View source for Atomoxetine

{{Short description|Medication used to treat ADHD}}
{{Use dmy dates|date=November 2024}}
{{cs1 config |name-list-style=vanc |display-authors=6}}
{{Infobox drug
| Verifiedfields = changed
| Watchedfields = changed
| verifiedrevid = 458780865
| image = Atomoxetine structure.svg
| image_class = skin-invert-image
| width = 220
| alt = 
| caption = 
| image2 = Atomoxetine ball-and-stick model.png
| width2 = 240
| alt2 =

<!-- Clinical data -->
| pronounce = 
| tradename = Strattera, [[#Brand_names|others]]
| Drugs.com = {{drugs.com|monograph|atomoxetine-hydrochloride}}
| MedlinePlus = a603013
| DailyMedID = Atomoxetine
| pregnancy_AU = B3
| pregnancy_AU_comment = <ref name="Drugs.com pregnancy">{{cite web | title=Atomoxetine (Strattera) Use During Pregnancy | website=Drugs.com | date=22 August 2019 | url=https://www.drugs.com/pregnancy/atomoxetine.html | access-date=7 February 2020 | archive-date=22 March 2019 | archive-url=https://web.archive.org/web/20190322181637/https://www.drugs.com/pregnancy/atomoxetine.html | url-status=live }}</ref>
| pregnancy_category = 
| routes_of_administration = [[Oral administration|By mouth]]
| class = [[Norepinephrine reuptake inhibitor]]
| ATC_prefix = N06
| ATC_suffix = BA09
| ATC_supplemental =

<!-- Legal status -->
| legal_AU = S4
| legal_AU_comment = 
| legal_BR = C1
| legal_BR_comment = <ref>{{cite web |author=Anvisa |author-link=Brazilian Health Regulatory Agency |date=15 September 2023 |title=RDC Nº 816 - Listas de Substâncias Entorpecentes, Psicotrópicas, Precursoras e Outras sob Controle Especial |trans-title=Collegiate Board Resolution No. 816 - Lists of Narcotic, Psychotropic, Precursor, and Other Substances under Special Control|url=https://www.in.gov.br/en/web/dou/-/resolucao-rdc-n-816-de-15-de-setembro-de-2023-510390164 |url-status=live |archive-url=https://web.archive.org/web/20231019120956/https://www.in.gov.br/en/web/dou/-/resolucao-rdc-n-816-de-15-de-setembro-de-2023-510390164 |archive-date=19 October 2023 |access-date=19 October 2023 |publisher=[[Diário Oficial da União]] |language=pt-BR |publication-date=18 September 2023}}</ref>
| legal_CA = Rx-only
| legal_CA_comment = 
| legal_DE = <!-- Anlage I, II, III or Unscheduled -->
| legal_DE_comment = 
| legal_NZ = Prescription only
| legal_UK = POM
| legal_UK_comment = <ref>{{cite web | title=Strattera 10mg hard capsules - Summary of Product Characteristics (SmPC) | website=(emc) | date=8 February 2021 | url=https://www.medicines.org.uk/emc/product/5531/smpc | access-date=11 June 2022 | archive-date=8 October 2021 | archive-url=https://web.archive.org/web/20211008174322/https://www.medicines.org.uk/emc/product/5531/smpc | url-status=live }}</ref>
| legal_US = Rx-only
| legal_US_comment = <ref name="Strattera FDA label" />
| legal_EU = Rx-only
| legal_EU_comment = <ref>{{cite web |url=https://www.ema.europa.eu/en/documents/psusa/atomoxetine-list-nationally-authorised-medicinal-products-psusa/00000262/201511_en.pdf |title=Active substance(s): atomoxetine | work = List of nationally authorised medicinal products| publisher =  European Medicines Agency | date = 2016 |access-date=12 June 2022 |archive-date=12 June 2022 |archive-url=https://web.archive.org/web/20220612030231/https://www.ema.europa.eu/en/documents/psusa/atomoxetine-list-nationally-authorised-medicinal-products-psusa/00000262/201511_en.pdf |url-status=live }}</ref>
| legal_UN = <!-- N I, II, III, IV / P I, II, III, IV -->
| legal_UN_comment = 
| legal_status = <!-- For countries not listed above -->

<!-- Pharmacokinetic data -->
| bioavailability = 63–94%<ref name = MSR>{{cite web|title= Atomoxetine (Rx) – Strattera|work=Medscape Reference|publisher=WebMD|access-date=10 November 2013|url=http://reference.medscape.com/drug/strattera-atomoxetine-342994|archive-url=https://web.archive.org/web/20131110153513/http://reference.medscape.com/drug/strattera-atomoxetine-342994|archive-date=10 November 2013|url-status=live}}</ref><ref name = TGA /><ref name = DM>{{cite web|title=Atomoxetine Hydrochloride capsule [Mylan Pharmaceuticals Inc.]|work=DailyMed|publisher=Mylan Pharmaceuticals Inc.|date=October 2011|access-date=10 November 2013|url=https://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=bdab7205-d0ff-41c3-8430-2d399dfaa759|archive-url=https://web.archive.org/web/20131110152856/http://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=bdab7205-d0ff-41c3-8430-2d399dfaa759|archive-date=10 November 2013|url-status=live}}</ref>
| protein_bound = 98%<ref name = MSR /><ref name = TGA /><ref name = DM />
| metabolism = [[Liver]], via [[CYP2D6]]<ref name = MSR /><ref name = TGA /><ref name = DM />
| metabolites = 
| onset = 
| elimination_half-life = 4.5–25 hours<ref name = MSR /><ref name = TGA /><ref name = DM /><ref name = Sa2005/><ref name = PMID26314574/>
| duration_of_action = 
| excretion = [[Kidney]] (80%) and faecal (17%)<ref name = MSR /><ref name = TGA /><ref name = DM />

<!-- Identifiers -->
| index2_label = as HCl
| CAS_number_Ref = {{cascite|correct|CAS}}
| CAS_number = 83015-26-3
| CAS_number2 = 82248-59-7
| CAS_supplemental = 
| PubChem = 54841
| PubChem2 = 54840
| IUPHAR_ligand = 7118
| DrugBank_Ref = {{drugbankcite|correct|drugbank}}
| DrugBank = DB00289
| DrugBank2 = DBSALT001207
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChemSpiderID = 49516
| ChemSpiderID2 = 49515
| UNII_Ref = {{fdacite|correct|FDA}}
| UNII = ASW034S0B8
| UNII2 = 57WVB6I2W0
| KEGG_Ref = {{keggcite|correct|kegg}}
| KEGG = D07473
| KEGG2 = D02574
| ChEBI_Ref = {{ebicite|correct|EBI}}
| ChEBI = 127342
| ChEBI2 = 331697
| ChEMBL_Ref = {{ebicite|correct|EBI}}
| ChEMBL = 641
| ChEMBL2 = 1702
| NIAID_ChemDB = 
| PDB_ligand = 
| synonyms = (''R'')-''N''-Methyl-3-phenyl-3-(''o''-tolyloxy)propan-1-amine

<!-- Chemical and physical data -->
| IUPAC_name = (3''R'')-''N''-Methyl-3-(2-methylphenoxy)-3-phenylpropan-1-amine
| C = 17
| H = 21
| N = 1
| O = 1
| SMILES = CC1=C(C=CC=C1)O[C@H](CCNC)C2=CC=CC=C2
| StdInChI_Ref = {{stdinchicite|correct|chemspider}}
| StdInChI = 1S/C17H21NO/c1-14-8-6-7-11-16(14)19-17(12-13-18-2)15-9-4-3-5-10-15/h3-11,17-18H,12-13H2,1-2H3/t17-/m1/s1
| StdInChI_comment = 
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = VHGCDTVCOLNTBX-QGZVFWFLSA-N
| density = 
| density_notes = 
| melting_point = 
| melting_high = 
| melting_notes = 
| boiling_point = 
| boiling_notes = 
| solubility = 
| sol_units = 
| specific_rotation = 
}}

