Generic Strattera is used for treating attention deficit hyperactivity disorder (ADHD).
Other names for this medication:
Also known as: Atomoxetine.
Generic Strattera is used for treating attention deficit hyperactivity disorder (ADHD).
Generic Strattera is a selective norepinephrine reuptake inhibitor. Exactly how Generic Strattera works to treat ADHD is not known. Generic Strattera increases certain chemicals (e.g., norepinephrine) in the brain. This may affect attention span and behavior.
Strattera is also known as Atomoxetine, Attentrol, Tomoxetin, Attentin, Axepta.
Generic name of Generic Strattera is Atomoxetine.
Brand name of Generic Strattera is Strattera.
Take Generic Strattera by mouth with or without food. If stomach upset occurs, take with food to reduce stomach irritation.
Swallow Generic Strattera whole. Do not open or take the capsules apart.
Taking Generic Strattera at the same time each day will help you remember to take it.
If you want to achieve most effective results do not stop taking Generic Strattera suddenly.
If you overdose Generic Strattera and you don't feel good you should visit your doctor or health care provider immediately.
Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Throw away any unused medication after the expiration date. Keep out of the reach of children.
The most common side effects associated with Strattera are:
Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.
Do not take Generic Strattera if you are allergic to Generic Strattera components.
Do not take Generic Strattera if you're pregnant or you plan to have a baby, or you are a nursing mother.
Do not Generic Strattera if you are taking or have taken a monoamine oxidase inhibitor (MAOI) (e.g., phenelzine) within the last 14 days.
Do not Generic Strattera if you have certain heart problems (e.g., heart defect, heart failure), certain types of irregular heartbeat, severe blood vessel problems, or narrow-angle glaucoma.
Children and teenagers who take Generic Strattera may be at increased risk for suicidal thoughts or actions. Adults may also be affected. The risk may be greater in patients who have had suicidal thoughts or actions in the past. The risk may also be greater in patients who have had bipolar (manic-depressive) illness, or if their family members have had it. Watch patients who take Generic Strattera closely!
Do not try to open the capsules or take them apart. Wash your hands immediately after using Generic Strattera. Do not get Generic Strattera in your eye. It may irritate your eye if you do. If you get Generic Strattera in your eyes or nose, rinse at once with cool water.
Lab tests, including heart rate, blood pressure, and liver function, may be performed while you use Generic Strattera.
Use Generic Strattera with caution in the elderly. They may be more sensitive to its effects, especially dizziness.
Corticosteroids may affect growth rate in children and teenagers in some cases. They may need regular growth checks while they take Generic Strattera.
Generic Strattera should be used with extreme caution in children younger than 6 years old. Safety and effectiveness in these children have not been confirmed.
Sit up or stand slowly, especially in the morning.
Avoid driving machine.
Do not stop taking Generic Strattera suddenly.
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An acute dose of MPH but not ATM or CIT was able to improve SSRT and reduce response time variability in nonclinical participants. Improvements in response inhibition and response variability might underlie the reported clinical benefits of MPH in disorders such as attention-deficit/hyperactivity disorder.
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This was a 3-arm, 9-week, randomized, placebo-controlled, double-blind study in ADHD patients (6-17 years) with comorbid ODD (Diagnostic and Statistical Manual of Mental Disorders, 4th edition [DSM-IV] criteria A-C) or conduct disorder (CD). ATX-treatment arms were as follows-ATX-fast: 7 days 0.5 mg/kg, then 1.2 mg/kg; ATX-slow: 7 days each at 0.5 and 0.8 mg/kg, then 1.2 mg/kg. Primary outcome was the Swanson, Nolan, and Pelham Rating Scale-Revised (SNAP-IV) ODD-score after 9 weeks (Mixed Effects Model for Repeated Measures, ATX-up-titration groups pooled).
The aim of this article was to assess the catalytic activities of 24 cytochrome P450 2D6 (CYP2D6) variants found in the Chinese population toward atomoxetine in vitro as well as CYP2D6.1.
