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ATOMOXETINE

EC / List no.: 617-427-9
CAS no.: 83015-26-3


Atomoxetine, sold under the brand name Strattera, among others, is a medication used to treat attention deficit hyperactivity disorder (ADHD).
Atomoxetine may be used alone or along with psychostimulants.
Use of atomoxetine is only recommended for those who are at least six years old.
Atomoxetine is taken by mouth.
Atomoxetine was approved for medical use in the United States in 2002.
In 2018, it was the 162nd most commonly prescribed medication in the United States, with more than 3 million prescriptions.

Common side effects of atomoxetine include abdominal pain, loss of appetite, nausea, feeling tired, and dizziness.
Serious side effects may include angioedema, liver problems, stroke, psychosis, heart problems, suicide, and aggression.
There is a lack of data regarding its safety during pregnancy; as of 2019, its safety during pregnancy and for use during breastfeeding is not certain.

Atomoxetine is a norepinephrine reuptake inhibitor and is believed to work by increasing norepinephrine and dopamine levels in the brain.


How atomoxetine works
Atomoxetine is a noradrenaline reuptake inhibitor.

Atomoxetine is not a central nervous stimulant, which makes it different from other treatments for attention deficit hyperactivity disorder (ADHD). 
Instead, it makes more noradrenaline available in your brain.

We are still not sure exactly how atomoxetine works – but this is what we know so far:

One of the chemicals in the brain is called noradrenaline (also known as norepinephrine). 
This transmitter is released from nerve endings to carry messages from one nerve cell to another in the brain.
After sending the message, noradrenaline is taken back up by the nerve endings in a recycling process.  Atomoxetine is a molecule that stops this process. 
This means that the levels of active noradrenaline in the brain increase.
Higher levels of noradrenaline in the brain help to make people more alert and ready for action. 
They feel like they have increased wellbeing and more energy.
Atomoxetine should help to increase your attention span and your concentration, and stop you acting on impulse without thinking.
Outside of the brain, higher levels of noradrenaline have other effects in different parts of the body, including the heart, the gut and the lungs. 
This can lead to unwanted side effects. 
Atomoxetine is hard to predict if and how you will be affected as each person is different.

Medical uses
Attention deficit hyperactivity disorder
Atomoxetine is approved for use in children, adolescents, and adults.
However, its efficacy has not been studied in children under six years old.
Its primary advantage over the standard stimulant treatments for ADHD is that it has little known abuse potential.
While it has been shown to significantly reduce inattentive and hyperactive symptoms, the responses were lower than the response to stimulants. 
Additionally, 40% of participants who were treated with atomoxetine experienced residual ADHD symptoms.

While its efficacy may be less than that of stimulant medications, there is some evidence that it may be used in combination with stimulants.
Doctors may prescribe non-stimulants including atomoxetine when a person has bothersome side effects from stimulants; when a stimulant was not effective; in combination with a stimulant to increase effectiveness; or when there is concern about the abuse potential of psychostimulants in a patient with a history of drug use disorder.

Unlike α2 adrenoceptor agonists such as guanfacine and clonidine, atomoxetine's use can be abruptly stopped without significant discontinuation effects being seen.

The initial therapeutic effects of atomoxetine usually take 1 to 4 weeks to become apparent.
A further 2 to 4 weeks may be required for the full therapeutic effects to be seen.
Incrementally increasing response may occur up to 1 year or longer.
The maximum recommended total daily dose in children and adolescents over 70 kg and adults is 100 mg.

Other uses:
Atomoxetine may be used in those with ADHD and bipolar disorder although such use has not been well studied.
Some benefit has also been seen in people with ADHD and autism.
As with other norepinephrine reuptake inhibitors it appears to reduce anxiety and depression symptoms, although attention has focused mainly on specific patient groups such as those with concurrent ADHD or methamphetamine dependence.

Contraindications
Contraindications include:

Hypersensitivity to atomoxetine or any of the inactive ingredients in the product
Symptomatic cardiovascular disease including:
-moderate to severe hypertension
-atrial fibrillation
-atrial flutter
-ventricular tachycardia
-ventricular fibrillation
-ventricular flutter
-advanced arteriosclerosis
Severe cardiovascular disorders
Pheochromocytoma
Concomitant treatment with monoamine oxidase inhibitors
Narrow angle glaucoma
Poor metabolizers (due to the metabolism of atomoxetine by CYP2D6)

Interactions
Atomoxetine is a substrate for CYP2D6. 
Concurrent treatment with a CYP2D6 inhibitor such as bupropion, fluoxetine, or paroxetine has been shown to increase plasma atomoxetine by 100% or more, as well as increase N-desmethylatomoxetine levels and decrease plasma 4-hydroxyatomoxetine levels by a similar degree.