'''Atomoxetine''', sold under the brand name '''Strattera''',<ref>{{cite web |date=3 March 2023 | title=STRATTERA® (atomoxetine capsules) to be discontinued as of March 2023 | url=https://www.caddra.ca/treatment-update-strattera-atomoxetine-capsules-to-be-discontinued-as-of-march-2023-2/}}</ref> is a [[selective norepinephrine reuptake inhibitor]] (sNRI) medication used to treat [[attention deficit hyperactivity disorder]] (ADHD)<ref name=AHFS2019>{{cite web |title=Atomoxetine Hydrochloride Monograph for Professionals |url=https://www.drugs.com/monograph/atomoxetine-hydrochloride.html |website=Drugs.com |publisher=American Society of Health-System Pharmacists |access-date=22 March 2019 |archive-url=https://web.archive.org/web/20190404041202/https://www.drugs.com/monograph/atomoxetine-hydrochloride.html |archive-date=4 April 2019 |url-status=live }}</ref> and, to a lesser extent, [[cognitive disengagement syndrome]] (CDS).<ref name="Atomoxetine-Related Change in Slugg">{{cite journal | vauthors = McBurnett K, Clemow D, Williams D, Villodas M, Wietecha L, Barkley R | title = Atomoxetine-Related Change in Sluggish Cognitive Tempo Is Partially Independent of Change in Attention-Deficit/Hyperactivity Disorder Inattentive Symptoms | journal = Journal of Child and Adolescent Psychopharmacology | volume = 27 | issue = 1 | pages = 38–42 | date = February 2017 | pmid = 27845858 | doi = 10.1089/cap.2016.0115 }}</ref><ref name="Report of a Work Group on Sluggish">{{cite journal | vauthors = Becker SP, Willcutt EG, Leopold DR, Fredrick JW, Smith ZR, Jacobson LA, Burns GL, Mayes SD, Waschbusch DA, Froehlich TE, McBurnett K, Servera M, Barkley RA | title = Report of a Work Group on Sluggish Cognitive Tempo: Key Research Directions and a Consensus Change in Terminology to Cognitive Disengagement Syndrome | journal = Journal of the American Academy of Child and Adolescent Psychiatry | volume = 62 | issue = 6 | pages = 629–645 | date = June 2023 | pmid = 36007816 | pmc = 9943858 | doi = 10.1016/j.jaac.2022.07.821 }}</ref><ref name="Atomoxetine improved attention in c">{{cite journal | vauthors = Wietecha L, Williams D, Shaywitz S, Shaywitz B, Hooper SR, Wigal SB, Dunn D, McBurnett K | title = Atomoxetine improved attention in children and adolescents with attention-deficit/hyperactivity disorder and dyslexia in a 16 week, acute, randomized, double-blind trial | journal = Journal of Child and Adolescent Psychopharmacology | volume = 23 | issue = 9 | pages = 605–613 | date = November 2013 | pmid = 24206099 | pmc = 3842866 | doi = 10.1089/cap.2013.0054 }}</ref> It may be used alone or along with [[Stimulant|stimulant medication]].<ref name="Tr2013">{{cite journal | vauthors = Treuer T, Gau SS, Méndez L, Montgomery W, Monk JA, Altin M, Wu S, Lin CC, Dueñas HJ | title = A systematic review of combination therapy with stimulants and atomoxetine for attention-deficit/hyperactivity disorder, including patient characteristics, treatment strategies, effectiveness, and tolerability | journal = Journal of Child and Adolescent Psychopharmacology | volume = 23 | issue = 3 | pages = 179–193 | date = April 2013 | pmid = 23560600 | pmc = 3696926 | doi = 10.1089/cap.2012.0093 }}</ref><ref>{{cite web |archive-url = https://web.archive.org/web/20170202064443/https://www.psychiatry.org/patients-families/adhd/what-is-adhd |type = Guidelines (Tertiary source) |archive-date = 2 February 2017 |url = https://www.psychiatry.org/patients-families/adhd/what-is-adhd |title = Parent's Medication Guide: ADHD |date = June 2013 |website = American Psychiatric Association |publisher = American Psychiatric Association & American Academy of Child and Adolescent Psychiatry (AACAP)|quote = Though not FDA-approved for combined treatment, atomoxetine (Strattera) is sometimes used in conjunction with stimulants as an off-label combination therapy.|url-status = live |access-date = 1 January 2017}}</ref> It enhances the [[executive functions]] of self-motivation, sustained attention, [[Cognitive inhibition|inhibition]], [[working memory]], [[reaction time]],<ref>{{cite journal | vauthors = Isfandnia F, El Masri S, Radua J, Rubia K | title = The effects of chronic administration of stimulant and non-stimulant medications on executive functions in ADHD: A systematic review and meta-analysis | journal = Neuroscience and Biobehavioral Reviews | volume = 162 | article-number = 105703 | date = July 2024 | pmid = 38718988 | doi = 10.1016/j.neubiorev.2024.105703 | url = https://kclpure.kcl.ac.uk/portal/en/publications/69dc26fe-1517-438e-9cd7-6788fc396dc9 }}</ref> and [[emotional self-regulation]].<ref>{{cite journal | vauthors = Faraone SV, Banaschewski T, Coghill D, Zheng Y, Biederman J, Bellgrove MA, Newcorn JH, Gignac M, Al Saud NM, Manor I, Rohde LA, Yang L, Cortese S, Almagor D, Stein MA, Albatti TH, Aljoudi HF, Alqahtani MM, Asherson P, Atwoli L, Bölte S, Buitelaar JK, Crunelle CL, Daley D, Dalsgaard S, Döpfner M, Espinet S, Fitzgerald M, Franke B, Gerlach M, Haavik J, Hartman CA, Hartung CM, Hinshaw SP, Hoekstra PJ, Hollis C, Kollins SH, Sandra Kooij JJ, Kuntsi J, Larsson H, Li T, Liu J, Merzon E, Mattingly G, Mattos P, McCarthy S, Mikami AY, Molina BS, Nigg JT, Purper-Ouakil D, Omigbodun OO, Polanczyk GV, Pollak Y, Poulton AS, Rajkumar RP, Reding A, Reif A, Rubia K, Rucklidge J, Romanos M, Ramos-Quiroga JA, Schellekens A, Scheres A, Schoeman R, Schweitzer JB, Shah H, Solanto MV, Sonuga-Barke E, Soutullo C, Steinhausen HC, Swanson JM, Thapar A, Tripp G, van de Glind G, van den Brink W, Van der Oord S, Venter A, Vitiello B, Walitza S, Wang Y | title = The World Federation of ADHD International Consensus Statement: 208 Evidence-based conclusions about the disorder | journal = Neuroscience and Biobehavioral Reviews | volume = 128 | pages = 789–818 | date = September 2021 | pmid = 33549739 | pmc = 8328933 | doi = 10.1016/j.neubiorev.2021.01.022 }}</ref><ref>{{cite journal | vauthors = Kamradt JM, Ullsperger JM, Nikolas MA | title = Executive function assessment and adult attention-deficit/hyperactivity disorder: tasks versus ratings on the Barkley deficits in executive functioning scale | journal = Psychological Assessment | volume = 26 | issue = 4 | pages = 1095–1105 | date = December 2014 | pmid = 24885846 | doi = 10.1037/pas0000006 }}</ref> Use of atomoxetine is only recommended for those who are at least six years old.<ref name="AHFS2019" /> It is taken [[Oral administration|orally]].<ref name="AHFS2019" /> The effectiveness of atomoxetine is comparable to the commonly prescribed stimulant medication [[methylphenidate]]<!-- Do not contextualise by adding "immediate release" as that is inaccurate. The systematic meta-analyses cited conclude that the effectiveness of ATX is comparable to OROS (extended-release) MTP and equivalent (not comparable) to IR in children and adolescents. In adults, it is equivalent to OROS MPH. Therefore, it's correct to leave simply "comparable to methylphenidate". -->.<ref name="Hanwella_2011" /><ref name="Rezaei_2016" /><ref name="Hazell_2011" /><ref name="Bushe_2016" />

Common side effects of atomoxetine include [[abdominal pain]], [[decreased appetite]], [[nausea]], feeling tired, and [[dizziness]].<ref name=AHFS2019/> Serious side effects may include [[angioedema]], liver problems, [[stroke]], [[psychosis]], heart problems, [[suicide]], and [[aggression]].<ref name=AHFS2019/><ref name=BNF76>{{cite book|title=British national formulary: BNF 76|date=2018|publisher=Pharmaceutical Press|isbn=978-0-85711-338-2|pages=344–345|edition=76}}</ref> 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.<ref name=Preg2019>{{cite web |title=Atomoxetine Pregnancy and Breastfeeding Warnings |url=https://www.drugs.com/pregnancy/atomoxetine.html |website=Drugs.com |access-date=3 March 2019 |archive-url=https://web.archive.org/web/20190322181637/https://www.drugs.com/pregnancy/atomoxetine.html |archive-date=22 March 2019 |url-status=live }}</ref><ref name= Ornoy2018/>

It was approved for medical use in the United States in 2002.<ref name=AHFS2019/> In 2023, it was the 161st most commonly prescribed medication in the United States, with more than 3{{nbsp}}million prescriptions.<ref name="Top 300">{{cite web | title=Top 300 of 2023 | url=https://clincalc.com/DrugStats/Top300Drugs.aspx | website=ClinCalc | access-date=12 August 2025 | archive-date=12 August 2025 | archive-url=https://web.archive.org/web/20250812130026/https://clincalc.com/DrugStats/Top300Drugs.aspx | url-status=live }}</ref><ref>{{cite web | title = Atomoxetine Drug Usage Statistics, United States, 2013 - 2023 | website = ClinCalc | url = https://clincalc.com/DrugStats/Drugs/Atomoxetine | access-date = 19 August 2025 }}</ref>

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==Medical uses==

Atomoxetine is [[indicated]] for the treatment of attention deficit hyperactivity disorder (ADHD).<ref name="Strattera FDA label" />

===Attention deficit hyperactivity disorder===
Atomoxetine is approved for use in children, adolescents, and adults.<ref name="Strattera FDA label" /> However, its efficacy has not been studied in children under six years old.<ref name = TGA>{{cite web|title=Strattera (atomoxetine hydrochloride)|work=TGA eBusiness Services|publisher=Eli Lilly Australia Pty. Limited|date=21 August 2013|access-date=10 November 2013|url=https://www.ebs.tga.gov.au/ebs/picmi/picmirepository.nsf/pdf?OpenAgent&id=CP-2010-PI-04269-3|archive-url=https://web.archive.org/web/20170406152455/https://www.ebs.tga.gov.au/ebs/picmi/picmirepository.nsf/pdf?OpenAgent&id=CP-2010-PI-04269-3|archive-date=6 April 2017|url-status=live}}</ref> One of the primary differences with the standard [[psychostimulant|stimulant]] treatments for ADHD is that it has little known abuse potential.<ref name = TGA /> [[Meta-analysis|Meta-analyses]] and [[systematic review]]s have found that atomoxetine has comparable efficacy and equal tolerability to [[methylphenidate]] in children and adolescents. In adults, efficacy and tolerability are equivalent.<ref name="Hanwella_2011">{{cite journal | vauthors = Hanwella R, Senanayake M, de Silva V | title = Comparative efficacy and acceptability of methylphenidate and atomoxetine in treatment of attention deficit hyperactivity disorder in children and adolescents: a meta-analysis | journal = BMC Psychiatry | volume = 11 | article-number = 176 | date = November 2011 | pmid = 22074258 | pmc = 3229459 | doi = 10.1186/1471-244X-11-176 | doi-access = free }}</ref><ref name="Rezaei_2016">{{cite journal | vauthors = Rezaei G, Hosseini SA, Akbari Sari A, Olyaeemanesh A, Lotfi MH, Yassini M, Bidaki R, Nouri B | title = Comparative efficacy of methylphenidate and atomoxetine in the treatment of attention deficit hyperactivity disorder in children and adolescents: A systematic review and meta-analysis | journal = Medical Journal of the Islamic Republic of Iran | volume = 30 | page = 325 | date = 10 February 2016 | pmid = 27390695 | pmc = 4898838 }}</ref><ref name="Hazell_2011">{{cite journal | vauthors = Hazell PL, Kohn MR, Dickson R, Walton RJ, Granger RE, Wyk GW | title = Core ADHD symptom improvement with atomoxetine versus methylphenidate: a direct comparison meta-analysis | journal = Journal of Attention Disorders | volume = 15 | issue = 8 | pages = 674–683 | date = November 2011 | pmid = 20837981 | doi = 10.1177/1087054710379737 | url = http://journals.sagepub.com/doi/10.1177/1087054710379737 | access-date = 7 December 2023 | url-status = live | s2cid = 43503227 | archive-url = https://web.archive.org/web/20231115073753/http://journals.sagepub.com/doi/10.1177/1087054710379737 | archive-date = 15 November 2023 | url-access = subscription }}</ref><ref name="Bushe_2016">{{cite journal | vauthors = Bushe C, Day K, Reed V, Karlsdotter K, Berggren L, Pitcher A, Televantou F, Haynes V | title = A network meta-analysis of atomoxetine and osmotic release oral system methylphenidate in the treatment of attention-deficit/hyperactivity disorder in adult patients | journal = Journal of Psychopharmacology | volume = 30 | issue = 5 | pages = 444–458 | date = May 2016 | pmid = 27005307 | doi = 10.1177/0269881116636105 | url = http://journals.sagepub.com/doi/10.1177/0269881116636105 | access-date = 7 December 2023 | url-status = live | s2cid = 104938 | archive-url = https://web.archive.org/web/20230523141246/https://journals.sagepub.com/doi/10.1177/0269881116636105 | archive-date = 23 May 2023 | url-access = subscription }}</ref>

