Delving into the Latest Updates on Atomoxetine Hydrochloride with Synapse

Overview

Basic Info

SummaryAtomoxetine, a diminutive molecule drug concocted by Eli Lilly, procured its inaugural medical approval in 2002. The drug functions as an inhibitor of norepinephrine reuptake in the brain, inducing augmented levels of norepinephrine in the synaptic cleft. The drug's primary indication is for Attention Deficit Disorder with Hyperactivity (ADHD), a disorder typified by inattentiveness, impulsivity, and hyperactivity. Atomoxetine is postulated to operate by enhancing focus and concentration in individuals grappling with ADHD. Taking everything into account, atomoxetine's intricate mechanism of action and clinical indications proffer it as a valuable therapeutic option for those affected by ADHD.

Drug Type

Small molecule drug

Synonyms

(-)-Tomoxetine, Atomoxetine, Atomoxetine hydrochloride (JAN/USP)

+ [9]

Target

NET

Action

inhibitors

Mechanism

NET inhibitors(Norepinephrine transporter inhibitors)

Therapeutic Areas

Other Diseases

Active Indication

Attention Deficit Disorder With Hyperactivity

Inactive Indication

Alzheimer DiseaseAttention Deficit and Disruptive Behavior DisordersAttention Deficit Disorder+ [9]

Originator Organization

Eli Lilly & Co.

Active Organization

Eli Lilly Australia Pty Ltd.Lilly SA

Jiangsu Chia Tai Fenghai Pharmaceutical Co., Ltd.

+ [1]

Inactive Organization-

Drug Highest PhaseApproved

First Approval Date

United States (26 Nov 2002),

Attention Deficit Disorder With Hyperactivity

RegulationOrphan Drug (United States), Priority Review (China)

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Structure/Sequence

Molecular FormulaC17H22ClNO

InChIKeyLUCXVPAZUDVVBT-UNTBIKODSA-N

CAS Registry82248-59-7

View All Structures (2)

Attention deficits (AD) frequently co-occur with posttraumatic stress disorder (PTSD). The presence of AD is associated with greater PTSD clinical severity and poorer clinical outcomes. Knowledge regarding the mechanism underlying this association is limited, though the emerging evidence has indicated that executive function deficit (EFD) is strongly correlated with AD and PTSD symptoms. While treatments developed for PTSD have existed for years, a substantial portion of individuals do not fully respond to conventional treatment. Accumulating evidence suggest that attention deficit (AD) and EFD may be a driving force for PTSD treatment resistance. However, treatment of executive impairment in PTSD is very limited. As a result, untreated co-occurring AD and EFD in PTSD poses severe negative impacts on patients' functional recovery, treatment outcomes, and quality of life (QoL). Given that up to 50% of patients do not respond well to the first-line pharmacological PTSD treatments, it is imperative to seek novel treatment strategies to improve EF that may improve both standard treatment response and QoL, social function. The proposed study directly addresses this knowledge gap by testing the efficacy of atomoxetine (ATX) in improving EF and attention among Veterans with PTSD, which will further improve Veterans' QoL and social function. ATX represents a promising novel candidate pharmacotherapy for individuals with PTSD. ATX is a non-stimulant selective norepinephrine reuptake inhibitor (SNRI), approved by the FDA for the treatment of ADHD. Studies suggest that ATX, unlike stimulants, lacks addictive properties and shows efficacy in the treatment of comorbid depression and anxiety, which is ideal in the treatment of PTSD. Data from the investigators' preliminary study provides encouraging support for the therapeutic potential of ATX in improving EF in Veterans with comorbid PTSD/ADHD. The investigators' recent research uncovered a higher rate of ADHD among Veterans with PTSD, and the comorbid AD symptoms were correlated with PTSD severity and poorer treatment outcomes. Treatment with ATX showed significant symptoms reduction in ADHD and improvement in inhibitory function in Veterans with ADHD/PTSD. In the proposed study, the investigators will focus on ATX in improvement of EF and attention, and further psycho-social life function and QoL. The investigators will (1) employ a randomized, double-blind design that will consist of 12 weeks of treatment with ATX or placebo medication; (2) use standardized, repeated dependent measures to rigorously assess AD and EFD symptomatology; (3) measure impairment in associated mental and behavioral health problems (e.g., attention deficit, depression, anxiety, suicidality, QoL, family/social functioning); and (4) use response inhibition task GoNogo, working memory and attention tests Digit Span and Trail Making to investigate the underlying pathophysiology of PTSD and prognostic indicators of treatment outcome. To achieve these goals, the investigators have assembled a multidisciplinary team with expertise in PTSD, ADHD clinical trials, and human laboratory paradigms who have successfully collaborated in the past and are uniquely qualified to implement this type of investigation. The proposed project is directly responsive to the mission of the VA-RRD "to maximize Veterans' functional independence, quality of life and participation in their lives and community." Successful completion of this study will provide a platform for a large multi-center trial to further confirm the important role of EF in PTSD treatment outcomes. The findings from this study will provide critically needed evidence to help inform clinical practice guidelines on the treatment of PTSD. The outcome of the proposed research will be significant, because it provides a knowledge base to allow for development of new PTSD intervention strategies. More importantly, this clinical trial may immediately benefit Veterans by enhancing their cognitive function, reducing AD related disability, and further improving quality of life for Veterans who suffer from PTSD.

