CLINICAL TRIALS PROFILE FOR CHLORPROTHIXENE
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All Clinical Trials for CHLORPROTHIXENE
| Trial ID | Title | Status | Sponsor | Phase | Start Date | Summary |
|---|---|---|---|---|---|---|
| NCT01309178 ↗ | Anti-inflammatory Pulmonal Therapy of Cystic Fibrosis (CF) Patients With Amitriptyline and Placebo | Unknown status | Universität Duisburg-Essen | Phase 2 | 2009-05-01 | Cystic fibrosis patients suffer from a chronic destruction of the lung, frequent and finally chronic pneumonia and a reduced life expectancy. Unfortunately, no curative treatment for cystic fibrosis is available, neither are treatments established that prevent the disease. Our data identify ceramide as a potential novel target to treat cystic fibrosis. Two smaller trials support the notion that inhibition of the acid sphingomyelinase by amitriptyline improves the lung function of CF-patients even at a dose that is low enough to avoid adverse effects. In the present proposal the investigators, therefore, aim to test in a larger cystic fibrosis patient population whether an inhibition of ceramide release in the lung caused by the lack of functional CFTR improves the lung function of cystic fibrosis patients. Inhibition of ceramide-release in the lung will be achieved by treatment with amitriptyline, which is used as an anti-depressant drug for almost 50 years. Although it is not absolutely specific, it seems to be relatively specific for the degradation of acid sphingomyelinase (typically 60-80% of cellular acid sphingomyelinase are degraded), which releases ceramide from sphingomyelin. If the data confirm the beneficial effect of amitriptyline already observed in our preliminary studies, the present clinical study may establish a novel treatment to improve clinical symptoms of cystic fibrosis and, moreover, to prevent or at least delay the onset of cystic fibrosis. Hypothesis - Amitriptyline reduces ceramide concentrations in respiratory epithelial cells (measured in nasal epithelial cells obtained by brushing nasal mucosa). - Amitriptyline treatment reduces cell death in bronchi and deposition of DNA on the respiratory epithelium, which permits elimination of P. aeruginosa from the lung (measured as P. aeruginosa counts in tracheal fluid). - Amitriptyline treatment results in normalization of the function of leukocytes (number determined in serum and tracheal fluid) - Amitriptyline reduces systemic and local inflammation (measured as cytokines in plasma and tracheal fluid). Based on these effects amitriptyline increases the lung function of cystic fibrosis patients (measured by FEV1). |
| NCT01309178 ↗ | Anti-inflammatory Pulmonal Therapy of Cystic Fibrosis (CF) Patients With Amitriptyline and Placebo | Unknown status | University of Ulm | Phase 2 | 2009-05-01 | Cystic fibrosis patients suffer from a chronic destruction of the lung, frequent and finally chronic pneumonia and a reduced life expectancy. Unfortunately, no curative treatment for cystic fibrosis is available, neither are treatments established that prevent the disease. Our data identify ceramide as a potential novel target to treat cystic fibrosis. Two smaller trials support the notion that inhibition of the acid sphingomyelinase by amitriptyline improves the lung function of CF-patients even at a dose that is low enough to avoid adverse effects. In the present proposal the investigators, therefore, aim to test in a larger cystic fibrosis patient population whether an inhibition of ceramide release in the lung caused by the lack of functional CFTR improves the lung function of cystic fibrosis patients. Inhibition of ceramide-release in the lung will be achieved by treatment with amitriptyline, which is used as an anti-depressant drug for almost 50 years. Although it is not absolutely specific, it seems to be relatively specific for the degradation of acid sphingomyelinase (typically 60-80% of cellular acid sphingomyelinase are degraded), which releases ceramide from sphingomyelin. If the data confirm the beneficial effect of amitriptyline already observed in our preliminary studies, the present clinical study may establish a novel treatment to improve clinical symptoms of cystic fibrosis and, moreover, to prevent or at least delay the onset of cystic fibrosis. Hypothesis - Amitriptyline reduces ceramide concentrations in respiratory epithelial cells (measured in nasal epithelial cells obtained by brushing nasal mucosa). - Amitriptyline treatment reduces cell death in bronchi and deposition of DNA on the respiratory epithelium, which permits elimination of P. aeruginosa from the lung (measured as P. aeruginosa counts in tracheal fluid). - Amitriptyline treatment results in normalization of the function of leukocytes (number determined in serum and tracheal fluid) - Amitriptyline reduces systemic and local inflammation (measured as cytokines in plasma and tracheal fluid). Based on these effects amitriptyline increases the lung function of cystic fibrosis patients (measured by FEV1). |
| NCT01309178 ↗ | Anti-inflammatory Pulmonal Therapy of Cystic Fibrosis (CF) Patients With Amitriptyline and Placebo | Unknown status | University Children's Hospital Tuebingen | Phase 2 | 2009-05-01 | Cystic fibrosis patients suffer from a chronic destruction of the lung, frequent and finally chronic pneumonia and a reduced life expectancy. Unfortunately, no curative treatment for cystic fibrosis is available, neither are treatments established that prevent the disease. Our data identify ceramide as a potential novel target to treat cystic fibrosis. Two smaller trials support the notion that inhibition of the acid sphingomyelinase by amitriptyline improves the lung function of CF-patients even at a dose that is low enough to avoid adverse effects. In the present proposal the investigators, therefore, aim to test in a larger cystic fibrosis patient population whether an inhibition of ceramide release in the lung caused by the lack of functional CFTR improves the lung function of cystic fibrosis patients. Inhibition of ceramide-release in the lung will be achieved by treatment with amitriptyline, which is used as an anti-depressant drug for almost 50 years. Although it is