While its efficacy may be less than that of [[Lisdexamfetamine|lisdexamfetamine]],<ref>{{cite journal | vauthors = Stuhec M, Munda B, Svab V, Locatelli I | title = Comparative efficacy and acceptability of atomoxetine, lisdexamfetamine, bupropion and methylphenidate in treatment of attention deficit hyperactivity disorder in children and adolescents: a meta-analysis with focus on bupropion | journal = Journal of Affective Disorders | volume = 178 | pages = 149–159 | date = June 2015 | pmid = 25813457 | doi = 10.1016/j.jad.2015.03.006 }}</ref> there is some evidence that it may be used in combination with stimulants.<ref name=Tr2013/> 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;<ref name="Home combination">{{cite web | title= Attention Deficit Hyperactivity Disorder | work = National Institute of Mental Health (NIMH) | url=https://www.nimh.nih.gov/health/topics/attention-deficit-hyperactivity-disorder-adhd | access-date=21 July 2018 |archive-url=https://web.archive.org/web/20161225231931/https://www.nimh.nih.gov/health/topics/attention-deficit-hyperactivity-disorder-adhd/index.shtml | archive-date=25 December 2016 | url-status=live }}</ref><ref name="NIMH 2019">{{cite web | title=Mental Health Medications | website=NIMH| url=https://www.nimh.nih.gov/health/topics/mental-health-medications | access-date=17 May 2019 | archive-url=https://web.archive.org/web/20190406082433/https://www.nimh.nih.gov/health/topics/mental-health-medications/index.shtml#part_149861 | archive-date=6 April 2019 | url-status=live }}</ref> when the cost of stimulants is prohibitive; or when there is concern about the abuse potential of stimulants in a patient with a history of [[drug use disorder|substance use disorder]].

Atomoxetine alleviates ADHD symptoms through [[norepinephrine]] reuptake inhibition and by indirectly increasing dopamine in the [[prefrontal cortex]],<ref name="Koda_2010">{{cite journal |vauthors=Koda K, Ago Y, Cong Y, Kita Y, Takuma K, Matsuda T |date=July 2010 |title=Effects of acute and chronic administration of atomoxetine and methylphenidate on extracellular levels of noradrenaline, dopamine and serotonin in the prefrontal cortex and striatum of mice |journal=Journal of Neurochemistry |volume=114 |issue=1 |pages=259–270 |doi=10.1111/j.1471-4159.2010.06750.x |pmid=20403082}}</ref> sharing 70-80% of the brain regions with stimulants in their produced effects.<ref name="Schulz_2012">{{cite journal |vauthors=Schulz KP, Fan J, Bédard AC, Clerkin SM, Ivanov I, Tang CY, Halperin JM, Newcorn JH |date=September 2012 |title=Common and unique therapeutic mechanisms of stimulant and nonstimulant treatments for attention-deficit/hyperactivity disorder |journal=Archives of General Psychiatry |volume=69 |issue=9 |pages=952–961 |doi=10.1001/archgenpsychiatry.2011.2053 |pmid=22945622}}</ref>

Unlike [[Alpha-adrenergic agonist|α<sub>2</sub>-adrenergic receptor agonists]] such as [[guanfacine]] and [[clonidine]], atomoxetine's use can be abruptly stopped without significant [[Drug withdrawal|withdrawal]] symptoms being observed.<ref name = TGA />

The initial therapeutic effects of atomoxetine usually take 1 to 4 weeks to become apparent.<ref name = MSR /><ref name="pmid23438503">{{cite journal | vauthors = Bushe CJ, Savill NC | title = Systematic review of atomoxetine data in childhood and adolescent attention-deficit hyperactivity disorder 2009-2011: focus on clinical efficacy and safety | journal = Journal of Psychopharmacology | volume = 28 | issue = 3 | pages = 204–211 | date = March 2014 | pmid = 23438503 | doi = 10.1177/0269881113478475 | s2cid = 793033 | doi-access = free }}</ref><ref name="pmid26730199">{{cite journal | vauthors = Childress AC | title = A critical appraisal of atomoxetine in the management of ADHD | journal = Therapeutics and Clinical Risk Management | volume = 12 | issue =  | pages = 27–39 | date = 2016 | pmid = 26730199 | pmc = 4694693 | doi = 10.2147/TCRM.S59270 | doi-access = free }}</ref> A further 2 to 4 weeks may be required for the full therapeutic effects to be seen.<ref name="Maudsley">{{cite book | isbn = 978-0-470-97948-8 | title = The Maudsley prescribing guidelines in psychiatry | vauthors = Taylor D, Paton C, Shitij K | year = 2012 | publisher = Wiley-Blackwell | location = West Sussex }}</ref><ref name="pmid23438503" /> Incrementally increasing response may occur up to 1 year or longer.<ref name="pmid26730199" /><ref name="pmid26349559">{{cite journal | vauthors = Clemow DB, Bushe CJ | title = Atomoxetine in patients with ADHD: A clinical and pharmacological review of the onset, trajectory, duration of response and implications for patients | journal = Journal of Psychopharmacology | volume = 29 | issue = 12 | pages = 1221–1230 | date = December 2015 | pmid = 26349559 | doi = 10.1177/0269881115602489 | s2cid = 22649093 }}</ref> The maximum recommended total daily dose in children and adolescents is 70&nbsp;mg and adults is 100&nbsp;mg.<ref name="Strattera FDA label">{{cite web | url = https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=309de576-c318-404a-bc15-660c2b1876fb | title = Strattera- atomoxetine hydrochloride capsule | date = 29 January 2020 | website = DailyMed.gov | publisher = Eli Lilly and Company | access-date = 26 February 2020 | archive-url = https://web.archive.org/web/20180607120316/https://dailymed.nlm.nih.gov/dailymed/getFile.cfm?setid=309de576-c318-404a-bc15-660c2b1876fb&type=pdf&name=309de576-c318-404a-bc15-660c2b1876fb | archive-date = 7 June 2018 | url-status = live }}</ref>

===Other uses===

==== Cognitive disengagement syndrome ====

Atomoxetine may be used to treat [[cognitive disengagement syndrome]] (CDS),<ref name="Report of a Work Group on Sluggish"/> as multiple [[Randomized controlled trial|randomised controlled clinical trials]] (RCTs) have found that it is an effective treatment.<ref name="Report of a Work Group on Sluggish"/><ref name="Atomoxetine-Related Change in Slugg"/><ref name="Atomoxetine improved attention in c"/> In contrast, multiple RCTs have shown that it responds poorly to the stimulant medication [[methylphenidate]].<ref>{{cite journal | vauthors = Fırat S, Gul H, Aysev A | title = An Open-Label Trial of Methylphenidate Treating Sluggish Cognitive Tempo, Inattention, and Hyperactivity/Impulsivity Symptoms Among 6- to 12-Year-Old ADHD Children: What Are the Predictors of Treatment Response at Home and School? | journal = Journal of Attention Disorders | volume = 25 | issue = 9 | pages = 1321–1330 | date = July 2021 | pmid = 32064995 | doi = 10.1177/1087054720902846 | s2cid = 211134241 }}</ref><ref>{{cite journal | vauthors = Froehlich TE, Becker SP, Nick TG, Brinkman WB, Stein MA, Peugh J, Epstein JN | title = Sluggish Cognitive Tempo as a Possible Predictor of Methylphenidate Response in Children With ADHD: A Randomized Controlled Trial | journal = The Journal of Clinical Psychiatry | volume = 79 | issue = 2 | article-number = 17m11553 | date = 2018 | pmid = 29489078 | pmc = 6558969 | doi = 10.4088/JCP.17m11553 }}</ref><ref>{{cite journal | vauthors = Barkley RA, DuPaul GJ, McMurray MB | title = Attention deficit disorder with and without hyperactivity: clinical response to three dose levels of methylphenidate | journal = Pediatrics | volume = 87 | issue = 4 | pages = 519–531 | date = April 1991 | doi = 10.1542/peds.87.4.519 | pmid = 2011430 | s2cid = 23501657 }}</ref><ref>{{cite book | vauthors = Barkley RA | chapter = Concentration deficit disorder (sluggish cognitive tempo). | title = Attention-deficit hyperactivity disorder: A handbook for diagnosis and treatment. | publisher = The Guilford Press | date = 2015 | pages = 81–115 | chapter-url = https://www.peterraabe.ca/docs/SCT_Barkley.pdf | access-date = 28 February 2024 | archive-date = 16 January 2024 | archive-url = https://web.archive.org/web/20240116211606/https://peterraabe.ca/docs/SCT_Barkley.pdf | url-status = live }}</ref><!-- For Barkley et al., 1991 (cited) found specifically ADHD-IN/CDS symptoms linked to a poor treatment response (20%) to methylphenidate; for those who responded, the benefits were small and low doses were best. Subsequently, Barkley, 2014 (cited) confirmed that the significant results are linked to CDS (Barkley, 2014). -->