Start Date01 Apr 2025

Sponsor / Collaborator

VA Office of Research and Development

[+1]

NCT06841666

/ Not yet recruitingEarly Phase 1IIT

Evaluating the Efficacy of Atomoxetine in Reducing Primary Nocturnal Enuresis in Children With ADHD

1. Primary Aim: To evaluate the efficacy of atomoxetine in reducing the frequency of primary nocturnal enuresis episodes in children with ADHD.
2. Secondary Aim: To determine if improvements in attention symptoms correlate with reductions in nocturnal enuresis episodes.

Start Date28 Feb 2025

Sponsor / Collaborator

Tanta University

IRCT20240925063160N1

/ RecruitingPhase 2/3IIT

Efficacy of Atomoxetine in the treatment of ADHD symptoms in autistic children

Start Date21 Nov 2024

Sponsor / Collaborator-

100 Clinical Results associated with Atomoxetine Hydrochloride

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100 Translational Medicine associated with Atomoxetine Hydrochloride

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100 Patents (Medical) associated with Atomoxetine Hydrochloride

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2,944

Literatures (Medical) associated with Atomoxetine Hydrochloride

01 May 2025·Environmental Research

Occurrence and risk assessment of different cyanotoxins and their relationship with environmental factors in six typical eutrophic lakes of China

Article

Author: Yao, Yujia ; Chen, Wei ; Mao, Zhigang ; Xiang, Tao ; Chen, Huihui ; Yang, Huiting ; Zeng, Qingfei ; Gu, Xiaohong

Cyanobacterial blooms can generate various toxic metabolites in freshwater, and pose serious threats to drinking water safety and human health. Although microcystins (MCs) have been detected in many freshwater ecosystems in China, little is known about the other cyanotoxins. An investigation of six eutrophic lakes (i.e. Hulun Lake, Wuliangsuhai Lake, Chaohu Lake, Taihu Lake, Xingyun Lake, and Dianchi Lake) in different geographical locations of China was performed during the summer of 2022 to determine the occurrence of various cyanotoxins (i.e. anatoxin-a (ATX), cylindrospermopsin (CYN), and MCs) in water column and their possible risks, and to evaluate the related environmental factors. MCs levels in sediment of these lakes were also investigated. MCs were the primary cyanotoxins in the water column of investigated lakes. The mean MCs contents in water column of Hulun Lake, Wuliangsuhai Lake, Chaohu Lake, Taihu Lake, Xingyun Lake, and Dianchi Lake were 3.61, 0.13, 3.60, 2.18, 0.57, and 2.56 μg/L, respectively. The total MCs levels in water column exceeded 1 μg/L in some areas of these lakes except Wuliangsuhai Lake. Replete nitrogen and/or phosphorus levels seemed to be related to MCs production. ATX can be detected in these lakes except Xingyun Lake at ng/L levels. CYN can be detected in all lakes at ng/L levels. However, the levels of ATX and CYN appear to be not significantly associated with environmental factors. MCs and CYN can pose a high or moderate risk for humans and aquatic organisms in some areas of these lakes, while ATX can pose a low or no risk for humans and aquatic organisms in most areas of these lakes. MCs can also be detected in sediment of all lakes at ng/g levels. This research emphasizes the necessity for long-term monitoring of different cyanotoxins in eutrophic lakes, and the implementation of nutrient control and management strategies.