not absolutely specific, it seems to be relatively specific for the degradation of acid sphingomyelinase (typically 60-80% of cellular acid sphingomyelinase are degraded), which releases ceramide from sphingomyelin. If the data confirm the beneficial effect of amitriptyline already observed in our preliminary studies, the present clinical study may establish a novel treatment to improve clinical symptoms of cystic fibrosis and, moreover, to prevent or at least delay the onset of cystic fibrosis. Hypothesis - Amitriptyline reduces ceramide concentrations in respiratory epithelial cells (measured in nasal epithelial cells obtained by brushing nasal mucosa). - Amitriptyline treatment reduces cell death in bronchi and deposition of DNA on the respiratory epithelium, which permits elimination of P. aeruginosa from the lung (measured as P. aeruginosa counts in tracheal fluid). - Amitriptyline treatment results in normalization of the function of leukocytes (number determined in serum and tracheal fluid) - Amitriptyline reduces systemic and local inflammation (measured as cytokines in plasma and tracheal fluid). Based on these effects amitriptyline increases the lung function of cystic fibrosis patients (measured by FEV1). |
| NCT01309178 ↗ | Anti-inflammatory Pulmonal Therapy of Cystic Fibrosis (CF) Patients With Amitriptyline and Placebo | Unknown status | University Children’s Hospital Tuebingen | Phase 2 | 2009-05-01 | Cystic fibrosis patients suffer from a chronic destruction of the lung, frequent and finally chronic pneumonia and a reduced life expectancy. Unfortunately, no curative treatment for cystic fibrosis is available, neither are treatments established that prevent the disease. Our data identify ceramide as a potential novel target to treat cystic fibrosis. Two smaller trials support the notion that inhibition of the acid sphingomyelinase by amitriptyline improves the lung function of CF-patients even at a dose that is low enough to avoid adverse effects. In the present proposal the investigators, therefore, aim to test in a larger cystic fibrosis patient population whether an inhibition of ceramide release in the lung caused by the lack of functional CFTR improves the lung function of cystic fibrosis patients. Inhibition of ceramide-release in the lung will be achieved by treatment with amitriptyline, which is used as an anti-depressant drug for almost 50 years. Although it is not absolutely specific, it seems to be relatively specific for the degradation of acid sphingomyelinase (typically 60-80% of cellular acid sphingomyelinase are degraded), which releases ceramide from sphingomyelin. If the data confirm the beneficial effect of amitriptyline already observed in our preliminary studies, the present clinical study may establish a novel treatment to improve clinical symptoms of cystic fibrosis and, moreover, to prevent or at least delay the onset of cystic fibrosis. Hypothesis - Amitriptyline reduces ceramide concentrations in respiratory epithelial cells (measured in nasal epithelial cells obtained by brushing nasal mucosa). - Amitriptyline treatment reduces cell death in bronchi and deposition of DNA on the respiratory epithelium, which permits elimination of P. aeruginosa from the lung (measured as P. aeruginosa counts in tracheal fluid). - Amitriptyline treatment results in normalization of the function of leukocytes (number determined in serum and tracheal fluid) - Amitriptyline reduces systemic and local inflammation (measured as cytokines in plasma and tracheal fluid). Based on these effects amitriptyline increases the lung function of cystic fibrosis patients (measured by FEV1). |
| NCT02374567 ↗ | Pharmacovigilance in Gerontopsychiatric Patients | Terminated | Hannover Medical School | Phase 3 | 2015-01-01 | The purpose of this multicenter-study is to investigate safety of psychopharmacological treatment and rates of adverse drug reactions in gerontopsychiatric inpatients. Elderly people are at higher risk for developing side effects under pharmacological treatment due to an altered metabolic situation, higher comorbidity rates and often polypharmacy. Furthermore gerontopsychiatric patients can often not articulate their symptoms clearly, for example due to pronounced cognitive impairment. The aim of the study is to gain valid data of possible adverse drug reaction rates, their potential risk factors and outcome, as well as medical prescription practises. To assess these outcomes an intensive pharmacovigilance-monitoring will be conducted at the five participating study sites. At Baseline demographic data, previous and present disorders, use of drugs, previous and present medication, quality of life, cognitive function, physical examination results, laboratory results and ECG will be assessed. Afterwards patients are visited weekly and screened for possible adverse drug reactions. All adverse drug reactions will be coded in the MedDRA-system. In case of a possible serious adverse drug reaction serum levels of all psychotropic substances applicated will be assessed. Drug combinations will be analysed using an established advanced bioinformatic tool (mediQ). Diagnosis, medication intake and possible adverse drug reactions are documented continually. 2 weeks after discharge from the ward, patients will be contacted by phone to assess catamnestic data. |
| NCT02582736 ↗ | Antipsychotics and Risk of Hyperglycemic Emergencies | Completed | Canadian Institutes of Health Research (CIHR) | 2012-04-01 | The purpose of this study is to determine whether the use of atypical antipsychotic medication increases the risk of hospitalization for a hyperglycemic emergency. The investigators will carry out separate population-based cohort studies using administrative health databases in eight jurisdictions in Canada and the UK. Cohort entry will be defined by the initiation of a new antipsychotic medication. Follow-up will continue until hospitalization for a hyperglycemic emergency or the end of 365 days. The results from the separate sites will be combined to provide an overall assessment of the risk of hyperglycemic emergencies among new users of various antipsychotic drugs. | |
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