Research and Clinical Trials on Atomoxetine (Strattera)

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By Dr Greg Mulhauser

This list of current clinical research trials on Atomoxetine (Strattera) is followed by a short set of abstracts from the most recent research articles published on the drug.

Article Contents

Atomoxetine (Strattera) Clinical Research Trials

From our searchable database at ClinicalTrialsFeeds.org, this list includes all the latest information about clinical trials involving Atomoxetine (Strattera).

 

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Current Research Literature on Atomoxetine (Strattera)

Here are abstracts for some of the latest research articles to have appeared on Atomoxetine (Strattera):

Pharmacological treatment patterns among patients with attention-deficit/hyperactivity disorder: retrospective claims-based analysis of a managed care population.

Curr Med Res Opin. 2010 Apr; 26(4): 977-89
Christensen L, Sasané R, Hodgkins P, Harley C, Tetali S
Abstract Objective: To develop a descriptive profile of attention-deficit/hyperactivity disorder (ADHD) pharmacological treatment patterns in terms of persistence, adherence, augmentation, switching, and dosing changes; and to assess differences in treatment patterns with regard to ADHD medication type, class, and duration of action. Methods: This retrospective claims database analysis used medical data, pharmacy data, and enrollment information to examine treatment patterns among patients with at least one claim with a diagnosis code for ADHD and a filled prescription for ADHD medication (index therapy) during the period 01 January 2004 through 30 September 2006. Treatment persistence and adherence (days supplied/days persistent) were calculated. Dose changes, medication switching, and augmentation were analyzed at three levels of comparison: class (stimulant vs nonstimulant [atomoxetine]), drug type (amphetamine vs methylphenidate), and duration of action (short, intermediate, long). Statistical comparisons were made using the chi-square test for proportions and Student's t-test or the F-test from one-way ANOVA for means. Results: Of 60,010 patients meeting eligibility criteria, 58.4% were younger than age 18. Most (78.4%) were prescribed a stimulant as their index therapy. Persistence and adherence were greater for patients on stimulants (vs the nonstimulant), for patients on amphetamines (vs methylphenidates), and for patients on long-acting medications (vs short- and intermediate-acting medications; all p < 0.0001). Index drug dose changes were least likely among individuals taking the nonstimulant (vs stimulants), methylphenidates (vs amphetamines), or intermediate-acting drugs (vs short- and long-acting drugs; all p < 0.0001), and medication switches were more frequent among those on nonstimulants, methylphenidates, or short-acting drugs (all p < 0.0001). Subjects taking long-acting medication were less likely to augment with a drug with a different duration of action than those taking intermediate- or short-acting medication (p < 0.0001). This claims-based study is limited by possible discrepancies between claims and patient behaviors (i.e., a claim for a prescription does not necessarily indicate that the medication was taken as prescribed). Conclusions: Patients were more stable on treatment compared with their respective comparator groups if their index therapy was a stimulant, long-acting drug, or amphetamine.

Trends in incidence and characteristics of children, adolescents, and adults initiating immediate- or extended-release methylphenidate or atomoxetine in the Netherlands during 2001-2006.

J Child Adolesc Psychopharmacol. 2010 Feb; 20(1): 55-61
van den Ban E, Souverein P, Swaab H, van Engeland H, Heerdink R, Egberts T
BACKGROUND: Previous Dutch studies showed increasing psychostimulant use, especially methylphenidate immediate-release (MPH-IR), between 1995 and 2003. In 2003 the extended-release (ER) formulation of MPH and in 2005 atomoxetine (ATX) were introduced in The Netherlands, which increased treatment options. OBJECTIVE: The aim of this study was to describe the change in incidence of attention-deficit/hyperactivity disorder (ADHD) drugs and the prescription profiles of patients younger than 45 years starting treatment with these medicines between 2001 and 2006. METHODS: Data were obtained from Dutch community pharmacies as collected by the Foundation for Pharmaceutical Statistics, covering 97% of all dispenses for prescription medicines to outpatients in The Netherlands. RESULTS: The overall incidence of ADHD drugs use increased 6.5-fold from 2001 to 2006 in men as well as in women. The absolute incidence was highest among 6- to 11-year-old boys. The percentage of first-time MPH-IR users decreased from 98.3% in 2001 to 75.9% in 2006. Likewise, MPH-ER use increased from 0% in 2001 to 18.9% in 2006, and ATX use increased from 0% in 2001 to 3.9% in 2006. The new nonstimulant drug ATX was prescribed more often to adults if they had been previously treated with selective serotonin reuptake inhibitors (SSRIs), benzodiazepines, or antipsychotics. Youngsters

