CLINICAL TRIALS PROFILE FOR TRICOR
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All Clinical Trials for Tricor
| Trial ID | Title | Status | Sponsor | Phase | Start Date | Summary |
|---|---|---|---|---|---|---|
| NCT00186537 ↗ | Comparing Tricor, Avandia, or Weight Loss to Lower Cardiovascular Risk Factors in People With High Triglycerides. | Completed | Abbott | N/A | 2003-09-01 | Approximately 1/4 of the US population has insulin resistance and the associated risk factors such as elevated lipid levels -triglycerides (type of fat from what we eat and what the liver produces and low HDL cholesterol which is the good cholesterol helping to protect against heart disease. Currently one known treatment for this a medication called fenofibrate, another medication that can improve insulin resistance is rosiglitazone, a third treatment known to improve insulin resistance an decrease triglycerides is weight loss. In this study insulin resistant individuals with elevated triglycerides and or a ratio of triglycerides to HDL cholesterol of 3:1 or greater will be randomized (selected by chance) to receive one of these treatments and results of insulin sensitivity and cardiac risk profiles will be compared at the end of the study. |
| NCT00186537 ↗ | Comparing Tricor, Avandia, or Weight Loss to Lower Cardiovascular Risk Factors in People With High Triglycerides. | Completed | Stanford University | N/A | 2003-09-01 | Approximately 1/4 of the US population has insulin resistance and the associated risk factors such as elevated lipid levels -triglycerides (type of fat from what we eat and what the liver produces and low HDL cholesterol which is the good cholesterol helping to protect against heart disease. Currently one known treatment for this a medication called fenofibrate, another medication that can improve insulin resistance is rosiglitazone, a third treatment known to improve insulin resistance an decrease triglycerides is weight loss. In this study insulin resistant individuals with elevated triglycerides and or a ratio of triglycerides to HDL cholesterol of 3:1 or greater will be randomized (selected by chance) to receive one of these treatments and results of insulin sensitivity and cardiac risk profiles will be compared at the end of the study. |
| NCT00195793 ↗ | A 16 Week Comparative Study of Fenofibrate Versus Ezetimibe as Add-on Therapy to Atorvastatin | Completed | Abbott | Phase 3 | 2004-08-01 | The objective of this study is to evaluate the effects of adding Tricor 145 mg to once daily atorvastatin 20 mg on CHD lipid laboratory parameters. |
| NCT00251680 ↗ | Efficacy of Lapaquistat Acetate in Subjects Currently Treated With Lipid-Lowering Therapy. | Completed | Takeda | Phase 3 | 2005-10-01 | The purpose of the study is to determine the efficacy of lapaquistat acetate, once daily (QD), taken with established lipid-lowering therapy in subjects with type 2 diabetes mellitus. |
| NCT00262964 ↗ | Obesity and Nonalcoholic Fatty Liver Disease | Completed | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) | N/A | 2004-10-01 | The primary goal of this study is to provide a better understanding of: 1) the pathogenesis and pathophysiology of non-alcoholic fatty liver disease (NAFLD) in obese subjects, and 2) the effect of marked weight loss on the histologic and metabolic abnormalities associated with NAFLD. The following hypotheses will be tested: 1. obesity causes hepatic fat accumulation because of excessive fatty acid release from fat tissue and increased free fatty acid availability, 2. increased hepatic (liver) fat content causes insulin-resistant glucose (sugar) production by the liver and altered liver protein synthesis, 3. increased hepatic fat content causes increased lipid (fat) peroxidation, hepatic inflammation, necrosis and fibrosis, and 4. marked weight loss improves NAFLD once patients are weight stable. |
| NCT00262964 ↗ | Obesity and Nonalcoholic Fatty Liver Disease | Completed | Washington University School of Medicine | N/A | 2004-10-01 | The primary goal of this study is to provide a better understanding of: 1) the pathogenesis and pathophysiology of non-alcoholic fatty liver disease (NAFLD) in obese subjects, and 2) the effect of marked weight loss on the histologic and metabolic abnormalities associated with NAFLD. The following hypotheses will be tested: 1. obesity causes hepatic fat accumulation because of excessive fatty acid release from fat tissue and increased free fatty acid availability, 2. increased hepatic (liver) fat content causes insulin-resistant glucose (sugar) production by the liver and altered liver protein synthesis, 3. increased hepatic fat content causes increased lipid (fat) peroxidation, hepatic inflammation, necrosis and fibrosis, and 4. marked weight loss improves NAFLD once patients are weight stable. |
| >Trial ID | >Title | >Status | >Sponsor | >Phase | >Start Date | >Summary |
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