Atomoxetine has been found to directly inhibit hERG potassium currents with an IC50 of 6.3 μM, which has the potential to cause arrhythmia.
QT prolongation has been reported with atomoxetine at therapeutic doses and in overdose; it is suggested that atomoxetine not be used with other medications that may prolong the QT interval, concomitantly with CYP2D6 inhibitors, and caution to be used in poor metabolizers.

Other notable drug interactions include:

Antihypertensive agents, due to atomoxetine acting as an indirect sympathomimetic
Indirect-acting sympathomimetics, such as pseudoephedrine, norepinephrine reuptake inhibitors, or MAOIs
Direct-acting sympathomimetics, such as phenylephrine or other α1 adrenoceptor agonists, including pressors such as dobutamine or isoprenaline and β2 adrenoceptor agonists
Highly plasma protein-bound drugs: atomoxetine has the potential to displace these drugs from plasma proteins which may potentiate their adverse or toxic effects. 
In vitro, atomoxetine does not affect the plasma protein binding of aspirin, desipramine, diazepam, paroxetine, phenytoin, or warfarin

Pharmacology
Pharmacodynamics
Atomoxetine inhibits the presynaptic norepinephrine transporter (NET), preventing the reuptake of norepinephrine throughout the brain along with inhibiting the reuptake of dopamine in specific brain regions such as the prefrontal cortex, where dopamine transporter (DAT) expression is minimal.


Pharmacokinetics
Orally administered atomoxetine is rapidly and completely absorbed.
First-pass metabolism by the liver is dependent on CYP2D6 activity, resulting in an absolute bioavailability of 63% for extensive metabolizers and 94% for poor metabolizers.
Maximum plasma concentration is reached in 1–2 hours.
If taken with food, the maximum plasma concentration decreases by 10-40% and delays the tmax by 3 hours.
Drugs affecting gastric pH have no effect on oral bioavailability.

Atomoxetine has a volume of distribution of 0.85 L/kg, with limited partitioning into red blood cells.
Atomoxetine is highly bound to plasma proteins (98.7%), mainly albumin, along with α1-acid glycoprotein (77%) and IgG (15%).
Its metabolite N-desmethylatomoxetine is 99.1% bound to plasma proteins, while 4-hydroxyatomoxetine is only 66.6% bound.

The half-life of atomoxetine varies widely between individuals, with an average range of 4.5 to 19 hours.
As atomoxetine is metabolized by CYP2D6, exposure may be increased 10-fold in CYP2D6 poor metabolizers.

Atomoxetine, N-desmethylatomoxetine, and 4-hydroxyatomoxetine produce minimal to no inhibition of CYP1A2 and CYP2C9, but inhibit CYP2D6 in human liver microsomes at concentrations between 3.6-17 μmol/L.
Plasma concentrations of 4-hydroxyatomoxetine and N-desmethylatomoxetine at steady state are 1.0% and 5% that of atomoxetine in CYP2D6 extensive metabolizers, and are 5% and 45% that of atomoxetine in CYP2D6 poor metabolizers.

Atomoxetine is excreted unchanged in urine at <3% in both extensive and poor CYP2D6 metabolizers, with >96% and 80% of a total dose being excreted in urine, respectively.
The fractions excreted in urine as 4-hydroxyatomoxetine and its glucuronide account for 86% of a given dose in extensive metabolizers, but only 40% in poor metabolizers.
CYP2D6 poor metabolizers excrete greater amounts of minor metabolites, namely N-desmethylatomoxetine and 2-hydroxymethylatomoxetine and their conjugates.

Pharmacogenomics
Chinese adults homozygous for the hypoactive CYP2D6*10 allele have been found to exhibit two-fold higher area-under-the-curve (AUCs) and 1.5-fold higher maximum plasma concentrations compared to extensive metabolizers.

Japanese men homozygous for CYP2D6*10 have similarly been found to experience two-fold higher AUCs compared to extensive metabolizers.