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Eight trials were finally included. IR-MPH, OROS-MPH and AHC were effective for ADHD. OROS-MPH was superior to IR-MPH in the improvement of peer relationship, CGI-I score, mother satisfaction and psychosomatic problems. There were no significant differences in the effectiveness between the AHC and IR-MPH groups. The adverse events related to the therapy with IR-MPH, OROS-MPH or AHC were mild and the incidence rates of adverse events were not significantly different among the three groups.
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The catecholamine agonists methylphenidate and atomoxetine effectively treat attention-deficit/hyperactivity disorder (ADHD). Furthermore, dopamine agonists have shown to improve time estimation in ADHD, a core cognitive deficit. However, few have compared the effects of methylphenidate and atomoxetine on brain function in ADHD, and none during time estimation. Using single dose challenges, we investigated shared and drug-specific effects in ADHD adolescents on the neural substrates of time discrimination (TD).
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Although our data provide reassurance of the safety of ATX and MPH, several unexpected or uncommon ADRs (hepatomegaly, suicidal ideation, weight gain, or drug interactions) were identified by our intensive pharmacosurveillance monitoring program. Our results show that an intensive pharmacosurveillance monitoring program that involves pharmacovigilance centers and clinicians can improve the collection of information on drug safety in children.
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This meta-analysis examined suicide-related events in the acute phases of double-blind, placebo-controlled atomoxetine trials in pediatric and adult patients with attention-deficit/hyperactivity disorder (ADHD).
To illustrate a matching-adjusted indirect comparison by comparing the efficacy of guanfacine extended release (GXR) and atomoxetine (ATX) in reducing oppositional symptoms in children with attention-deficit/hyperactivity disorder and comorbid oppositional defiant disorder.
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Eli Lilly is developing tomoxetine, a norepinephrine reuptake inhibitor, for the potential treatment of attention deficit hyperactivity disorder (ADHD) and depression. As of May 2000, tomoxetine was undergoing phase III trials in the US . An NDA was filed with the FDA in October 2001, with a launch expected in the second half of 2002 . Tomoxetine was first investigated by Lilly in the 1980s as a potential treatment for depressive illness. The compound was selected from a series of potent inhibitors of norepinephrine reuptake, and reached large-scale phase II clinical trials for depression in 1990. Development for this indication appeared to stop at that time, despite some evidence that tomoxetine wasfairly effective . In 1996, Lilly apparently restarted preclinical development of tomoxetine as a potential therapyfor ADHD, and submitted EP-00721777 claiming tomoxetine's utility for this disorder in July of that year . In June 2001, ABN AMRO predicted sales of $121 million in 2002, rising to $4,064 million in 2012 . In October 2001, analysts at Salomon Smith Barney predicted that the product would make sales of $24 million in 2002, rising to $305 million in 2005 .
By the author.
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The objective of the study is to evaluate the effectiveness and tolerability of atomoxetine in youth, ages 6-17 years with ADHD, who had a prior trial of stimulant treatment. This was a 6-week prospective open-label study of atomoxetine, dosage up to 1.4 mg/kg per day in 34 children and adolescents with DSM-IV ADHD. Primary measures of response included the ADHD Rating Scale (ADHD RS) and the Clinical Global Impression (CGI) Scale. Analyses were intention-to-treat. The treatment with atomoxetine was associated with statistical and clinical significant reduction in clinician rated ADHD RS symptoms, compared with baseline. Statistical significant improvement was attained by the second week of treatment. Fifty-six percent (N = 18) met criteria for our a priori definition of response; much or very much improved on the CGI plus more than 30% reduction in ADHD RS symptoms. In conclusion, atomoxetine was generally well tolerated; 85% of subjects completed the trial. Atomoxetine was effective and well tolerated in a 6-week open study of ADHD youth with a prior history of stimulant treatment.
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Pediatric patients from 14 trials of atomoxetine were subdivided into a placebo-controlled (atomoxetine n = 1308, placebo n = 806) or active comparator databases (atomoxetine n = 566, methylphenidate n = 472). A third database comprised adult patients from placebo-controlled studies (atomoxetine n = 541, placebo n = 405). A computerized search of adverse events and comments identified patients with potential aggression/hostility events. Mantel-Haenszel incidence differences (MHID) were calculated.