Prepuberal subchronic methylphenidate and atomoxetine induce different long-term effects on adult behaviour and forebrain dopamine, norepinephrine and serotonin in Naples High-Excitability rats.

Behav Brain Res. 2010 Feb 13;
Ruocco LA, Gironi Carnevale UA, Treno C, Sadile AG, Melisi D, Arra C, Ibba M, Schirru C, Carboni E
The psychostimulant methylphenidate and the non-stimulant atomoxetine are two approved drugs for attention-deficit hyperactivity disorder (ADHD) therapy. The aim of this study was to investigate the long-term effects of prepuberal subchronic methylphenidate and atomoxetine on adult behaviour and the forebrain neurotransmitter and metabolite content of Naples High-Excitability (NHE) rats, a genetic model for the mesocortical variant of ADHD. Male NHE rats were given a daily intraperitoneal injection (1.0mg/kg) of methylphenidate, atomoxetine or vehicle from postnatal day 29 to 42. At postnatal day 70-75, rats were exposed to spatial novelty in the Làt and radial (Olton) mazes. Behavioural analysis for indices of horizontal, vertical, non-selective (NSA) and selective spatial attention (SSA) indicated that only methylphenidate significantly reduced horizontal activity to a different extent, i.e., 39 and 16% respectively. Moreover methylphenidate increased NSA as assessed by higher leaning duration. The high-performance liquid chromatography (HPLC) tissue content assessment of dopamine, norepinephrine, serotonin and relative metabolites in the prefrontal cortex (PFC), cortical motor area (MC), dorsal striatum (DS), ventral striatum (VS), hippocampus and mesencephalon indicated that methylphenidate decreased (i) dopamine, DOPAC, norepinephrine, MHPG, 5-HT and 5-HIAA in the PFC, (ii) dopamine, DOPAC, HVA, serotonin, 5-HIAA in the DS, (iii) dopamine, DOPAC, HVA and MHPG (but increased norepinephrine) in the VS and (iv) norepinephrine, MHPG, serotonin and 5-HIAA in the hippocampus. Atomoxetine increased dopamine and decreased MHPG in the PFC. Like methylphenidate, atomoxetine decreased dopamine, DOPAC, HVA, serotonin and 5-HIAA in the DS, but decreased MHPG in the VS. These results suggest that methylphenidate determined long-term effects on behavioural and neurochemical parameters, whereas atomoxetine affected only the latter.

Gateways to clinical trials.