Chemistry
Atomoxetine, or (−)-methyl[(3R)-3-(2-methylphenoxy)-3-phenylpropylamine, is a white, granular powder that is highly soluble in water.

Detection in biological fluids
Atomoxetine may be quantitated in plasma, serum or whole blood in order to distinguish extensive versus poor metabolizers in those receiving the drug therapeutically, to confirm the diagnosis in potential poisoning victims or to assist in the forensic investigation in a case of fatal overdosage.

History
Atomoxetine is manufactured, marketed, and sold in the United States as the hydrochloride salt (atomoxetine HCl) under the brand name Strattera by Eli Lilly and Company, the original patent-filing company and current U.S. patent owner. 
Atomoxetine was initially intended to be developed as an antidepressant, but it was found to be insufficiently efficacious for treating depression. 
Atomoxetine was, however, found to be effective for ADHD and was approved by the FDA in 2002, for the treatment of ADHD. 
Its patent expired in May 2017.
On 12 August 2010, Lilly lost a lawsuit that challenged its patent on Strattera, increasing the likelihood of an earlier entry of a generic into the US market.
On 1 September 2010, Sun Pharmaceuticals announced it would begin manufacturing a generic in the United States.In a 29 July 2011 conference call, however, Sun Pharmaceutical's Chairman stated "Lilly won that litigation on appeal so I think [generic Strattera]'s deferred."

In 2017 the FDA approved the generic production of atomoxetine by four pharmaceutical companies.

Society and culture
Brand names
In India, atomoxetine is sold under brand names including Axetra, Axepta, Attera, Tomoxetin, and Attentin. 
In Australia, Portugal, the US, Canada, Italy and Romania, atomoxetine is sold under the brand name Strattera. 
In Iran, atomoxetine is sold under brand names including Stramox. In 2017, a generic version was approved in the United States.


Atomoxetine is a selective norepinephrine reuptake inhibitor used primarily for therapy of attention deficit hyperactivity disorder. 
Atomoxetine has been linked to a low rate of serum aminotransferase elevations and to rare cases of acute, clinically apparent liver injury.

Atomoxetine is a secondary amino compound having methyl and 3-(2-methylphenoxy)-3-phenylpropan-1-yl substituents. 
Atomoxetine has a role as an adrenergic uptake inhibitor, an antidepressant, a xenobiotic and an environmental contaminant. 
Atomoxetine is an aromatic ether, a secondary amino compound and a member of toluenes.

Atomoxetine is a selective norepinephrine (NE) reuptake inhibitor used for the treatment of attention deficit hyperactivity disorder (ADHD). 
Also known as the marketed product Strattera, atomoxetine is used with other treatment modalities (psychological, educational, cognitive behaviour therapy, etc) to improve developmentally inappropriate symptoms associated with ADHD including distractibility, short attention span, hyperactivity, emotional lability, and impulsivity. 
Although the underlying pathophysiology that causes ADHD remains unclear, evidence suggests that dysregulation in noradrenergic and dopaminergic pathways plays a critical role in suboptimal executive functioning within prefrontal regions of the brain, which are involved in attention and memory. 
Atomoxetine has been shown to specifically increase NA and DA within the prefrontal cortex, but not in the nucleus accumbens (NA) or striatum. 
This is beneficial in the treatment of ADHD as DA activation in the subcortical NA and striatum is associated with many stimulant-associated side effects and an increase in abuse potential, which is a limiting factor associated with the use of stimulant medications such as [DB00422], [DB01576], and [DB01255]. 
Use of non-stimulant medications such as atomoxetine is therefore thought to offer a clinical advantage over the use of traditional medications for the management of ADHD. 
More recently, positron emission tomography (PET) imaging studies in rhesus monkeys have shown that atomoxetine also binds to the serotonin transporter (SERT), and blocks the N-methyl-d-aspartate (NMDA) receptor, indicating a role for the glutamatergic system in the pathophysiology of ADHD. 
Long-acting formulations of psychostimulants (such as [DB00422], [DB01576], and [DB01255]) are typically considered the most effective and first-line treatment for ADHD in adults and children as recommended by CADDRA (Canadian ADHD Resource Alliance). 
However, these stimulant medications are limited by dose-related side effects and concerns of abuse. 
Many contain a blackbox warning stating that CNS stimulants, including methylphenidate-containing products and amphetamines, have a high potential for abuse and dependence. 
In particular, increased dopamine in key areas caused by these stimulant medications is associated with their reinforcing and addictive properties, and even amplifies the potency and reinforcing effects of other drugs of abuse such as amphetamines, making ADHD sufferers more susceptible to their addictive effects. 
Concerns about abuse potential have spurred research into medications with fewer effects on DA and the use of non-stimulant ADHD medications including atomoxetine, and. 
The non-stimulant norepinephrine/dopamine reuptake inhibitor (commonly used for the treatment of depression and for smoking cessation) has also been shown to be effective in the treatment of ADHD.


