What is Kamaptin used for?

Atomoxetine is indicated for the treatment of Attention-Deficit/Hyperactivity Disorder (ADHD) in children of 6 years and older, in adolescents and in adults as part of a comprehensive treatment programme. Treatment must be initiated by a specialist in the treatment of ADHD, such as a paediatrician, child/adolescent psychiatrist, or psychiatrist. Diagnosis should be made according to current DSM criteria or the guidelines in ICD. In adults, the presence of symptoms of ADHD that

What pharmaceutical form is Kamaptin available in?

Kamaptin: Kapsułki twarde 10 mg (doustna)

Is Kamaptin OTC or prescription only?

Kamaptin requires a doctor's prescription.

What are the side effects of Kamaptin?

Paediatric population : Summary of the safety profile In paediatric placebo-controlled trials, headache, abdominal pain 1 and decreased appetite are the adverse events most commonly associated with atomoxetine, and are reported by about 19%, 18% and 16% of patients respectively, but seldom lead to drug discontinuation (discontinuation rates are 0.1% for headache, 0.2% for abdominal pain and 0.0% for decreased appetite). Abdominal pain and decreased appetite are usually transien

Who should NOT take Kamaptin?

Hypersensitivity to the active substance or to any of the excipients listed in section 6.1. Atomoxetine should not be used in combination with monoamine oxidase inhibitors (MAOI). Atomoxetine should not be used within a minimum of 2 weeks after discontinuing therapy with MAOI. Treatment with MAOI should not be initiated within 2 weeks after discontinuing atomoxetine. Atomoxetine should not be used in patients with narrow angle glaucoma, as in clinical trials the use of atomoxet

Does Kamaptin interact with other medications?

Effects of other drugs on atomoxetine: MAOIs: Atomoxetine should not be used with MAOIs (see section 4.3). CYP2D6 inhibitors (SSRIs (e.g. fluoxetine, paroxetine), quinidine, terbinafine): In patients receiving these drugs, atomoxetine exposure may be 6-to 8-fold increased and Css max 3 to 4 times higher, because it is metabolised by the CYP2D6 pathway. Slower titration and final lower dosage of atomoxetine may be necessary in patients who are already taking CYP2D6 inhibitor dru

Can Kamaptin be used during pregnancy?

Pregnancy Animal studies in general do not indicate direct harmful effects with respect to pregnancy, embryonal/foetal development, parturition or postnatal development (see section 5.3). For atomoxetine clinical data on exposed pregnancies are limited. Such data are insufficient to indicate either an association or a lack of association between atomoxetine and adverse pregnancy and/or lactation outcomes. Atomoxetine should not be used during pregnancy unless the potential bene

What precautions should be taken with Kamaptin?

Any unused medicinal product or waste material should be disposed of in accordance with local requirements.

Who manufactures Kamaptin?

Ranbaxy (Poland) Sp. z o.o. (Niemcy)

What ATC class does Kamaptin belong to?

Kamaptin: ATC N06BA09. ATC is the WHO Anatomical Therapeutic Chemical classification — it groups drugs by organ system and pharmacological mechanism.

Kamaptin

This information is for educational purposes only. It is not intended as medical advice. Always consult a qualified healthcare professional.