01 Apr 2025·Psychological Reports

Examination of Excessive Mind-Wandering Following Attention-Deficit and Hyperactivity Disorder Treatment in Adults

Article

Author: Takım, Uğur ; Gökçay, Hasan

Although mind-wandering (MW) is a part of attention deficit and hyperactivity disorder (ADHD), the impact of psychostimulants on excessive MW remains unclear. We aimed to elucidate how psychostimulants impact the MW of adult ADHD patients post treatment. This cross-sectional cohort study consisted of 54 randomly selected ADHD patients who applied to our psychiatry outpatient clinic and 40 healthy controls. The ADHD patients were administered methylphenidate or atomoxetine. A Semi-Structured Sociodemographic and Clinical Data Form, the Adult ADHD Self-Report Scale (ASRS), and the Mind Excessively Wandering Scale (MEWS) were applied. Routine psychiatric assessments in the 1st, 2nd, and 3rd months of pharmacological treatment were carried out by a psychiatrist. The pre-treatment MEWS score of the ADHD patients was 26.09 ± 1.92, which significantly decreased to 12.78 ± 2.54 post-treatment (F = 715.250, p < .001). A statistically significant difference was identified between the mean pre-treatment ASRS total score (44.07 ± 10.09) and post-treatment score (27.34 ± 11.22; F = 50.364, p < .001). A lifetime history of alcohol/substance use was positively associated with the MEWS score. ADHD pharmacotherapy led to significant reductions in MW. Recognizing the interaction between MW and ADHD could help in the design of more specific and comprehensive interventions.

01 Apr 2025·Cytotechnology

Autotaxin regulates the expression and the activity of P-glycoprotein in lipopolysaccharide -activated microglial cells

Article

Author: Awada, Rana ; Fayyad-Kazan, Hussein ; Soayfane, Zeina ; Faour, Wissam ; Fayyad-Kazan, Mohammad

Neurodegenerative diseases (NDs), such as Alzheimer's and Parkinson's, are characterized by chronic inflammation and oxidative stress, often mediated by activated microglial cells. Microglia-induced neuroinflammation is essential to neuronal damage, driven by the overproduction of pro-inflammatory cytokines and reactive oxygen species. Autotaxin (ATX), a lysophospholipase D enzyme, can modulate inflammation through its enzymatic product lysophosphatidic acid (LPA). While previous studies highlighted ATX's anti-inflammatory properties, its impact on P-glycoprotein (P-gp), a key efflux transporter involved in drug resistance and neuroinflammation, remains not fully understood. The objective of this study was to explore how ATX modulates the expression and activity of P-gp in lipopolysaccharide (LPS)-activated and H2O2-stressed BV-2 microglial cells. Microglial cells were transfected with either an empty vector (EV) or an ATX cDNA vector (A +) and exposed to LPS (1 µg/mL) or H2O2 (100 µM). The mRNA expression levels of P-gp and pro-inflammatory cytokines were analyzed using qRT-PCR, and P-gp activity was assessed using the NBD-CSA fluorescence efflux assay. Our findings revealed that while LPS- and H₂O₂-treated microglial cells were characterized by an abnormal cellular morphology with long ramified processes, ATX overexpression restored the round shape morphology normally observed in the control untreated cells. Interestingly, ATX overexpression significantly reduced the mRNA levels of pro-inflammatory cytokines, such as TNF-α, in LPS- and H₂O₂-treated microglial cells. Moreover, ATX overexpression reduced both the mRNA levels and efflux activity of P-gp under inflammatory and oxidative stress conditions. These results suggest that ATX mitigates microglial activation and its downstream effects, highlighting its therapeutic potential in reducing neuroinflammation.