IDENTIFICATION AND USE: 
Atomoxetine, as Strattera, is indicated for the treatment of Attention-Deficit/Hyperactivity Disorder (ADHD).


Pharmacokinetics    
Atomoxetine is well absorbed from the GItract and cleared primarily by metabolism, with the majority of the dose being excreted into the urine. 
Atomoxetine is metabolized primarily by CYP2D6 to its major active metabolite, 4-hydroxyatomoxetine, which is eliminated as its glucuronide. 
Peak plasma concentrations of atomoxetine occur 1 to 2 hours after oral administration. 
Significant differences are seen in the elimination half-life between normal metabolizers, extensive metabolizers, and poor metabolizers. 
Atomoxetine exhibited an elimination half-life of 3 to 6 hours for normal and extensive metabolizers and 17 to 21 hours for poor metabolizers. 
CYP2C19 is the other enzyme primarily responsible for the formation of its minor metabolite N-desmethylatomoxetine.

Clinical Use:    
Atomoxetine is used as a safe and well-tolerated “nonstimulant” treatment of ADHD in both adults and children and of depression. 
Among children and adolescents aged 8 to 18 years, atomoxetine was superior to placebo in reducing symptoms of ADHD and in improving social and family functioning symptoms. 
Oral atomoxetine is promoted as an alternative to conventional ADHD therapy with methylphenidate, dextroamphetamine, and pemoline. 
Atomoxetine also can be a replacement for bupropion or for TCAs. 
Onset of action is approximately 7 days.


Description    
Atomoxetine is the first non-stimulant marketed for the treatment of attention deficit hyperactivity disorder (ADHD). 
Atomoxetine is the R-stereoisomer of the racemate tomoxetine and is a selective and potent norepinephrine uptake inhibitor (Ki=0.7–1.9 nM) that is devoid of binding to monoamine receptor. 
Atomoxetine also has little effect on dopamine and serotonin reuptake or acetylcholine, H1 histamine, alpha1 or alpha1-adrenergic or dopamine receptors. 
Atomoxetine is prepared from racemic 1-phenylbut-3-en-1-ol via a selective enzymatic acylation leaving the desired S-stereoisomer as the alcohol. 
This alcohol is converted via a Mitsunobu reaction with ortho-cresol to the corresponding ether with isomeric R-configuration. 
Ozonolysis and reduction steps provided the terminal alcohol that is mesylated and displaced with methylamine. 
Its selectivity for norepinephrine relative to dopamine inhibition was demonstrated in vivo preclinically. 
In a two-lever (two condition) discriminative stimulus effect study in squirrel monkeys, tomoxetine and other norepinephrine uptake inhibitors substituted for cocaine under low-dose training conditions, whereas dopamine uptake inhibitors substituted for cocaine in both low and high-dose conditions. 
In clinical ADHD studies in adolescents, it was significantly different from placebo in 1.2 and 1.8 mpk/day dosing. 
In the clinical study in adults using the CAARS scale a 95 mg/day dose provided greater than 30% improvement in total scores. 
Atomoxetine is about 63% orally bioavailable, is highly protein bound (98%, primarily to albumin) and has a half-life of about 5.2 h. 
Atomoxetine is metabolized by CYP2D6 resulting in differential clearance for poor metabolizers (halflife of 19 h with a 10 times higher AUC) relative to extensive metabolizers. 
The total daily dose for children, adolescents and adults is a maximum of 100 mg/day. 
Common side effects in children and adults include nausea, decreased appetite, and dizziness. 
Adults may also have insomnia.


Biological Activity    
Potent and selective noradrenalin re-uptake inhibitor (K i values are 5, 77 and 1451 nM for inhibition of radioligand binding to human NET, SERT and DAT respectively). 
Displays minimal affinity for a range of other neurotransmitter receptors and transporters (K i > 1 μ M). Antidepressant.