Kamaptin — Description, Dosage, Side Effects | PillsCard

Pharmacotherapeutic group: Psychoanaleptics, centrally acting sympathomimetics ATC code: N06BA09 Mechanism of action and Pharmacodynamic effects Atomoxetine is a highly selective and potent inhibitor of the pre-synaptic noradrenaline transporter, its presumed mechanism of action, without directly affecting the serotonin or dopamine transporters.‍‍‍‍‍‍‍‍‍‍‍‍‍ Atomoxetine has minimal affinity for other noradrenergic receptors or for other neurotransmitter transporters or receptors. Atomoxetine has two major oxidative metabolites: 4-hydroxyatomoxetine and N-desmethylatomoxetine. 4-Hydroxyatomoxetine is equipotent to atomoxetine as an inhibitor of the noradrenaline transporter but unlike atomoxetine, this metabolite also exerts some inhibitory activity at the serotonin transporter. However, any effect on this transporter is likely to be minimal as the majority of 4-hydroxyatomoxetine is further metabolised such that it circulates in plasma at much lower concentrations (1% of atomoxetine concentration in extensive metabolisers and 0.1% of atomoxetine concentration in poor metabolisers). N-Desmethylatomoxetine has substantially less pharmacological activity compared with atomoxetine. It circulates in plasma at lower concentrations in extensive metabolisers and at comparable concentrations to the parent drug in poor metabolisers at steady state. Atomoxetine is not a psychostimulant and is not an amphetamine derivative. In a randomised, double-blind, placebo-controlled, abuse-potential study in adults comparing effects of atomoxetine and placebo, atomoxetine was not associated with a pattern of response that suggested stimulant or euphoriant properties. Clinical efficacy and safety Paediatric population Atomoxetine has been studied in trials in over 5000 children and adolescents with ADHD. The acute efficacy of Atomoxetine in the treatment of ADHD was initially established in six randomised, double-blind, placebo-controlled trials of six to nine weeks duration. Signs and symptoms of ADHD were evaluated by a comparison of mean change from baseline to endpoint for Atomoxetine treated and placebo treated patients. In each of the six trials, atomoxetine was statistically significantly superior to placebo in reducing ADHD signs and symptoms. Additionally, the efficacy of atomoxetine in maintaining symptom response was demonstrated in a 1 year, placebo-controlled trial with over 400 children and adolescents, primarily conducted in Europe (approximately 3 months of open label acute treatment followed by 9 months of double-blind, placebo-controlled maintenance treatment). The proportion of patients relapsing after 1 year was 18.7% and 31.4% (atomoxetine and placebo, respectively). After 1 year of atomoxetine treatment, patients who continued atomoxetine for 6 additional months were less likely to relapse or to experience partial symptom return compared with patients who discontinued active treatment and switched to placebo (2% vs. 12% respectively). For children and adolescents periodic assessment of the value of ongoing treatment during long-term treatment should be performed. Atomoxetine was effective as a single daily dose and as a divided dose administered in the morning, and late afternoon/early evening. Atomoxetine administered once daily demonstrated statistically significantly greater reduction in severity of ADHD symptoms compared with placebo as judged by teachers and parents. Active Comparator Studies In a randomised, double-blind, parallel group, 6 week paediatric study to test the noninferiority of atomoxetine to a standard extended-release methylphenidate comparator, the comparator was shown to be associated with superior response rates compared to atomoxetine. The percentage of patients classified as responders was 23.5% (placebo), 44.6% (atomoxetine) and 56.4% (methylphenidate). Both atomoxetine and the comparator were statistically superior to placebo and methylphenidate was statistically superior to atomoxetine (p=0.016). However, this study excluded patients who were stimulant nonresponders. Adult population Atomoxetine has been studied in trials in over 4800 adults who met DSM-IV diagnostic criteria for ADHD. The acute efficacy of Atomoxetine in the treatment of adults was established in six randomised, double-blind, placebo-controlled trials of ten to sixteen weeks' duration. Signs and symptoms of ADHD were evaluated by a comparison of mean change from baseline to endpoint for atomoxetine treated and placebo treated patients. In each of the six trials, atomoxetine was statistically significantly superior to placebo in reducing ADHD signs and symptoms (Table X). Atomoxetine-treated patients had statistically