CYP2C9.”