==== Traumatic brain injury ====

Atomoxetine is sometimes used in the treatment of [[cognitive impairment]] and [[frontal lobe]] symptoms due to conditions like [[traumatic brain injury]] (TBI).<ref name="pmid16456396">{{cite journal | vauthors = Ripley DL | title = Atomoxetine for individuals with traumatic brain injury | journal = The Journal of Head Trauma Rehabilitation | volume = 21 | issue = 1 | pages = 85–88 | date = 2006 | pmid = 16456396 | doi = 10.1097/00001199-200601000-00010 }}</ref><ref name="pmid32044373">{{cite journal | vauthors = Arnts H, van Erp WS, Lavrijsen JC, van Gaal S, Groenewegen HJ, van den Munckhof P | title = On the pathophysiology and treatment of akinetic mutism | journal = Neuroscience and Biobehavioral Reviews | volume = 112 | issue =  | pages = 270–278 | date = May 2020 | pmid = 32044373 | doi = 10.1016/j.neubiorev.2020.02.006 | hdl-access = free | s2cid = 211053123 | doi-access = free | hdl = 2066/225901 }}</ref> It is used to treat ADHD-like symptoms such as [[attention|sustained attention]]al problems, disinhibition,<ref name="pmid24295630">{{cite journal | vauthors = Termine C, Selvini C, Rossi G, Balottin U | title = Emerging treatment strategies in Tourette syndrome: what's in the pipeline? | journal = International Review of Neurobiology | volume = 112 | issue = | pages = 445–80 | date = 2013 | pmid = 24295630 | doi = 10.1016/B978-0-12-411546-0.00015-9 | quote = Atomoxetine is a nonstimulant drug used to treat ADHD (Perwien et al., 2006) that acts as a presynaptic blocker of noradrenalin reuptake (Swanson et al., 2006). }}</ref> lack of [[arousal]], [[fatigue (medical)|fatigue]], and [[depression (mood)|depression]], including symptoms from [[cognitive disengagement syndrome]].<ref name="pmid16456396" /> A 2015 [[Cochrane review]] identified only one study of atomoxetine for TBI and found no positive effects.<ref name="pmid26624881">{{cite journal | vauthors = Dougall D, Poole N, Agrawal N | title = Pharmacotherapy for chronic cognitive impairment in traumatic brain injury | journal = The Cochrane Database of Systematic Reviews | volume =  | issue = 12 | article-number = CD009221 | date = December 2015 | pmid = 26624881 | doi = 10.1002/14651858.CD009221.pub2 | pmc = 11092927 }}</ref> Aside from TBI, atomoxetine was found to be effective in the treatment of [[akinetic mutism]] following [[subarachnoid hemorrhage]] in a [[case report]].<ref name="pmid32044373" /><ref name="pmid20661027">{{cite journal | vauthors = Kim YW, Shin JC, An YS | title = Treatment of chronic akinetic mutism with atomoxetine: subtraction analysis of brain f-18 fluorodeoxyglucose positron emission tomographic images before and after medication: a case report | journal = Clinical Neuropharmacology | volume = 33 | issue = 4 | pages = 209–211 | date = July 2010 | pmid = 20661027 | doi = 10.1097/WNF.0b013e3181dca948 | url = https://ir.ymlib.yonsei.ac.kr/handle/22282913/101391 }}</ref>

==Contraindications==
[[Contraindications]] include:<ref name = TGA />

* Any [[cardiovascular disease]] including:
** Moderate to severe [[hypertension]]
** [[Atrial fibrillation]]
** [[Atrial flutter]]
** [[Ventricular tachycardia]]
** [[Ventricular fibrillation]]
** [[Ventricular flutter]]
** Advanced [[arteriosclerosis]]
* Severe cardiovascular disorders
* Uncontrolled [[hyperthyroidism]]
* [[Pheochromocytoma]]
* Concomitant treatment with [[monoamine oxidase inhibitors]] (MAOIs)
* Narrow-angle [[glaucoma]]

== Adverse effects ==
Common side effects include [[abdominal pain]], [[decreased appetite]], [[nausea]], [[erectile dysfunction]], feeling tired, [[dizziness]]<ref name="AHFS2019" /> and [[urinary retention]].<ref>{{cite journal | vauthors = Whiskey E, Taylor D | title = A review of the adverse effects and safety of noradrenergic antidepressants | journal = Journal of Psychopharmacology | volume = 27 | issue = 8 | pages = 732–739 | date = August 2013 | pmid = 23784737 | doi = 10.1177/0269881113492027 | quote = In adult ADHD controlled trials, the rates of urinary retention (1.7%, 9/540) and urinary hesitation (5.6%, 30/540) were increased among atomoxetine subjects compared with placebo subjects (0%, 0/402; 0.5%, 2/402, respectively). }}</ref> Serious side effects may include [[angioedema]], liver problems, [[stroke]], [[psychosis]], heart problems, [[suicide]], and aggression.<ref name="AHFS2019" /><ref name="BNF76" /> A 2020 meta-analysis found that atomoxetine was associated with [[Anorexia (symptom)|anorexia]], [[weight loss]], and [[hypertension]], rating it as a "potentially least preferred agent based on safety" for treating ADHD.<ref name= Solmi2020>{{cite journal | vauthors = Solmi M, Fornaro M, Ostinelli EG, Zangani C, Croatto G, Monaco F, Krinitski D, Fusar-Poli P, Correll CU | title = Safety of 80 antidepressants, antipsychotics, anti-attention-deficit/hyperactivity medications and mood stabilizers in children and adolescents with psychiatric disorders: a large scale systematic meta-review of 78 adverse effects | journal = World Psychiatry | volume = 19 | issue = 2 | pages = 214–232 | date = June 2020 | pmid = 32394557 | pmc = 7215080 | doi = 10.1002/wps.20765 | type = Meta-analysis }}</ref><ref>{{cite journal |date=1 September 2020 |title=Psychiatric drugs given to children and adolescents have been ranked in order of safety |url=https://evidence.nihr.ac.uk/alert/psychiatric-drugs-given-to-children-and-adolescents-have-been-ranked-in-order-of-safety/ |journal=NIHR Evidence |type=Plain English summary |doi=10.3310/alert_40795 |s2cid=241309451 |access-date=12 March 2022 |archive-date=21 January 2022 |archive-url=https://web.archive.org/web/20220121102841/https://evidence.nihr.ac.uk/alert/psychiatric-drugs-given-to-children-and-adolescents-have-been-ranked-in-order-of-safety/ |url-status=live |url-access=subscription }}</ref> As of 2019, safety in [[pregnancy]] and [[breastfeeding]] is not clear;<ref name="Preg2019" /> a 2018 review stated that, "because of lack of data, the treating
physician should consider stopping atomoxetine treatment in women with ADHD during pregnancy."<ref name= Ornoy2018>{{cite journal | vauthors = Ornoy A | title = Pharmacological Treatment of Attention Deficit Hyperactivity Disorder During Pregnancy and Lactation | journal = Pharmaceutical Research | volume = 35 | issue = 3 | article-number = 46 | date = February 2018 | pmid = 29411149 | doi = 10.1007/s11095-017-2323-z | type = Review | s2cid = 3663423 }}</ref>

The U.S. [[Food and Drug Administration]] (FDA) has issued a [[black box warning]] for [[Suicidal ideation|suicidal behavior/ideation]].<ref name="DM" /> Similar warnings have been issued in Australia.<ref name="TGA" /><ref>{{cite journal | url = http://www.australianprescriber.com/magazine/36/5/166/9|title=Atomoxetine and suicidality in children and adolescents|date=October 2013| journal = Australian Prescriber | volume = 4 | issue =  5 | page = 166 |access-date=10 November 2013|archive-url=https://web.archive.org/web/20150330113305/http://www.australianprescriber.com/magazine/36/5/166/9 |archive-date=30 March 2015 |url-status=usurped }}</ref> Unlike stimulant medications, atomoxetine does not have abuse liability or the potential to cause [[Drug withdrawal|withdrawal]] effects upon abrupt discontinuation.<ref name="TGA" /><ref>{{cite journal | vauthors = Wernicke JF, Adler L, Spencer T, West SA, Allen AJ, Heiligenstein J, Milton D, Ruff D, Brown WJ, Kelsey D, Michelson D | title = Changes in symptoms and adverse events after discontinuation of atomoxetine in children and adults with attention deficit/hyperactivity disorder: a prospective, placebo-controlled assessment | journal = Journal of Clinical Psychopharmacology | volume = 24 | issue = 1 | pages = 30–35 | date = February 2004 | pmid = 14709944 | doi = 10.1097/01.jcp.0000104907.75206.c2 | s2cid = 37636280 }}</ref>

==Overdose==
Atomoxetine can lead to cardiac complications, with severe overdose requiring intensive medical care to avoid death.<ref>{{cite journal | title=Refractory cardiogenic shock due to atomoxetine overdose rescued by venoarterial extracorporeal membrane oxygenation: A case report | journal=Acute Medicine & Surgery | date=29 August 2024 | doi=10.1002/ams2.70001 | volume=11 | issue=1 | article-number=e70001 | pmid=39211522 | pmc=11359704 | vauthors = Komoriya K, Kitagawa K, Mihara Y, Hagiwara K, Hatanaka Y, Hikone M, Sugiyama K }}</ref>