Chemical Synthesis    
The 3-aryloxy substituent was introduced utilizing a chiral alcohol by either the Mitsunobu reaction or by nucleophilic aromatic displacement. 
Because of the expense and difficulty of the Mitsunobu reaction on large scale, the commercial process adopts the nucleophilic aromatic substitution method. 
3- Chloropropiophenone (37) was asymmetrically reduced with borane and catalytic amount of (S)-oxazaborolidine (8) in THF at 0°C to give chiral alcohol 38 in 99% yield and 94% e.e. 
The chiral alcohol was further purified by recrystallization to greater than 99% e.e.. Subsequent treatment of chloride 38 with excess dimethylamine (40% in water) in ethanol gave dimethylamine alcohol 39 in 90% yield. 
Alcohol 39 was then subjected to nucleophilic aromatic displacement in the presence of NaH in DMSO with 1- fluoro-2-(t-butylimino)benzene (41), which was prepared in high yield from 2-fluorobenzaldehyde (40). 
The displacement product 42 was obtained in 98% yield, and the imine 42 was subsequently hydrolyzed with acetic acid in water at low temperature to give the corresponding aldehyde 43 in 96% yield.
Sodium borohydride was employed to reduce aldehyde 43 to alcohol in cold methanol and the intermediate alcohol was converted to chloride 44 with thionyl chloride. 
Chloride 44 was then reduced with zinc metal under acidic conditions to give methyl adduct 45 in 95% yield and 94% e.e. 
Finally, phenyl chloroformate and triethylamine was used to transform dimethylamine 45 to monomethyl amine, which was subsequently treated with HCl in EtOAc under reflux to give atomoxetin hydrochloride (IV) in 98% yield and 99% e.e. from 45.


Atomoxetine is used to treat attention-deficit hyperactivity disorder (ADHD) as part of a total treatment plan, including psychological, social, and other treatments. 
Atomoxetine may help to increase the ability to pay attention, concentrate, stay focused, and stop fidgeting. 
Atomoxetine is thought to work by restoring the balance of certain natural substances (neurotransmitters) in the brain.

How to use Atomoxetine Capsule
Read the Medication Guide provided by your pharmacist before you start using atomoxetine and each time you get a refill. 
If you have any questions, ask your doctor or pharmacist.

Take this medication with or without food as directed by your doctor, usually 1 to 2 times a day. 
The first dose is usually taken when you wake up in the morning. 
If a second dose is prescribed, take it as directed by your doctor, usually in the late afternoon/early evening. Taking this medication late in the day may cause trouble sleeping (insomnia).

Swallow the capsules whole. 
Do not crush, chew, or open the capsules. 
If the capsule is accidentally opened or broken, avoid contact with the powder and wash away any loose powder as soon as possible with water. 
If the powder gets in your eyes, flush with plenty of water right away and contact your doctor.

The dosage is based on your medical condition, response to treatment, and other drugs you may be taking. 
Be sure to tell your doctor and pharmacist about all the products you use (including prescription drugs, nonprescription drugs, and herbal products). 
Do not increase your dose or take this drug more often than directed.

Use this medication regularly to get the most benefit from it. 
To help you remember, take it at the same time(s) each day.

Tell your doctor if your condition does not improve or if it worsens.

Precautions
Before taking atomoxetine, tell your doctor or pharmacist if you are allergic to it; or if you have any other allergies. 
This product may contain inactive ingredients, which can cause allergic reactions or other problems.
Talk to your pharmacist for more details.

Before using this medication, tell your doctor or pharmacist your medical history, especially of: a certain adrenal problem (pheochromocytoma), bladder or prostate problems, glaucoma, heart problems (such as irregular heartbeat, heart failure, previous heart attack, problems with heart structure), family history of heart problems (such as sudden cardiac death, irregular heartbeat), high blood pressure, liver disease, personal/family history of mental/mood disorders (such as bipolar disorder, depression, psychosis, suicidal thoughts), stroke.

This drug may make you dizzy or drowsy. Alcohol or marijuana (cannabis) can make you more dizzy or drowsy. 
Do not drive, use machinery, or do anything that needs alertness until you can do it safely. 
Limit alcoholic beverages. 
Talk to your doctor if you are using marijuana (cannabis).

Before having surgery, tell your doctor or dentist about all the products you use (including prescription drugs, nonprescription drugs, and herbal products).