56

News (Medical) associated with Atomoxetine Hydrochloride

11 Mar 2025

·www.prnewswire.com

Apnimed Appoints Kevin R. Lind as Non-Executive Chairman of the Board of Directors

– Larry Miller, CEO, to Continue Serving as Non-Independent Board Director – Phase 3 SynAIRgy and LunAIRo Clinical Trials on Track for Topline Results in 2Q2025 and 3Q2025, Respectively CAMBRIDGE, Mass., March 11, 2025 /PRNewswire/ -- Apnimed, Inc., a pharmaceutical company focused on discovering, developing, and commercializing first-in-class oral therapies for the neuromuscular dysfunction associated with obstructive sleep apnea (OSA) and other sleep-related breathing diseases, today announced the expansion of its Board of Directors with the appointment of Kevin R. Lind as non-executive Chairman of the Board. Mr. Lind brings decades of experience from the biotech and financial sectors. "We are thrilled to welcome Kevin to Apnimed's Board," said Larry Miller, MD, Chief Executive Officer of Apnimed. "His proven leadership in biotechnology and corporate strategy will provide invaluable insights as we approach Phase 3 clinical trial results for AD109 and prepare for its potential commercial launch as a once-nightly oral therapy for OSA. Our team has been executing to our stated milestones and, most importantly, our ongoing Phase 3 trials are on track to report top-line results in 2Q2025 and 3Q2025, respectively." "Apnimed is well-positioned for growth with both its promising late-stage asset, AD109, and its synergistic partnership with Shionogi to drive long-term value," said Mr. Lind. "I am excited to join Apnimed at this pivotal time and look forward to contributing to the company's continued clinical and future commercial successes." About Kevin Lind Kevin Lind recently served as Longboard Pharmaceuticals' President and Chief Executive Officer and as a member of its board from the company's inception in 2020 until Longboard was acquired by H. Lundbeck A/S in December 2024. Prior to co-founding Longboard Pharmaceuticals, Mr. Lind served as EVP and Chief Financial Officer during the turnaround of Arena Pharmaceuticals (acquired by Pfizer) from 2016 to 2020. As an executive leader at these organizations, he successfully raised over $1.1B in equity capital (including Longboard's IPO), secured valuable business development partnerships (including ~$1B in upfront payments), spun out two organizations, and was instrumental in activities resulting in the successful acquisitions of both companies for a cumulative value of ~$9.3B. At Longboard, Mr. Lind also led the initiation of a global Phase 3 program for a neurological drug candidate, bexicaserin, and innovative drug development strategies resulting in the conceptualization of a novel medical indication and securing of Breakthrough Therapy designation from the U.S. FDA. Prior to Longboard, Mr. Lind focused on healthcare investing at TPG Special Situations Partners from 2009 to 2016 and at TPG-Axon from 2006 to 2008. He served in various capacities as a healthcare investment banker at Lehman Brothers, Inc., a former global financial services firm, from 1998 to 2002 and 2004 to 2006. Mr. Lind received a B.S. from Stanford University in Biological Sciences and an MBA from UCLA Anderson School of Management. About AD109 AD109 is a once-nightly oral pill that could be the first pharmacological treatment to improve oxygenation during sleep by directly targeting the underlying neuromuscular dysfunction that causes the upper airway to collapse in people with obstructive sleep apnea (OSA). It is a first-in-class combination of aroxybutynin, a novel antimuscarinic, and atomoxetine, a selective norepinephrine reuptake inhibitor (NRI). Their combined pharmacological synergy targets the root neuromuscular cause of OSA. In a disease characterized by complex and invasive treatment options, AD109 may offer a simple solution to help improve oxygenation and overall health for people living with OSA. AD109 has successfully completed multiple Phase 1 and Phase 2 trials in OSA. The Phase 3 program is fully enrolled with topline results expected in mid-2025. About Obstructive Sleep Apnea Obstructive sleep apnea (OSA) is a serious, chronic sleep-related breathing disease in which the upper airway repeatedly collapses during sleep, leading to intermittent oxygen deprivation. It is caused by two overlapping mechanisms: neuromuscular dysfunction during sleep and predisposing anatomic abnormalities. It has been demonstrated that OSA affects people of all body types, ages and genders —there is no single "face" of the disease. An estimated 80 million people in the United States and 1 billion people worldwide suffer from OSA. An individual with OSA can experience hundreds of sleep apnea events in a single night, each one reducing the blood oxygen levels and negatively impacting cellular functions vital to normal health and function. Failure to effectively treat OSA increases the risk of serious long-term health consequences, such as high blood pressure, cardiovascular disease and type 2 diabetes, along with impacts on quality of life, including daytime fatigue and impaired judgement. Yet, the majority of those diagnosed with OSA refuse, abandon, or underutilize treatment. Currently, no available pharmacological treatments directly address the underlying neuromuscular dysfunction that is present in all people with OSA. About Apnimed Apnimed is a privately held clinical-stage pharmaceutical company dedicated to transforming the treatment landscape for sleep-related breathing diseases. Apnimed envisions a new era where novel oral therapies simplify intervention, expand the reach of diagnosis and treatment, and help more people get the oxygen and restorative sleep needed to thrive. Based in Cambridge, Mass., Apnimed is advancing a robust pipeline of oral pharmaceutical product candidates designed to improve oxygenation in individuals living with OSA and other sleep-related breathing disorders. This includes AD109, which is currently in Phase 3 clinical trials for the treatment of mild, moderate and severe OSA, as well as several therapies being developed as part of our joint venture with Shionogi & Co., Ltd, through Shionogi Apnimed Sleep Science (SASS). Learn more at apnimed.com or follow us on X and LinkedIn. Media Contact: [email protected] Investor Contact: Ramzi Benamar [email protected] SOURCE Apnimed, Inc. WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