Methods Find Exp Clin Pharmacol. 2009 Nov; 31(9): 597-633
Tomillero A, Moral MA
Abacavir sulfate/lamivudine, Adalimumab, AdCD40L, Adefovir, Adefovir dipivoxil, Ambrisentan, Amlodipine, Amlodipine besylate/olmesartan medoxomil, AN-2728, Apixaban, Aripiprazole, Armodafinil, Atazanavir sulfate, Atomoxetine hydrochloride, Atrasentan, Azacitidine, Bevacizumab, Blinatumomab, Bortezomib, Bosentan, Carfilzomib, Caspofungin acetate, Cediranib, Cetuximab, Choriogonadotropin alfa, Clevudine, Clindamycin phosphate/benzoyl peroxide, Clofarabine, Daidzeol, Darunavir, Dasatinib, Decitabine, Deferasirox, Deforolimus, Degarelix acetate, Denenicokin, Dexlansoprazole, Duloxetine hydrochloride, Elacytarabine, Enfuvirtide, Enoxaparin, Entecavir, Eribulin mesilate, Erlotinib hydrochloride, Escitalopram oxalate, Eslicarbazepine acetate, Eszopiclone, Etravirine, Ezetimibe/simvastatin, Forodesine hydrochloride, Fosamprenavir calcium, Gefitinib, Gemtuzumab ozogamicin, Golimumab, Imatinib mesylate, Imetelstat, Insulin gl'argine, Insulin glulisine, Interferon alfa-2b XL, Ivabradine hydrochloride, Lacosamide, Lenalidomide, Lintuzumab, Liposomal adriamycin, Liposomal belotecan, Liposome-encapsulated fentanyl, Lopinavir/ritonavir, Lutropin alfa, LY-207320, Maraviroc, Mecasermin, MKC-253, MP-470, NGR-TNF, Nilotinib hydrochloride monohydrate, Ofatumumab, Olmesartan medoxomil, Omacetaxine mepesuccinate, PAN-811, Panobinostat, Pegfilgrastim, Peginterferon alfa-2a, Peginterferon alfa-2b, Peginterferon alfa-2b/ribavirin, Pemetrexed disodium, Perospirone hydrochloride, PF-734200, Phentermine/topiramate, Pimecrolimus, Pitavastatin calcium, Plerixafor hydrochloride, Pregabalin, Raltegravir potassium, Ramelteon, Ranibizumab, Recombinant Bet V1, Recombinant human insulin, Regadenoson, rhITF, Romidepsin, Rosuvastatin calcium, Ruboxistaurin hydrochloride, Rufinamide, Sapropterin dihydrochloride Saracatinib, SB-73, SC-599, Seliciclib, Sirolimus-eluting stent, Sorafenib, Sunitinib malate, Tadalafil, Tanespimycin, Tapentadol hydrochloride, Tegaserod maleate, Telbivudine, Tenofovir disoproxil fumarate, Tenofovir disoproxil fumarate/emtricitabine, Tenofovir disoproxil fumarate/emtricitabine/efavirenz, Ticlopidine hydrochloride, Tigecycline, TST-10088, Tularemia vaccine, Valsartan/amlodipine besylate, Vandetanib, Vardenafil hydrochloride hydrate, Vincristine, Vorinostat, Yttrium 90 (90Y) ibritumomab tiuxetan.

Cognitive enhancement as a pharmacotherapy target for stimulant addiction.

Addiction. 2010 Jan; 105(1): 38-48
Sofuoglu M
BACKGROUND: No medications have been proven to be effective for cocaine and methamphetamine addiction. Attenuation of drug reward has been the main strategy for medications development, but this approach has not led to effective treatments. Thus, there is a need to identify novel treatment targets in addition to the brain reward system. AIM: To propose a novel treatment strategy for stimulant addiction that will focus on medications enhancing cognitive function and attenuating drug reward. METHODS: Pre-clinical and clinical literature on potential use of cognitive enhancers for stimulant addiction pharmacotherapy was reviewed. RESULTS AND CONCLUSIONS: Cocaine and methamphetamine users show significant cognitive impairments, especially in attention, working memory and response inhibition functions. The cognitive impairments seem to be predictive of poor treatment retention and outcome. Medications targeting acetylcholine and norepinephrine are particularly well suited for enhancing cognitive function in stimulant users. Many cholinergic and noradrenergic medications are on the market and have a good safety profile and low abuse potential. These include galantamine, donepezil and rivastigmine (cholinesterase inhibitors), varenicline (partial nicotine agonist), guanfacine (alpha(2)-adrenergic agonist) and atomoxetine (norepinephrine transporter inhibitor). Future clinical studies designed optimally to measure cognitive function as well as drug use behavior would be needed to test the efficacy of these cognitive enhancers for stimulant addiction.

 

This page was last reviewed by Dr Greg Mulhauser, Sunday, 31 January 2010.

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http://counsellingresource.com/medications/trials-and-research/atomoxetine-research.html