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To investigate predictors of beginning treatment with atomoxetine, a new attention-deficit-hyperactivity disorder (ADHD) drug, shortly after it was introduced into the marketplace compared with well-established stimulants for children in a managed care setting.
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To examine the influence of comorbid oppositional defiant disorder (ODD) on the relative risk (RR) of relapse during 9 months of treatment with atomoxetine for attention-deficit/hyperactivity disorder (ADHD).
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The design, synthesis, and SAR of a series of ring-constrained norepinephrine reuptake inhibitors are described. A substantially rigid inhibitor with potent functional activity at the transporter (IC(50)=8 nM) was used to develop a model for the distance and orientation of key features necessary for interaction with the norepinephrine transporter (NET).
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Attention deficit hyperactivity disorder (ADHD) may exist in up to 60% of adults, whose first symptoms appeared before they were seven years old. Since it is a neurobiological condition, its basic symptoms -lack of attention, hyperactivity and impulsiveness- are similar at all ages, but in adults the clinical manifestations are specific to the subgroup with more frequent comorbidities than in childhood. Manifestations that characteristically appear in adults are difficulty in concentrating, poorer memory and short-term memory, disorganisation, difficulties with self-discipline, impulsiveness, low self-esteem, mental restlessness, frustration and limited social skills.
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The goal of this review was to describe the chemistry, mechanism of action, pharmacokinetics, drug interactions, and efficacy and safety profiles of atomoxetine in pediatric and adult patients with ADHD, as well as relevant pharmacoeconomic considerations.
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The primary outcome measure for both studies was mean ADHD Rating Scale (ADHD RS) total score. For study 1 (N = 122), decreases in ADHD RS total scores were not significantly different between treatment groups (mean change [SD]: continued same dose, -8.9 [11.2]; high dose, -9.8 [13.1]; p = .595). Likewise, for study 2 (N = 125), treatment groups did not differ (mean change [SD]: continued same dose, -6.2 [12.2]; high dose, -8.9 [10.0], p =.110). Tolerability was not significantly different between the continued same-dose and high-dose groups.
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We included 35 original studies on the pharmacogenetics of childhood psychiatric disorders. Thirty-three studies addressed the association between genes particularly dopamine transporter gene (DAT1) and dopamine D4 receptor gene (DRD4) and response to medication for the treatment of attention-deficit/hyperactivity disorder (ADHD). Only two studies investigated atomoxetine as the pharmacological intervention, and the other 31 studies investigated methylphenidate (MPH). One study assessed children with depression and anxiety disorders and another assessed children with autism; in both of them selective serotonin reuptake inhibitors (SSRIs) were the pharmacological intervention.
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The study objective was to assess the efficacy and tolerability of atomoxetine in the treatment of attention deficit hyperactivity disorder symptoms in patients with mental retardation. In a 16-week, open-label, prospective study, 48 children with mental retardation and attention deficit hyperactivity disorder were recruited; the patients received atomoxetine, with a single final dose of 1.2 mg/kg per day reached at 3 weeks. The measure of efficacy was scores on Clinical Global Impression Severity scale (CGI-S), Conners, and Attention Deficit Hyperactivity Disorder Rating Scale ADHDRS-IV. A statistically significant difference was documented between the mean CGI-S scores before and after treatment: baseline CGI-S = 5.31 (S.D. = 0.85); post-treatment CGI-S = 4.13 (S.D. = 0.97), with a difference of 1.18 points (S.D. = 0.84) and a 95% confidence interval for the difference of 0.92-1.43 (P < 0.001). A statistically significant reduction (P < 0.01) was observed with respect to all the variables of the ADHDRS-IV and Conners scales. Slightly less than one third of the patients (31%) presented adverse events, the majority of which were mild, with irritability being the most frequent event. Atomoxetine appears to be to useful in improving attention deficit hyperactivity disorder symptoms in mentally retarded patients. Larger, randomized, controlled, double-blind studies are required to confirm the efficacy observed in this first study.
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A post hoc analysis was conducted using data from two double-blind, placebo-controlled clinical trials. Data from patients aged 18-25 years were compared with data from patients older than 25 years.
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This evidence that atomoxetine reduces hyperactive/impulsive behaviours in NK1R(-/-) mice consolidates the validity of using NK1R(-/-) mice in research of the aetiology and treatment of ADHD.