Phase 2Executive ChangePhase 3IPO

04 Mar 2025

·www.fiercepharma.com

Glenmark issues another recall, this time for nearly 1.5M bottles of generic ADHD drug

Glenmark Pharma is recalling nearly 1.5 million bottles of the attention-deficit/hyperactivity disorder drug atomoxetin. Glenmark Pharma, an India-based drug manufacturer that has been the focal point of a spate of recalls in recent years, has issued another. This time, the product pull covers about 1.48 million bottles of the generic attention-deficit/hyperactivity disorder (ADHD) drug atomoxetine.Eli Lilly previously sold the branded version of the drug, Strattera, but discontinued all strengths in 2023 after the arrival of generics.Unlike stimulant-based drugs that make up the bulk of ADHD treatment, including those like Vyvanse and Adderall, atomoxetine is a selective norepinephrine reuptake inhibitor (sNRI).The recall was triggered by the presence of unacceptable levels of N-nitroso atomoxetine, a possible carcinogen, in multiple Glenmark atomoxetine batches, according to the FDA. The voluntary pull, which began Jan. 29, covers bottles of the drug in strengths ranging from 10 mg to 100 mg, the FDA said on its Enforcement Report webpage. The ADHD drugs were manufactured in Glenmark’s facility in Goa, India, and were distributed nationwide. Glenmark has weathered a string of recalls in recent years due to both manufacturing and labelling issues.In June 2024, the company recalled 114 batches of 750 mg potassium chloride extended-release capsules—or roughly 47 million capsules—over concerns that they failed to dissolve properly.In December, the company recalled 90,528 bottles of the high blood pressure drug diltiazem hydrochloride in tablet and extended-release forms due to unacceptable levels of another N-nitroso compound, N-nitroso-Desmethyl-Diltiazem.In separate actions in 2023, Glemark recalled 1,200 bottles of trandolapril and verapamil hydrochloride extended-release tablets used to treat high blood pressure; 37,200 bottles of Indomethacin, which is a non-steroidal anti-inflammatory used to treat pain and arthritis symptoms; and five lots (no bottle count provided) of Naproxen that is used to reduce fever or relieve mild pain.The previous year it recalled 98,307 packs of mometasone furoate topical solution, a corticosteroid lotion that treats skin conditions such as eczema, psoriasis, allergies and rash.