== Interactions ==

Atomoxetine is a [[substrate (biochemistry)|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.<ref name = PMID27518170>{{cite journal | vauthors = Todor I, Popa A, Neag M, Muntean D, Bocsan C, Buzoianu A, Vlase L, Gheldiu AM, Briciu C | title = Evaluation of a Potential Metabolism-Mediated Drug-Drug Interaction Between Atomoxetine and Bupropion in Healthy Volunteers | journal = Journal of Pharmacy & Pharmaceutical Sciences | volume = 19 | issue = 2 | pages = 198–207 | date = April–June 2016 | pmid = 27518170 | doi = 10.18433/j3h03r | doi-access = free }}</ref><ref name = PMID21765848>{{cite journal | vauthors = Kasi PM, Mounzer R, Gleeson GH | title = Cardiovascular side effects of atomoxetine and its interactions with inhibitors of the cytochrome p450 system | journal = Case Reports in Medicine | volume = 2011 | article-number = 952584 | date = 2011 | pmid = 21765848 | pmc = 3135225 | doi = 10.1155/2011/952584 | doi-access = free }}</ref><ref name = PMID12412820>{{cite journal | vauthors = Belle DJ, Ernest CS, Sauer JM, Smith BP, Thomasson HR, Witcher JW | title = Effect of potent CYP2D6 inhibition by paroxetine on atomoxetine pharmacokinetics | journal = Journal of Clinical Pharmacology | volume = 42 | issue = 11 | pages = 1219–1227 | date = November 2002 | pmid = 12412820 | doi = 10.1177/009127002762491307 | s2cid = 40283275 | doi-access = free }}</ref>

Atomoxetine has been found to directly inhibit [[hERG]] potassium currents with an [[IC50|IC<sub>50</sub>]] of 6.3&nbsp;μM, which has the potential to cause [[Heart arrhythmia|arrhythmia]].<ref name = PMID21765848/><ref name = PMID19154426>{{cite journal | vauthors = Scherer D, Hassel D, Bloehs R, Zitron E, von Löwenstern K, Seyler C, Thomas D, Konrad F, Bürgers HF, Seemann G, Rottbauer W, Katus HA, Karle CA, Scholz EP | title = Selective noradrenaline reuptake inhibitor atomoxetine directly blocks hERG currents | journal = British Journal of Pharmacology | volume = 156 | issue = 2 | pages = 226–236 | date = January 2009 | pmid = 19154426 | pmc = 2697834 | doi = 10.1111/j.1476-5381.2008.00018.x }}</ref> [[QT prolongation]] has been reported with atomoxetine at therapeutic doses and in overdose; it is suggested that atomoxetine not be used with other [[Drug-induced QT prolongation|medications that may prolong the QT interval]], concomitantly with CYP2D6 inhibitors, and caution to be used in poor metabolizers.<ref name = PMID21765848/>

Other notable drug interactions include:

* [[Antihypertensive]] agents, due to atomoxetine acting as an indirect sympathomimetic
* Indirect-acting [[sympathomimetic]]s, such as [[pseudoephedrine]], other [[norepinephrine reuptake inhibitors]] (NRIs), or [[Monoamine oxidase inhibitor|MAOIs]]
* Direct-acting sympathomimetics, such as [[phenylephrine]] or other [[Alpha-1 adrenergic receptor#Ligands|α<sub>1</sub>-adrenergic receptor agonists]], including [[vasopressors]] such as [[dobutamine]] or [[isoprenaline]] and [[Beta2-adrenergic agonist|β<sub>2</sub>-adrenergic receptor 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]]<ref name="Sa2005">{{cite journal |vauthors=Sauer JM, Ring BJ, Witcher JW |date=2005 |title=Clinical pharmacokinetics of atomoxetine |journal=Clinical Pharmacokinetics |volume=44 |issue=6 |pages=571–590 |doi=10.2165/00003088-200544060-00002 |pmid=15910008 |s2cid=25708096}}</ref><ref name = part2>{{cite web|title=21-411 Strattera Clinical Pharmacology Biopharmaceutics Review Part 2|url=https://www.accessdata.fda.gov/drugsatfda_docs/nda/2002/21-411_Strattera_biopharmr_P2.pdf|website=U.S. [[Food and Drug Administration]] (FDA)|access-date=6 August 2017|archive-url=https://web.archive.org/web/20170301134914/http://www.accessdata.fda.gov/drugsatfda_docs/nda/2002/21-411_Strattera_biopharmr_P2.pdf|archive-date=1 March 2017}}</ref>

Atomoxetine prevents [[norepinephrine]] release induced by [[amphetamine-type stimulant|amphetamine]]s and has been found to reduce the [[stimulant]], [[euphoriant]], and [[sympathomimetic]] effects of [[dextroamphetamine]] in humans.<ref name="TreuerGauMéndez2013">{{cite journal | vauthors = Treuer T, Gau SS, Méndez L, Montgomery W, Monk JA, Altin M, Wu S, Lin CC, Dueñas HJ | title = A systematic review of combination therapy with stimulants and atomoxetine for attention-deficit/hyperactivity disorder, including patient characteristics, treatment strategies, effectiveness, and tolerability | journal = J Child Adolesc Psychopharmacol | volume = 23 | issue = 3 | pages = 179–193 | date = April 2013 | pmid = 23560600 | pmc = 3696926 | doi = 10.1089/cap.2012.0093 | url = }}</ref><ref name="HealSmithFindling2012">{{cite book | vauthors = Heal DJ, Smith SL, Findling RL | title = Behavioral Neuroscience of Attention Deficit Hyperactivity Disorder and Its Treatment | chapter = ADHD: current and future therapeutics | series = Current Topics in Behavioral Neurosciences | volume = 9 | pages = 361–390 | date = 2012 | pmid = 21487953 | doi = 10.1007/7854_2011_125 | isbn = 978-3-642-24611-1 | chapter-url = | quote = Adjunctive therapy with DL-methylphenidate in atomoxetine partial responders has been successful (Wilens et al. 2009), but this also increases the rates of insomnia, irritability and loss of appetite (Hammerness et al. 2009). This combination therapy has not included amphetamine because blockade of NET by atomoxetine prevents entry of amphetamine into presynaptic noradrenergic terminals (Sofuoglu et al. 2009). }}</ref><ref name="SofuogluPolingHill2009">{{cite journal | vauthors = Sofuoglu M, Poling J, Hill K, Kosten T | title = Atomoxetine attenuates dextroamphetamine effects in humans | journal = Am J Drug Alcohol Abuse | volume = 35 | issue = 6 | pages = 412–416 | date = 2009 | pmid = 20014909 | pmc = 2796580 | doi = 10.3109/00952990903383961 | url = }}</ref>