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Atomoxetine demonstrated significant ADHD symptom reduction over 24 weeks. Although both groups demonstrated baseline-to-end point changes on many marital and parenting measure items, there were no treatment differences. Maladaptive behaviors of long-standing ADHD may benefit from both medication and behavioral-psychosocial intervention.
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Population, observational, cross-sectional study in a health department, using prevalence data (November 2013) of treatment for ADHD in children aged 6-12 years. Data was obtained from the information systems of the Valencia Ministry of Health and multivariate models were used to estimate the prevalence ratio of treatment according to the month of birth of children in each grade.
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Non-stimulant agents have been shown to be effective in treatment of ADHD. Especially, atomoxetine seems promising and newline drugs are in development.
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Two hundred twenty-eight patients were randomized (atomoxetine n = 184, methylphenidate n = 44). Both drugs were associated with marked improvement in inattentive and hyperactive-impulsive symptom clusters as assessed by parents and investigators. No statistically significant differences between treatment groups were observed on the primary outcome measure (investigator-rated ADHD-IV Rating Scale total score: atomoxetine baseline: 39.4 [8.5], endpoint: 20.0 [13.9]; methylphenidate baseline: 37.6 [9.7], endpoint: 19.8 (16.6); p = .66). Safety and tolerability were also similar between the 2 drugs. Discontinuations due to adverse events were 10/184 (5.4%) for atomoxetine and 5/44 (11.4%) for methylphenidate; p = .175.
Atomoxetine speeded SSRT and increased accuracy for go-trials. Citalopram slowed go reaction time and decreased go accuracy at the highest dose (1 mg/kg). GBR-12909 speeded go reaction time and impaired both go and stop accuracy. Guanfacine negatively modulated all principal stop and go measures at the highest dose used (0.3 mg/kg).
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A total of 44 patients aged ≥18 years who met the Conners' Adult ADHD Diagnostic Interview for DSM-IV diagnostic criteria for ADHD were enrolled from China, Korea, and Taiwan. In this open-label, dose-escalation study, patients received atomoxetine orally once daily over a period of eight weeks, starting at 40 mg/day (one week) up to a maximum dosage of 120 mg/day. Tolerability was evaluated by rate of discontinuation due to adverse events. Safety was assessed by recording all adverse events, laboratory tests, vital signs, and electrocardiograms. ADHD symptoms were evaluated by the Conners' Adult ADHD Rating Scale-Investigator Rated: Screening Version (CAARS-Inv:SV) for efficacy assessment.
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Relative to control subjects, patients under placebo showed TD deficits and reduced activation of ventrolateral prefrontal cortex (VLPFC)/insula, inferior frontal cortex, and supplementary motor area. Performance differences were normalized only by methylphenidate, relative to both atomoxetine and placebo. Both medications, however, significantly upregulated right VLPFC/insula activation within patients and normalized its underactivation in ADHD boys under placebo relative to control subjects. The supplementary motor area and inferior frontal cortex activation differences that were observed under placebo were reduced by methylphenidate and atomoxetine, respectively, but neither survived rigorous testing for normalization.
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The comorbidity of seizures, epilepsy, and attention-deficit-hyperactivity disorder (ADHD) prompted the examination of whether atomoxetine use for ADHD is associated with an increased risk of seizures. Seizures and seizure-related symptoms were reviewed from two independent Eli Lilly and Company databases: the atomoxetine clinical trials database and the atomoxetine postmarketing spontaneous adverse event database. Review of clinical trial data indicated that the crude incidence rates of seizure adverse events were between 0.1 and 0.2%, and were not significantly different between atomoxetine, placebo, and methylphenidate. Only 2% of the postmarketing spontaneous reports of seizure events were classified as having no clear contributing or confounding factors, and the reporting rate (8 per 100 000 patients exposed) was within the expected range of population-based incidence. Although children with ADHD are increasingly recognized as being at an elevated risk for seizures, treatment of ADHD symptoms with atomoxetine does not appear to elevate this risk further. The shared vulnerability between ADHD and seizure activity should be taken into account when making treatment decisions for populations of children with epilepsy and children with ADHD.
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