significantly greater improvements in clinical global impression of severity (CGI-S) at endpoint compared to placebo-treated patients in all of the 6 acute studies, and statistically significantly greater improvements in ADHD related functioning in all 3 of the acute studies in which this was assessed (Table X). Long-term efficacy was confirmed in 2 six-month placebo controlled studies, but not demonstrated in a third (Table X). Table X Mean Changes in Efficacy Measures for Placebo-Controlled Studies Changes from Baseline in Patients with at Least One Post baseline Value (LOCF) CAARS-Inv:SV or AISRS a CGI-S AAQoL Study Treatment N Mean Change p-value Mean Change p-value Mean Change p-value Acute Studies LYAA ATX PBO 133 134 -9.5 -6.0 0.006 -0.8 -0.4 0.011 - - LYAO ATX PBO 124 124 -10.5 -6.7 0.002 -0.9 -0.5 0.002 - - LYBY ATX PBO 72 75 -13.6 -8.3 0.007 -1.0 -0.7 0.048 - - LYDQ ATX PBO 171 158 -8.7 -5.6 <0.001 -0.8 -0.6 0.022 14.9 11.1 0.030 LYDZ ATX PBO 192 198 -10.7 -7.2 <0.001 -1.1 -0.7 <0.001 15.8 11.0 0.005 LYEE ATX PBO 191 195 -14.3 -8.8 <0.001 -1.3 -0.8 <0.001 12.83 8.20 <0.001 Long-Term Studies LYBV ATX PBO 185 109 -11.6 -11.5 0.412 -1.0 -0.9 0.173 13.90 11.18 0.045 LYCU ATX PBO 214 216 -13.2 -10.2 0.005 -1.2 -0.9 0.001 13.14 8.62 0.004 LYCW ATX PBO 113 120 -14.3 -8.3 <0.001 -1.2 -0.7 <0.001 - - Abbreviations: AAQoL = Adult ADHD Quality of Life Total Score; AISRS = Adult ADHD Investigator Symptom Rating Scale Total Score; ATX = atomoxetine; CAARS-Inv:SV = Conners Adult ADHD Rating Scale, Investigator Rated, screening version Total ADHD Symptom Score; CGI-S = Clinical Global Impression of Severity; LOCF = last observation carried forward; PBO = placebo. a ADHD symptom scales; results shown for Study LYBY are for AISRS; results for all others are for CAARS-Inv:SV. In sensitivity analyses using a baseline-observation-carried-forward method for patients with no postbaseline measure (i.e. all patients treated), results were consistent with results shown in Table X. In analyses of clinically meaningful response in all 6 acute and both successful longterm studies, using a variety of a priori and post hoc definitions, atomoxetine-treated patients consistently had statistically significantly higher rates of response than placebo-treated patients (Table Y). Table Y Number (n) and Percent of Patients Meeting Criteria for Response in Pooled Placebo-Controlled Studies Group Treatment Response Defined by Improvement of at least 1 point on CGI-S Response Defined by 40% Improvement on CAARS-Inv:SV at Endpoint N n (%) p-value N n (%) p-value Pooled Acute Studies a ATX PBO 640 652 401 (62.7%) 283 (43.4%) <0.001 841 851 347 (41.3%) 215 (25.3%) <0.001 Pooled Long-Term Studies a ATX PBO 758 611 482 (63.6%) 301 (49.3%) <0.001 663 557 292 (44.0%) 175 (31.4%) <0.001 a Includes all studies in Table X except: Acute CGI-S response analysis excludes 2 studies in patients with comorbid disorders (LYBY, LYDQ); Acute CAARS response analysis excludes 1 study in which the CAARS was not administered (LYBY). In two of the acute studies, patients with ADHD and comorbid alcoholism or social anxiety disorder were studied and in both studies ADHD symptoms were improved. In the study with comorbid alcohol abuse, there were no differences between atomoxetine and placebo with respect to alcohol use behaviours. In the study with comorbid anxiety, the comorbid condition of anxiety did not deteriorate with atomoxetine treatment. The efficacy of atomoxetine in maintaining symptom response was demonstrated in a study where after an initial active treatment period of 24 weeks, patients who met criteria for clinically meaningful response (as defined by improvement on both CAARS-Inv:SV and CGI-S scores) were randomized to receive atomoxetine or placebo for an additional 6 months of double-blind treatment. Higher proportions of atomoxetine-treated patients than placebo-treated patients met criteria for maintaining clinically meaningful response at the end of 6 months (64.3% vs. 50.0%; p=0.001). Atomoxetine-treated patients demonstrated statistically significantly better maintenance of functioning than placebo-treated patients as shown by lesser mean change on the Adult ADHD Quality of Life (AAQoL) total score at the 3-month interval (p=0.003) and at the 6-month interval (p=0.002). QT/QTc study A thorough QT/QTc study, conducted in healthy adult CYP2D6 poor metabolizer (PM) subjects dosed up to 60 mg of atomoxetine BID, demonstrated that at maximum expected concentrations the effect of atomoxetine on QTc interval was not significantly different from placebo. There was a slight increase in QTc interval with increased atomoxetine concentration.

Kamaptin

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