==Pharmacology==

===Pharmacodynamics===
{| class="wikitable floatright" style="font-size:small;"
|+Atomoxetine (and metabolites)<ref name="PDSP">{{cite web | title = PDSP K<sub>i</sub> Database | work = Psychoactive Drug Screening Program (PDSP) | vauthors = Roth BL, Driscol J | author1-link = Bryan Roth | publisher = University of North Carolina at Chapel Hill and the United States National Institute of Mental Health | access-date = 14 August 2017 | url = https://pdsp.unc.edu/databases/pdsp.php?knowID=0&kiKey=&receptorDD=&receptor=&speciesDD=&species=&sourcesDD=&source=&hotLigandDD=&hotLigand=&testLigandDD=&testFreeRadio=testFreeRadio&testLigand=atomoxetine&referenceDD=&reference=&KiGreater=&KiLess=&kiAllRadio=all&doQuery=Submit+Query | archive-date = 27 August 2021 | archive-url = https://web.archive.org/web/20210827232047/https://pdsp.unc.edu/databases/pdsp.php?knowID=0&kiKey=&receptorDD=&receptor=&speciesDD=&species=&sourcesDD=&source=&hotLigandDD=&hotLigand=&testLigandDD=&testFreeRadio=testFreeRadio&testLigand=atomoxetine&referenceDD=&reference=&KiGreater=&KiLess=&kiAllRadio=all&doQuery=Submit+Query | url-status = live }}</ref><ref name="Upadhyaya Desaiah Schuh Bymaster pp. 189–200">{{cite journal | vauthors = Upadhyaya HP, Desaiah D, Schuh KJ, Bymaster FP, Kallman MJ, Clarke DO, Durell TM, Trzepacz PT, Calligaro DO, Nisenbaum ES, Emmerson PJ, Schuh LM, Bickel WK, Allen AJ | title = A review of the abuse potential assessment of atomoxetine: a nonstimulant medication for attention-deficit/hyperactivity disorder | journal = Psychopharmacology | volume = 226 | issue = 2 | pages = 189–200 | date = March 2013 | pmid = 23397050 | pmc = 3579642 | doi = 10.1007/s00213-013-2986-z | publisher = Springer Nature }}</ref>
|-
! Site !! {{abbr|ATX|Atomoxetine}} !! {{abbr|4-OH-ATX|4-Hydroxyatomoxetine}} !! {{abbr|N-DM-ATX|''N''-Desmethylatomoxetine}}
|-
| '''{{abbrlink|SERT|Serotonin transporter}}''' || '''77''' || '''43''' || {{abbr|ND|No data}}
|-
| '''{{abbrlink|NET|Norepinephrine transporter}}''' || '''5''' || '''3''' || '''92'''
|-
| [[Dopamine transporter|DAT]] || 1,451 || {{abbr|ND|No data}} || {{abbr|ND|No data}}
|-
| '''{{abbrlink|MOR|μ-Opioid receptor}}''' || >1,000<ref name="PMID15225731" /> || '''422''' (antagonist?) || {{abbr|ND|No data}}
|-
| {{abbrlink|DOR|δ-Opioid receptor}} || {{abbr|ND|No data}} || '''300''' (antagonist?) || {{abbr|ND|No data}}
|-
| '''{{abbrlink|KOR|κ-Opioid receptor}}''' || >1,000?<ref name="PMID15225731" /> || '''95''' (partial agonist) || {{abbr|ND|No data}}
|-
| [[Sigma-1 receptor|σ<sub>1</sub>]] || >1,000 || {{abbr|ND|No data}} || {{abbr|ND|No data}}
|-
| '''[[GABAA receptor|GABA<sub>A</sub>]]''' || '''200''' || >30,000 || >10,000
|-
| '''[[NMDA receptor|NMDA]]''' || '''0.66 - 3,470<sup>a</sup>''' || {{abbr|ND|No data}} || {{abbr|ND|No data}}
|-
|
|-
| [[5-HT1A receptor|5-HT<sub>1A</sub>]] || >1,000 || {{abbr|ND|No data}} || {{abbr|ND|No data}}
|-
| [[5-HT1B receptor|5-HT<sub>1B</sub>]] || >1,000 || {{abbr|ND|No data}} || {{abbr|ND|No data}}
|-
| [[5-HT1D receptor|5-HT<sub>1D</sub>]] || >1,000 || {{abbr|ND|No data}} || {{abbr|ND|No data}}
|-
| [[5-HT2 receptor|5-HT<sub>2</sub>]] || 2,000 || 1,000 || 1,700
|-
| [[5-HT6 receptor|5-HT<sub>6</sub>]] || >1,000 || {{abbr|ND|No data}} || {{abbr|ND|No data}}
|-
| [[5-HT7 receptor|5-HT<sub>7</sub>]] || >1,000 || {{abbr|ND|No data}} || {{abbr|ND|No data}}
|-
| [[Alpha-1 adrenergic receptor|α<sub>1</sub>]] || 11,400 || 20,000 || 19,600
|-
| [[Alpha-2A adrenergic receptor|α<sub>2A</sub>]] || 29,800 || >30,000 || >10,000
|-
| [[Beta-1 adrenergic receptor|β<sub>1</sub>]] || 18,000 || 56,100 || 32,100
|-
| [[Muscarinic acetylcholine receptor M1|M<sub>1</sub>]] || >100,000 || >100,000 || >100,000
|-
| [[Muscarinic acetylcholine receptor M2|M<sub>2</sub>]] || >100,000 || >100,000 || >100,000
|-
| [[Dopamine receptor D1|D<sub>1</sub>]] || >10,000 || >10,000 || >10,000
|-
| [[Dopamine receptor D2|D<sub>2</sub>]] || >10,000 || >10,000 || >10,000
|-
| [[Histamine receptor|H<sub>1</sub>]] || 12,100 || >100,000 || >100,000
|-
| [[G protein-coupled inwardly-rectifying potassium channel|K<sub>ir</sub>3.1/3.2]] || 10,900<sup>b</sup> || {{abbr|ND|No data}} || {{abbr|ND|No data}}
|-
| [[G protein-coupled inwardly-rectifying potassium channel|K<sub>ir</sub>3.2]] || 12,400<sup>b</sup> || {{abbr|ND|No data}} || {{abbr|ND|No data}}
|-
| [[G protein-coupled inwardly-rectifying potassium channel|K<sub>ir</sub>3.1/3.4]] || 6,500<sup>b</sup> || {{abbr|ND|No data}} || {{abbr|ND|No data}}
|-
| [[hERG]] || 6,300 || 20,000 || 5,710
|- class="sortbottom"
| colspan="5" style="width: 1px;" | Values are K<sub>i</sub> (nM). The smaller the value, the more strongly the drug binds to the site. All values are for human receptors unless otherwise specified. <sup>a</sup>rat cortex. <sup>b</sup>''Xenopus'' oocytes. Additional sources:<ref name = NPP2002 /><ref name="PMID15225731" /><ref name = Sa2005/><ref name = part2 />
|}

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.<ref name = Sa2005/> In rats, atomoxetine increased [[prefrontal cortex]] [[catecholamine]] concentrations without altering [[dopamine]] levels in the [[striatum]] or [[nucleus accumbens]]; in contrast, [[methylphenidate]], a [[dopamine reuptake inhibitor]], was found to increase prefrontal, striatal, and accumbal dopamine levels to the same degree.<ref name="HodgkinsShawMcCarthy2012">{{cite journal | vauthors = Hodgkins P, Shaw M, McCarthy S, Sallee FR | title = The pharmacology and clinical outcomes of amphetamines to treat ADHD: does composition matter? | journal = CNS Drugs | volume = 26 | issue = 3 | pages = 245–268 | date = March 2012 | pmid = 22329564 | doi = 10.2165/11599630-000000000-00000 | url = }}</ref><ref name = NPP2002>{{cite journal | vauthors = Bymaster FP, Katner JS, Nelson DL, Hemrick-Luecke SK, Threlkeld PG, Heiligenstein JH, Morin SM, Gehlert DR, Perry KW | title = Atomoxetine increases extracellular levels of norepinephrine and dopamine in prefrontal cortex of rat: a potential mechanism for efficacy in attention deficit/hyperactivity disorder | journal = Neuropsychopharmacology | volume = 27 | issue = 5 | pages = 699–711 | date = November 2002 | pmid = 12431845 | doi = 10.1016/S0893-133X(02)00346-9 | doi-access = free }}</ref> In addition to rats, atomoxetine has also been found to induce similar region-specific catecholamine level alteration in mice.<ref name = PMID20403082>{{cite journal | vauthors = Koda K, Ago Y, Cong Y, Kita Y, Takuma K, Matsuda T | title = Effects of acute and chronic administration of atomoxetine and methylphenidate on extracellular levels of noradrenaline, dopamine and serotonin in the prefrontal cortex and striatum of mice | journal = Journal of Neurochemistry | volume = 114 | issue = 1 | pages = 259–270 | date = July 2010 | pmid = 20403082 | doi = 10.1111/j.1471-4159.2010.06750.x | doi-access = free }}</ref>

Atomoxetine's status as a [[serotonin transporter]] (SERT) inhibitor at clinical doses in humans is uncertain. A [[Positron emission tomography|PET imaging]] study on [[rhesus monkey]]s found that atomoxetine occupied >90% and >85% of neural NET and SERT, respectively.<ref name="DingNaganawa2014">{{cite journal | vauthors = Ding YS, Naganawa M, Gallezot JD, Nabulsi N, Lin SF, Ropchan J, Weinzimmer D, McCarthy TJ, Carson RE, Huang Y, Laruelle M | title = Clinical doses of atomoxetine significantly occupy both norepinephrine and serotonin transports: Implications on treatment of depression and ADHD | journal = NeuroImage | volume = 86 | pages = 164–171 | date = February 2014 | pmid = 23933039 | doi = 10.1016/j.neuroimage.2013.08.001 | quote = The noradrenergic action also exerts an important clinical effect in different antidepressant classes such as desipramine and nortriptyline (tricyclics, prevalent noradrenergic effect), reboxetine and atomoxetine (relatively pure noradrenergic reuptake inhibitor (NRIs)), and dual action antidepressants such as the serotonin noradrenaline reuptake inhibitors (SNRIs), the noradrenergic and dopaminergic reuptake inhibitor (NDRI) bupropion, and other compounds (e.g., mianserin, mirtazapine), which enhance the noradrenergic transmission | s2cid = 16958660 }}</ref> However, both mouse and rat [[microdialysis]] studies have failed to find an increase in extracellular [[serotonin]] in the prefrontal cortex following acute or chronic atomoxetine treatment.<ref name = NPP2002/><ref name = PMID20403082/> Supporting atomoxetine's selectivity, a human study found no effects on platelet serotonin uptake (a marker of SERT inhibition) and inhibition of the [[Antihypotensive agent|pressor]] effects of [[tyramine]] (a marker of NET inhibition).<ref>{{cite journal | vauthors = Zerbe RL, Rowe H, Enas GG, Wong D, Farid N, Lemberger L | title = Clinical pharmacology of tomoxetine, a potential antidepressant | journal = The Journal of Pharmacology and Experimental Therapeutics | volume = 232 | issue = 1 | pages = 139–143 | date = January 1985 | doi = 10.1016/S0022-3565(25)20085-4 | pmid = 3965689 }}</ref>

Atomoxetine has been found to act as an [[NMDA receptor antagonist]] in rat cortical neurons at therapeutic concentrations.<ref name = PMID20423340>{{cite journal | vauthors = Ludolph AG, Udvardi PT, Schaz U, Henes C, Adolph O, Weigt HU, Fegert JM, Boeckers TM, Föhr KJ | title = Atomoxetine acts as an NMDA receptor blocker in clinically relevant concentrations | journal = British Journal of Pharmacology | volume = 160 | issue = 2 | pages = 283–291 | date = May 2010 | pmid = 20423340 | pmc = 2874851 | doi = 10.1111/j.1476-5381.2010.00707.x }}</ref><ref name = PMID28167075>{{cite journal | vauthors = Barygin OI, Nagaeva EI, Tikhonov DB, Belinskaya DA, Vanchakova NP, Shestakova NN | title = Inhibition of the NMDA and AMPA receptor channels by antidepressants and antipsychotics | journal = Brain Research | volume = 1660 | pages = 58–66 | date = April 2017 | pmid = 28167075 | doi = 10.1016/j.brainres.2017.01.028 | s2cid = 27647092 }}</ref> It causes a use-dependent open-channel block and its binding site overlaps with the Mg<sup>2+</sup> binding site.<ref name = PMID20423340/><ref name = PMID28167075/> Atomoxetine's ability to increase prefrontal cortex firing rate in anesthetized rats could not be blocked by [[D1 receptor|D<sub>1</sub>]] or [[alpha-1 blocker|α<sub>1</sub>-adrenergic receptor antagonist]]s, but could be potentiated by [[NMDA]] or an [[alpha-2 blocker|α<sub>2</sub>-adrenergic receptor antagonist]], suggesting a glutaminergic mechanism.<ref>{{cite journal | vauthors = Di Miceli M, Gronier B | title = Psychostimulants and atomoxetine alter the electrophysiological activity of prefrontal cortex neurons, interaction with catecholamine and glutamate NMDA receptors | journal = Psychopharmacology | volume = 232 | issue = 12 | pages = 2191–2205 | date = June 2015 | pmid = 25572531 | doi = 10.1007/s00213-014-3849-y | s2cid = 18339166 }}</ref> In [[Laboratory rat|Sprague Dawley rats]], atomoxetine reduces [[GRIN2B|NR2B]] protein content without altering transcript levels.<ref name = PMID24348020>{{cite journal | vauthors = Udvardi PT, Föhr KJ, Henes C, Liebau S, Dreyhaupt J, Boeckers TM, Ludolph AG | title = Atomoxetine affects transcription/translation of the NMDA receptor and the norepinephrine transporter in the rat brain--an in vivo study | journal = Drug Design, Development and Therapy | volume = 7 | pages = 1433–1446 | date = 2013 | pmid = 24348020 | pmc = 3857115 | doi = 10.2147/DDDT.S50448 | doi-access = free }}</ref> Aberrant glutamate and NMDA receptor function have been implicated in the etiology of [[ADHD]].<ref>{{cite journal | vauthors = Maltezos S, Horder J, Coghlan S, Skirrow C, O'Gorman R, Lavender TJ, Mendez MA, Mehta M, Daly E, Xenitidis K, Paliokosta E, Spain D, Pitts M, Asherson P, Lythgoe DJ, Barker GJ, Murphy DG | title = Glutamate/glutamine and neuronal integrity in adults with ADHD: a proton MRS study | journal = Translational Psychiatry | volume = 4 | issue = 3 | pages = e373 | date = March 2014 | pmid = 24643164 | pmc = 3966039 | doi = 10.1038/tp.2014.11 }}</ref><ref>{{cite journal | vauthors = Chang JP, Lane HY, Tsai GE | title = Attention deficit hyperactivity disorder and N-methyl-D-aspartate (NMDA) dysregulation | journal = Current Pharmaceutical Design | volume = 20 | issue = 32 | pages = 5180–5185 | date = 2014 | pmid = 24410567 | doi = 10.2174/1381612819666140110115227 }}</ref>