If used for a long time, this drug may affect a child's growth rate, weight, and final adult height. 
To reduce the risk, the doctor may recommend briefly stopping the medication from time to time. 
Check the child's weight and height regularly, and consult your doctor or pharmacist for more details.

During pregnancy, this medication should be used only when clearly needed. 
Discuss the risks and benefits with your doctor.

Atomoxetine is unknown if this drug passes into breast milk. 
Consult your doctor before breast-feeding.


Why is this medication prescribed?
Atomoxetine is used as part of a total treatment program to increase the ability to pay attention and decrease impulsiveness and hyperactivity in children and adults with ADHD. 
Atomoxetine is in a class of medications called selective norepinephrine reuptake inhibitors. 
Atomoxetine works by increasing the levels of norepinephrine, a natural substance in the brain that is needed to control behavior.

How should this medicine be used?
Atomoxetine comes as a capsule to take by mouth. 
Atomoxetine is usually taken either once a day in the morning, or twice a day in the morning and late afternoon or early evening. Atomoxetine may be taken with or without food. 
Take atomoxetine at around the same time(s) every day. 
Follow the directions on your prescription label carefully, and ask your doctor or pharmacist to explain any part you do not understand. 
Take atomoxetine exactly as directed. Do not take more or less of it or take it more often than prescribed by your doctor.

Swallow atomoxetine capsules whole; do not open, chew, or crush them. 
If a capsule is accidentally broken or opened, wash away the loose powder with water right away. 
Try not to touch the powder and be especially careful not to get the powder in your eyes. 
If you do get powder in your eyes, rinse them with water right away and call your doctor.

Your doctor will probably start you on a low dose of atomoxetine and increase your dose after at least 3 days. Your doctor may increase your dose again after 2–4 weeks. 
You may notice improvement in your symptoms during the first week of your treatment, but it may take up to one month for you to feel the full benefit of atomoxetine.

Atomoxetine may help to control the symptoms of ADHD but will not cure the condition. 
Continue to take atomoxetine even if you feel well. Do not stop taking atomoxetine without talking to your doctor.

Other uses for this medicine
This medication may be prescribed for other uses; ask your doctor or pharmacist for more information.


Atomoxetine is a selective norepinephrine (NE) reuptake inhibitor used for the treatment of attention deficit hyperactivity disorder (ADHD). 
Also known as the marketed product Strattera, atomoxetine is used with other treatment modalities (psychological, educational, cognitive behaviour therapy, etc) to improve developmentally inappropriate symptoms associated with ADHD including distractibility, short attention span, hyperactivity, emotional lability, and impulsivity. 
Although the underlying pathophysiology that causes ADHD remains unclear, evidence suggests that dysregulation in noradrenergic and dopaminergic pathways plays a critical role in suboptimal executive functioning within prefrontal regions of the brain, which are involved in attention and memory.
Atomoxetine has been shown to specifically increase NA and DA within the prefrontal cortex, but not in the nucleus accumbens (NA) or striatum.
This is beneficial in the treatment of ADHD as DA activation in the subcortical NA and striatum is associated with many stimulant-associated side effects and an increase in abuse potential, which is a limiting factor associated with the use of stimulant medications such as Methylphenidate, Dextroamphetamine, and Lisdexamfetamine.
Use of non-stimulant medications such as atomoxetine is therefore thought to offer a clinical advantage over the use of traditional medications for the management of ADHD. 
More recently, positron emission tomography (PET) imaging studies in rhesus monkeys have shown that atomoxetine also binds to the serotonin transporter (SERT), and blocks the N-methyl-d-aspartate (NMDA) receptor,10 indicating a role for the glutamatergic system in the pathophysiology of ADHD.

Long-acting formulations of psychostimulants (such as Methylphenidate, Dextroamphetamine, and Lisdexamfetamine) are typically considered the most effective and first-line treatment for ADHD in adults and children as recommended by CADDRA (Canadian ADHD Resource Alliance).
However, these stimulant medications are limited by dose-related side effects and concerns of abuse. 
Many contain a blackbox warning stating that CNS stimulants, including methylphenidate-containing products and amphetamines, have a high potential for abuse and dependence. 
In particular, increased dopamine in key areas caused by these stimulant medications is associated with their reinforcing and addictive properties, and even amplifies the potency and reinforcing effects of other drugs of abuse such as amphetamines, making ADHD sufferers more susceptible to their addictive effects.
Concerns about abuse potential have spurred research into medications with fewer effects on DA and the use of non-stimulant ADHD medications including atomoxetine, Modafinil and Guanfacine. 
The non-stimulant norepinephrine/dopamine reuptake inhibitor Bupropion (commonly used for the treatment of depression and for smoking cessation) has also been shown to be effective in the treatment of ADHD.