Clinical Result

04 Mar 2025

·www.echemi.com

Glenmark Recalls 1.5 Million ADHD Medication Bottles Over Safety Concerns

Glenmark Pharmaceuticals has initiated a recall of approximately 1.5 million bottles of its ADHD medication in the U.S., following findings of safety violations. The U.S. Food and Drug Administration (FDA) announced the recall due to "CGMP Deviations," which refers to violations of current good manufacturing practices. The recall affects around 1.476 million bottles of Atomoxetine Capsules, available in various strengths ranging from 10 mg to 100 mg. The FDA reported that the recall was prompted by the presence of N-Nitroso Atomoxetine impurity exceeding the recommended limits. Glenmark Pharmaceuticals Inc., based in New Jersey and a subsidiary of the Mumbai-based company, initiated this Class II recall on January 29, 2025. A Class II recall indicates that exposure to the violative product may lead to temporary or medically reversible adverse health consequences, though the likelihood of serious consequences is considered remote. ADHD, or Attention Deficit Hyperactivity Disorder, is a prevalent neurodevelopmental disorder, primarily affecting children's ability to focus and control impulses. The recall highlights ongoing concerns regarding drug safety and regulatory compliance in the pharmaceutical industry.

100 Deals associated with Atomoxetine Hydrochloride

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External Link

KEGG	Wiki	ATC	Drug Bank
D02574	Atomoxetine Hydrochloride	N06BA09	DB00289

R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
Attention Deficit Disorder With Hyperactivity	United States	Eli Lilly & Co.	26 Nov 2002

Developing

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Attention Deficit Disorder With Hyperactivity	Discovery	United Kingdom	Eli Lilly & Co.	01 Aug 2000
Attention Deficit Disorder With Hyperactivity	Discovery	Sweden	Eli Lilly & Co.	01 Aug 2000
Attention Deficit Disorder With Hyperactivity	Discovery	Norway	Eli Lilly & Co.	01 Aug 2000
Attention Deficit Disorder With Hyperactivity	Discovery	Netherlands	Eli Lilly & Co.	01 Aug 2000
Attention Deficit Disorder With Hyperactivity	Discovery	Belgium	Eli Lilly & Co.	01 Aug 2000
Attention Deficit Disorder With Hyperactivity	Discovery	Puerto Rico	Eli Lilly & Co.	01 Aug 2000
Attention Deficit Disorder With Hyperactivity	Discovery	Italy	Eli Lilly & Co.	01 Aug 2000
Attention Deficit Disorder With Hyperactivity	Discovery	Germany	Eli Lilly & Co.	01 Aug 2000
Attention Deficit Disorder With Hyperactivity	Discovery	South Africa	Eli Lilly & Co.	01 Aug 2000
Attention Deficit Disorder With Hyperactivity	Discovery	Israel	Eli Lilly & Co.	01 Aug 2000