Atomoxetine also reversibly inhibits [[GIRK]] currents in [[Xenopus|''Xenopus'' oocytes]] in a concentration-dependent, voltage-independent, and time-independent manner.<ref name = PMID20393461>{{cite journal | vauthors = Kobayashi T, Washiyama K, Ikeda K | title = Inhibition of G-protein-activated inwardly rectifying K+ channels by the selective norepinephrine reuptake inhibitors atomoxetine and reboxetine | journal = Neuropsychopharmacology | volume = 35 | issue = 7 | pages = 1560–1569 | date = June 2010 | pmid = 20393461 | pmc = 3055469 | doi = 10.1038/npp.2010.27 }}</ref> K<sub>ir</sub>3.1/3.2 [[ion channel]]s are opened downstream of [[Muscarinic acetylcholine receptor M2|M<sub>2</sub>]], [[Alpha-2 adrenergic receptor|α<sub>2</sub>]], [[Dopamine receptor D2|D<sub>2</sub>]], and [[Adenosine A1 receptor|A<sub>1</sub>]] stimulation, as well as other [[Gi alpha subunit|G<sub>i</sub>]]-coupled receptors.<ref name = PMID20393461/> Therapeutic concentrations of atomoxetine are within range of interacting with GIRKs, especially in CYP2D6 poor metabolizers.<ref name = PMID20393461/> It is not known whether this contributes to the therapeutic effects of atomoxetine in ADHD.

4-Hydroxyatomoxetine, the major active metabolite of atomoxetine in CYP2D6 extensive metabolizers, has been found to have sub-micromolar affinity for [[opioid receptor]]s, acting as an antagonist at [[Mu opioid receptor|μ-opioid receptors]] and a partial agonist at [[Kappa opioid receptor|κ-opioid receptors]].<ref name="PMID15225731">{{cite journal | vauthors = Creighton CJ, Ramabadran K, Ciccone PE, Liu J, Orsini MJ, Reitz AB | title = Synthesis and biological evaluation of the major metabolite of atomoxetine: elucidation of a partial kappa-opioid agonist effect | journal = Bioorganic & Medicinal Chemistry Letters | volume = 14 | issue = 15 | pages = 4083–4085 | date = August 2004 | pmid = 15225731 | doi = 10.1016/j.bmcl.2004.05.018 }}</ref> It is not known whether this action at the kappa-opioid receptor leads to CNS-related adverse effects.

===Pharmacokinetics===
Orally administered atomoxetine is rapidly and completely absorbed.<ref name = Sa2005/> First-pass metabolism by the liver is dependent on [[CYP2D6]] activity, resulting in an [[bioavailability|absolute bioavailability]] of 63% for extensive metabolizers and 94% for poor metabolizers.<ref name = Sa2005/> Maximum plasma concentration is reached in 1–2 hours.<ref name = Sa2005/> If taken with food, the maximum plasma concentration decreases by 10–40% and delays the [[Pharmacokinetics|t<sub>max</sub>]] by 3 hours.<ref name = Sa2005/> Drugs affecting gastric pH have no effect on oral bioavailability.<ref name="Strattera FDA label" />

Following [[Intravenous therapy|intravenous delivery]], atomoxetine has a [[volume of distribution]] of 0.85 L/kg (indicating distribution primarily in total body water), with limited partitioning into red blood cells.<ref name = Sa2005/><ref>{{cite web|url=https://www.accessdata.fda.gov/drugsatfda_docs/label/2007/021411s004s012s013s015s021lbl.pdf|title=atomoxetine HC|website=FDA|access-date=30 November 2023|archive-date=18 October 2023|archive-url=https://web.archive.org/web/20231018171341/https://www.accessdata.fda.gov/drugsatfda_docs/label/2007/021411s004s012s013s015s021lbl.pdf}}</ref> It is highly bound to plasma proteins (98.7%), mainly albumin, along with α<sub>1</sub>-acid glycoprotein (77%) and IgG (15%).<ref name = Sa2005/><ref name = part2/> Its metabolite ''N''-desmethylatomoxetine is 99.1% bound to plasma proteins, while 4-hydroxyatomoxetine is only 66.6% bound.<ref name = Sa2005/>

The half-life of atomoxetine varies widely between individuals, with an average range of 4.5 to 19 hours.<ref name = Sa2005/><ref name = PMID26314574>{{cite journal | vauthors = Brown JT, Bishop JR | title = Atomoxetine pharmacogenetics: associations with pharmacokinetics, treatment response and tolerability | journal = Pharmacogenomics | volume = 16 | issue = 13 | pages = 1513–1520 | date = 2015 | pmid = 26314574 | doi = 10.2217/PGS.15.93 }}</ref> As atomoxetine is metabolized by CYP2D6, exposure may be increased 10-fold in CYP2D6 poor metabolizers.<ref name = PMID26314574/> Among CYP2D6 extensive metabolizers, the half-life of atomoxetine averaged 5.34 hours and the half-life of the active metabolite ''N''-desmethylatomoxetine was 8.9 hours.<ref name = Sa2005/><ref name="sa2003">{{cite journal | vauthors = Sauer JM, Ponsler GD, Mattiuz EL, Long AJ, Witcher JW, Thomasson HR, Desante KA | title = Disposition and metabolic fate of atomoxetine hydrochloride: the role of CYP2D6 in human disposition and metabolism | journal = Drug Metabolism and Disposition | volume = 31 | issue = 1 | pages = 98–107 | date = January 2003 | pmid = 12485958 | doi = 10.1124/dmd.31.1.98 | s2cid = 13032441 }}</ref> By contrast, among CYP2D6 poor metabolizers the half-life of atomoxetine averaged 20.0 hours and the half-life of ''N''-desmethylatomoxetine averaged 33.3 hours.<ref name = Sa2005/><ref name="sa2003"/> [[Steady state (biochemistry)|Steady-state]] levels of atomoxetine are typically achieved at or around day 10 of regular dosing, with [[Trough (pharmacology)|trough plasma concentrations]] ([[Trough (pharmacology)|C<sub>trough</sub>]]) residing around 30–40°ng/mL; however, both the time to steady-state levels and C<sub>trough</sub> are expected to vary based on a patient's [[CYP2D6]] profile.<ref>{{cite journal | vauthors = Sauer JM, Ring BJ, Witcher JW | title = Clinical pharmacokinetics of atomoxetine | journal = Clinical Pharmacokinetics | volume = 44 | issue = 6 | pages = 571–590 | date = 2005 | pmid = 15910008 | doi = 10.2165/00003088-200544060-00002 | s2cid = 25708096 }}</ref><ref>{{cite encyclopedia | vauthors = Chamberlain SR, Sahakian BJ |title=Atomoxetine |date=2010 |encyclopedia=Encyclopedia of Psychopharmacology |pages=158–160 | veditors = Stolerman IP |place=Berlin, Heidelberg |publisher=Springer |language=en |doi=10.1007/978-3-540-68706-1_35 |isbn=978-3-540-68706-1 }}</ref>

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 and 17 μmol/L.{{citation needed|date=November 2018}} Plasma concentrations of 4-hydroxyatomoxetine and ''N''-desmethylatomoxetine at steady state are 1% and 5% that of atomoxetine in CYP2D6 extensive metabolizers, and 0.1% and 45% that of atomoxetine in CYP2D6 poor metabolizers, respectively.<ref name="Strattera FDA label" />

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.<ref name = Sa2005/> 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.<ref name = Sa2005/> CYP2D6 poor metabolizers excrete greater amounts of minor metabolites, namely ''N''-desmethylatomoxetine and 2-hydroxymethylatomoxetine and their [[Drug metabolism|conjugates]].<ref name = Sa2005/>

[[File:Atomoxetine metabolism.png|class=skin-invert-image|700px|thumb|center|Major metabolites of atomoxetine in humans.<ref name = Sa2005/>]]

====Pharmacogenomics====
Chinese adults homozygous for the hypoactive CYP2D6*10 allele have been found to exhibit two-fold higher [[Area under the curve (pharmacokinetics)|area-under-the-curve]] (AUCs) and 1.5-fold higher maximum plasma concentrations compared to extensive metabolizers.<ref name = Sa2005/>