What is atomoxetine?
Atomoxetine is used to treat attention deficit hyperactivity disorder (ADHD).

Atomoxetine may also be used for purposes not listed in this medication guide.


SYNONYMS:
ATOMOXETINE
Atomoxetine EP Impurity C HCl
(R)-N-methyl-3-phenyl-3-(p-tolyloxy)propan-1-amine
(R)-N-methyl-3-phenyl-3-(p-tolyloxy)propan-1-amine hydrochloride
p-Tolyloxy Atomoxetine Hydrochloride
ATOMOXETINE
ATOMOXETINE HCL
ATOMOXETINE HYDROCHLORIDE
METHYL-(3-PHENYL-3-O-TOLYLOXY-PROPYL)-AMINE HYDROCHLORIDE
(R)-N-METHYL-GAMMA-(2-METHYLPHENOXY)-BENZENEPROPANAMINE HYDROCHLORIDE
(r)-tomoxetine hydrochloride
TOMOXETINE HYDROCHLORIDE
Atomoxetine HCI
(R)-N-methyl-gamma-(2-methylphenoxy)-benzenepropanamine
(R)-N-Methyl-g-(2-methylphenoxy)benzenepropanaminehydrochloride
R-Tomexetine, Hydrochloride, (R)-N-Methyl--(2-methylphenoxy)benzenepropanamine, Hydrochloride
(r)-n-methyl-γ-(2-methyl-phenoxy)benzenepropanamine hydrochloride
ATOMOXETINEHYDROCHLORIDE(FORR&DONLY)
ATOMOXITINE
Atomexine Hydrochloride
(R)-N-Methyl-3-(2-methylphenoxy)-3-phenylpropylamine Hydrochloride
Methyl-((R)-3-phenyl-3-o-tolyloxy-propyl)-amine hydrochloride
Atomoxetine hydrochloride, 99%, a selective norepinephrine reuptake inhibitor
(R)-N-METHYL-3-PHENYL-3-(O-TOLYLOXY)PROPAN-1-AMINE HCL
Atomoxetine hydrochloride, (R)-N-Methyl-γ-(2-methylphenoxy)benzenepropanamine hydrochloride
Atomoxitine HCL
LY 139603
R-Tomexetine Hydrochloride
Strattera
(3R)-N-methyl-3-(2-methylphenoxy)-3-phenyl-propan-1-amine hydrochloride
(3R)-N-methyl-3-(2-methylphenoxy)-3-phenylpropan-1-amine hydrochloride
methyl-[(3R)-3-(2-methylphenoxy)-3-phenyl-propyl]amine hydrochloride
BenzenepropanaMine,N-Methyl-g-(2-Methylphenoxy)-,hydrochloride (
(R)-N-Methyl-3-(2-methylphenoxy)-3-phenylpropylamine Hydrochloride (R)-Tomoxetine Hydrochloride
(R)-N-Methyl-3-phenyl-3-(o-tolyloxy)propan-1-aMine hydrochloride
BenzenepropanaMine,N-Methyl-g-(2-Methylphenoxy)-,hydrochloride (1:1), (gR)-
(R)-N-Methyl-3-phenyl-3-(o-tolyloxy)-propan-1-aMine hydrochloride, 95+%
LY 139603 HCl
Atomoxetine hydrochloride (R)-Tomoxetine hydrochloride
(R)-Atomoxetine hydrochloride
Atomoxetine for impurity A identification
Atomoxetine hydrochloride solution
Atomoxetine Hydrochloride (125 mg)
Atomoxetine Hydrochloride Impurity
Benzenepropanamine,N-methyl-g-(2-methylphenoxy)-,hydrochloride,(R)-
Atomoxetine Hydrochloride IMP
Atazanavir HCl
Atomoxetine hydrochloride CRS
Atomoxetine Hydrochloride >
(R)-Atomoxetine HCl
Atomoxetine hydrochloride USP/EP/BP
Tomoxetine hydrochloride impurity


 

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