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Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT04905979 (Pubmed \| Sleep Breath)	Phase 2	Sleep Apnea, Obstructive \| Hypertension	-	Atomoxetine 80 mg	(uewghfctxd) = agaketdbop qfjdkkgbxs (tjmyhronnx, 18.8 - 28.5) View more	Positive	01 Dec 2024
				Atomoxetine 80 mg + Spironolactone 80/50 mg	(uewghfctxd) = mvaasvltog qfjdkkgbxs (tjmyhronnx, 5.7 - 14.1)
WSC2022	Phase 2	-	30	Atomoxetine 75 mg + Aroxybutynin 2.5 mg	msievxjjhl(hrpfzyfkbn) = wldupevzoq cygtzenxvj (ostihwrity ) View more	Positive	11 Mar 2022
				Atomoxetine 37.5 mg + Aroxybutynin 2.5 mg	msievxjjhl(hrpfzyfkbn) = fbfyzldyzr cygtzenxvj (ostihwrity ) View more
NCT01340885 (CTgov)	Phase 4	Cognitive Dysfunction \| Parkinson Disease	9	Strattera (Atomoxetine)	xcsgnohaih(oxubdbswzr) = ahdovjlwed yebsacxuzl (tjztddmkqw, esvnatuahf - uworhciusm) View more	-	07 Jul 2020
				Exelon (Rivastigimine)	xcsgnohaih(oxubdbswzr) = skopmqgrbi yebsacxuzl (tjztddmkqw, fakqukklct - vaueqyarth) View more
NCT02500732 (POST6, CTgov)	Phase 2	Syncope, Vasovagal	57	Placebo (Placebo)	zkvztqrzzg(elmpjjqcut) = dffmmctftc wxmoqkjtay (csmwzfixsv, xixhyhmffs - zjsbsdnify) View more	-	21 Apr 2020
				Atomoxetine (Atomoxetine)	zkvztqrzzg(elmpjjqcut) = uqcrdbnxvk wxmoqkjtay (csmwzfixsv, xtawlfwrqn - chilewgwog) View more
NCT00918567 (CTgov)	Phase 4	Attention Deficit Disorder With Hyperactivity	56	Behavior Modification Therapy+atomoxetine (Combined Therapy)	hxvnmvpmte(awhctixhde) = enbccrvahk hajafobbdz (udpgoglvjg, nhtrkrryts - jvacqcuule) View more	-	07 Apr 2020
				atomoxetine (Drug Therapy)	hxvnmvpmte(awhctixhde) = smnzdhidqv hajafobbdz (udpgoglvjg, hngcpkvvip - szsvltjhlb) View more
NCT03091400 (CTgov)	Phase 2	Amnesia, Anterograde \| Multiple Sclerosis	11	Atomoxetine (Atomoxetine)	ostpiftoeo(ewatjcfuwo) = vahwqhlnrw yvudiirmhp (odslpobqfx, qkcfbunygx - iijijonlcr) View more	-	13 Mar 2020
				Placebo (Placebo)	ostpiftoeo(ewatjcfuwo) = vwjdnedpwm yvudiirmhp (odslpobqfx, kbgcncakud - dzlldlrhzi) View more
NCT01522404 (ATX-001, CTgov)	Phase 2	Mild cognitive disorder	39	Placebo+Atomoxetine (Atomoxetine / Inactive Compound)	iozbshzxxt(ecxhdtznlr) = usegnvytcb pwfsuohhnt (blohnikapn, attcjwvldf - zhlyahgcso) View more	-	05 Dec 2018
				Placebo+Atomoxetine (Inactive Compound / Atomoxetine)	iozbshzxxt(ecxhdtznlr) = xdqqrcetrf pwfsuohhnt (blohnikapn, xkniwhefxe - oemqznbscx) View more
NCT01738191 (ATM-Cog, CTgov)	Phase 2	Cognitive Dysfunction \| Parkinson Disease	30	Atomoxetine (Atomoxetine)	uxqerjwkkb(ttotpmezhi) = wqdqncgxik ypwvrezwts (yqpdmjlyso, nbqtkvolzs - grlcughfdw) View more	-	23 Aug 2018
				Placebo (Placebo)	uxqerjwkkb(ttotpmezhi) = sbaayawwnt ypwvrezwts (yqpdmjlyso, dxbyrccpgm - ygpnhjcvnf) View more
NCT00183391 (CTgov)	Phase 4	Attention Deficit Disorder With Hyperactivity	232	Methylphenidate+Atomoxetine (Atomoxetine Then Methylphenidate)	qhnlilheom(fwqdpehwhk) = qytektqdpl whimbqqxnq (hevhkfihqv, natypvysia - dblnbvcrng) View more	-	06 Jun 2018
				Methylphenidate+Atomoxetine (Methylphenidate Then Atomoxetine)	qhnlilheom(fwqdpehwhk) = qqxrdydioy whimbqqxnq (hevhkfihqv, rlprsgdogu - mpsowojxng) View more
NCT00286949 (CTgov)	Not Applicable	Parkinson Disease	12	Atomoxetine	jljsonfilo(wnruvbihxr) = qbfemyshvy fxodwkbgzm (aaojoohcwa, psqpfakxkd - xiieukeauv) View more	-	18 Sep 2017