Japanese men homozygous for CYP2D6*10 have similarly been found to experience two-fold higher AUCs compared to extensive metabolizers.<ref name = Sa2005/>

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

<gallery>
File:Strattera 60mg capsule back.jpg|Strattera 60-mg capsule back
File:Lilly Strattera 60mg Capsule.jpg|Strattera 60-mg capsule front with Lilly logo
</gallery>

===Synthesis===
[[File:Atomoxetine-synthesis.png|class=skin-invert-image|thumb|none|1000px|Original synthesis of atomoxetine, as patented by [[Eli Lilly and Company]]<ref>{{cite patent |country= US|number= 4018895 A|status= patent|title= Aryloxyphenylpropylamines in treating depression|pubdate= 19 April 1977|fdate= 17 September 1975|pridate= 10 January 1974|invent1= Bryan B. Molloy|invent2= Klaus K. Schmiegel|assign1= Eli Lilly And Company}}</ref><ref>{{cite patent |country= US|number= EP0052492 B1|status= patent|title= 3-aryloxy-3-phenylpropylamines|pubdate= 29 February 1984|fdate= 13 November 1981|pridate= 14 November 1980|invent1= Bennie Joe Foster|invent2= Edward Ralph Lavagnino|assign1= Eli Lilly And Company|url=}}</ref>]]

===Detection in biological fluids===
Atomoxetine may be quantitated in plasma, serum, or whole blood 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.<ref>{{cite book | vauthors = Baselt RC |title=Disposition of Toxic Drugs and Chemicals in Man |edition=8th |publisher=Biomedical Publications |location=Foster City, CA |year=2008 |pages=[https://archive.org/details/dispositionoftoxe2base/page/118 118–20] |isbn=978-0-931890-08-6 |url-access=registration |url=https://archive.org/details/dispositionoftoxe2base/page/118 }}</ref>

==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 [[drug development|developed]] as an antidepressant, but it was found to be insufficiently efficacious for treating depression. It 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.<ref name="orangeBook">{{cite web |url=http://www.accessdata.fda.gov/scripts/cder/ob/docs/patexclnew.cfm?Appl_No=021411&Product_No=002&table1=OB_Rx |title=Patent and Exclusivity Search Results |access-date=26 April 2009 |work=Electronic Orange Book |publisher=U.S. [[Food and Drug Administration]] (FDA) |archive-url=https://web.archive.org/web/20120322100021/http://www.accessdata.fda.gov/scripts/cder/ob/docs/patexclnew.cfm?Appl_No=021411&Product_No=002&table1=OB_Rx |archive-date=22 March 2012 }}</ref> 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.<ref name="w934">{{cite web | title=Lilly loses ADD patent case, cuts revenue outlook | website=Reuters | date=12 August 2010 | url=https://www.reuters.com/article/idUSN12148299/ | access-date=23 July 2024}}</ref> On 1&nbsp;September 2010, Sun Pharmaceuticals announced it would begin manufacturing a generic in the United States.<ref>{{cite news|url=http://www.ibtimes.com/articles/48022/20100901/sun-pharma-usfda-strattera-capsules-eli-lilly-atomoxetine-hydrochloride-attention-deficit-hyperactiv.htm |title=Sun Pharma receives USFDA approval for generic Strattera capsules |work=International Business Times |archive-url=https://web.archive.org/web/20110407100949/http://www.ibtimes.com/articles/48022/20100901/sun-pharma-usfda-strattera-capsules-eli-lilly-atomoxetine-hydrochloride-attention-deficit-hyperactiv.htm |archive-date=7 April 2011 }}</ref> 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."<ref>{{cite news|url=http://www.sunpharma.com/images/finance/FY12%20Q1%20Earnings%20Call%20Transcript.pdf |title=Sun Pharma Q1 2011-12 Earnings Call Transcript 10.00 am, July 29, 2011 |archive-url=https://web.archive.org/web/20110929013747/http://www.sunpharma.com/images/finance/FY12%20Q1%20Earnings%20Call%20Transcript.pdf |archive-date=29 September 2011 }}</ref>

In 2017 the FDA approved the generic production of atomoxetine by four pharmaceutical companies.<ref name="FDA PR">{{cite press release |url=https://www.fda.gov/news-events/press-announcements/fda-approves-first-generic-strattera-treatment-adhd|title=FDA approves first generic Strattera for the treatment of ADHD|date=30 May 2017|website=U.S. [[Food and Drug Administration]] (FDA) |access-date=1 January 2018|archive-url=https://web.archive.org/web/20170604122624/https://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm561096.htm|archive-date=4 June 2017}}</ref>

==Society and culture==
The drug was originally known as tomoxetine. It was renamed to avoid [[medication error]]s, as the name may be confused with [[tamoxifen]].<ref>{{cite journal | vauthors = Ledbetter M | title = Atomoxetine: a novel treatment for child and adult ADHD | journal = Neuropsychiatric Disease and Treatment | volume = 2 | issue = 4 | pages = 455–466 | date = December 2006 | pmid = 19412494 | pmc = 2671957 | doi = 10.2147/nedt.2006.2.4.455 | doi-access = free }}</ref>

===Brand names===
In India, atomoxetine is sold under brand names including Axetra, Axepta, Attera, Tomoxetin, and Attentin. In Australia, Canada, Italy, Portugal, Romania, Spain, Switzerland, and the US, atomoxetine is sold under the brand name Strattera. In France, hospitals dispense atomoxetine under the brand name Strattera (it is not marketed in France). In the Czech Republic, it is sold under brand names including Mylan. In Poland, it is sold under the brand name Auroxetyn. In Indonesia, it is sold under the brand name Xenocy. In Iran, atomoxetine is sold under brand names including Stramox. In Brazil, it is sold under the brand name Atentah. In Turkey, it is sold under the brand names Attex, Setinox, and Atominex. In 2017, a [[generic medication|generic]] version was approved in the United States.<ref name="FDA PR" />

==Research==
There has been some suggestion that atomoxetine might be a helpful adjunct in people with [[major depression]], particularly in cases with concomitant ADHD.<ref name="NHMH">{{cite book | vauthors = Malenka RC, Nestler EJ, Hyman SE, Holtzman DM | title = Molecular Neuropharmacology: A Foundation for Clinical Neuroscience | year = 2015 | publisher = McGraw-Hill Medical | location = New York | isbn = 978-0-07-182770-6 | edition = 3rd}}{{page needed|date=September 2021}}</ref>

Atomoxetine may be used in those with ADHD and [[bipolar disorder]] although such use has not been well established.<ref>{{cite journal | vauthors = Perugi G, Vannucchi G | title = The use of stimulants and atomoxetine in adults with comorbid ADHD and bipolar disorder | journal = Expert Opinion on Pharmacotherapy | volume = 16 | issue = 14 | pages = 2193–2204 | date = 2015 | pmid = 26364896 | doi = 10.1517/14656566.2015.1079620 | s2cid = 28907560 }}</ref> Some benefit has also been seen in people with ADHD and [[autism]].<ref>{{cite book | collaboration = Autism Society of America | vauthors = Siegel M, Erickson C, Frazier JA, Ferguson T, Goepfert E, Joshi G, Humberd QM, King BH, Lutz A, Kraus L, Mao A, Robb A, Veenstra-VanderWeele J, Wang P, Head CJ |title = Autism Spectrum Disorder Parents Medication Guide |publisher = American Academy of Child and Adolescent Psychiatry |date = 2016 |location = Washington, DC |page = 13 |url = https://www.aacap.org/App_Themes/AACAP/Docs/resource_centers/autism/Autism_Spectrum_Disorder_Parents_Medication_Guide.pdf |quote = Atomoxetine (Strattera) has also been researched in controlled studies for treatment of ADHD in children with autism, and showed some improvements, particularly for hyperactivity and impulsivity |url-status = live |archive-url = https://web.archive.org/web/20170411220740/https://www.aacap.org/App_Themes/AACAP/Docs/resource_centers/autism/Autism_Spectrum_Disorder_Parents_Medication_Guide.pdf |archive-date = 11 April 2017}}</ref> As with other norepinephrine reuptake inhibitors it appears to reduce anxiety and depression symptoms, although research has focused mainly on specific patient groups such as those with concurrent ADHD<ref>{{cite journal | vauthors = Snircova E, Marcincakova-Husarova V, Hrtanek I, Kulhan T, Ondrejka I, Nosalova G | title = Anxiety reduction on atomoxetine and methylphenidate medication in children with ADHD | journal = Pediatrics International | volume = 58 | issue = 6 | pages = 476–481 | date = June 2016 | pmid = 26579704 | doi = 10.1111/ped.12847 | s2cid = 6229741 }}</ref> or methamphetamine dependence.<ref>{{cite journal | vauthors = Rabiey A, Hassani-Abharian P, Farhad M, Moravveji AR, Akasheh G, Banafshe HR | title = Atomoxetine Efficacy in Methamphetamine Dependence during Methadone Maintenance Therapy | journal = Archives of Iranian Medicine | volume = 22 | issue = 12 | pages = 692–698 | date = December 2019 | pmid = 31823620 }}</ref>

== References ==
{{Reflist}}

== Further reading ==
{{refbegin}}
* {{cite book | title=Medical Genetics Summaries | chapter=Atomoxetine Therapy and CYP2D6 Genotype | chapter-url=https://www.ncbi.nlm.nih.gov/books/NBK315951/ | veditors=Pratt VM, McLeod HL, Rubinstein WS, Scott SA, Dean LC, Kattman BL, Malheiro AJ | display-editors=3 | publisher=[[National Center for Biotechnology Information]] (NCBI) | year=2015 | pmid=28520366 | id=Bookshelf ID: NBK315951 | vauthors=Dean L | url=https://www.ncbi.nlm.nih.gov/books/NBK61999/ | access-date=7 February 2020 | archive-date=26 October 2020 | archive-url=https://web.archive.org/web/20201026145821/https://www.ncbi.nlm.nih.gov/books/NBK61999/ | url-status=live }}
{{refend}}

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