CLINICAL TRIALS PROFILE FOR CYTOMEL
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All Clinical Trials for Cytomel
| Trial ID | Title | Status | Sponsor | Phase | Start Date | Summary |
|---|---|---|---|---|---|---|
| NCT00208702 ↗ | Thyroid Medication and Antidepressants for Treating Major Depression | Completed | National Institute of Mental Health (NIMH) | Phase 4 | 1996-09-01 | This study will evaluate the effectiveness of treatment with supplemental triiodothyronine (T3, Cytomel) and sertraline (Zoloft), a selective serotonin reuptake inhibitor (SSRI), in improving symptoms of major depressive disorder (MDD). |
| NCT00208702 ↗ | Thyroid Medication and Antidepressants for Treating Major Depression | Completed | Emory University | Phase 4 | 1996-09-01 | This study will evaluate the effectiveness of treatment with supplemental triiodothyronine (T3, Cytomel) and sertraline (Zoloft), a selective serotonin reuptake inhibitor (SSRI), in improving symptoms of major depressive disorder (MDD). |
| NCT00265980 ↗ | Leptin in Human Energy and Neuroendocrine Homeostasis | Terminated | Columbia University | N/A | 2002-07-01 | Previous work in our laboratory, and many others, has shown that body weight is regulated. When anyone, fat or thin, tries to maintain a reduced body weight, many systems affecting energy balance (skeletal muscle, neuroendocrine, and autonomic systems) conspire to slow metabolic rate thus favoring the regain of lost weight. Individuals with leptin deficiency are remarkably similar to weight-reduced individuals. Their metabolism, thyroid hormones, and sympathetic nervous system activity are all low despite their obesity. While administration of leptin to leptin-deficient humans results in substantial weight loss and increases in energy expenditure. However, leptin administration to leptin-sufficient humans at usual body weight has little or no effect on weight unless given in doses 10-20 times what would be considered to be in the normal physiological range. This study examines the hypothesis that leptin is "read" by various systems regulating energy balance as an indicator of how much energy we have stored and that the body perceives the weight-reduced state as a condition of relative leptin insufficiency. Within this model, restoration of leptin to levels present prior to weight loss should relieve much of the metabolic opposition to keeping weight off. Preliminary studies support this hypothesis. |
| NCT00265980 ↗ | Leptin in Human Energy and Neuroendocrine Homeostasis | Terminated | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) | N/A | 2002-07-01 | Previous work in our laboratory, and many others, has shown that body weight is regulated. When anyone, fat or thin, tries to maintain a reduced body weight, many systems affecting energy balance (skeletal muscle, neuroendocrine, and autonomic systems) conspire to slow metabolic rate thus favoring the regain of lost weight. Individuals with leptin deficiency are remarkably similar to weight-reduced individuals. Their metabolism, thyroid hormones, and sympathetic nervous system activity are all low despite their obesity. While administration of leptin to leptin-deficient humans results in substantial weight loss and increases in energy expenditure. However, leptin administration to leptin-sufficient humans at usual body weight has little or no effect on weight unless given in doses 10-20 times what would be considered to be in the normal physiological range. This study examines the hypothesis that leptin is "read" by various systems regulating energy balance as an indicator of how much energy we have stored and that the body perceives the weight-reduced state as a condition of relative leptin insufficiency. Within this model, restoration of leptin to levels present prior to weight loss should relieve much of the metabolic opposition to keeping weight off. Preliminary studies support this hypothesis. |
| NCT00265980 ↗ | Leptin in Human Energy and Neuroendocrine Homeostasis | Terminated | Michael Rosenbaum | N/A | 2002-07-01 | Previous work in our laboratory, and many others, has shown that body weight is regulated. When anyone, fat or thin, tries to maintain a reduced body weight, many systems affecting energy balance (skeletal muscle, neuroendocrine, and autonomic systems) conspire to slow metabolic rate thus favoring the regain of lost weight. Individuals with leptin deficiency are remarkably similar to weight-reduced individuals. Their metabolism, thyroid hormones, and sympathetic nervous system activity are all low despite their obesity. While administration of leptin to leptin-deficient humans results in substantial weight loss and increases in energy expenditure. However, leptin administration to leptin-sufficient humans at usual body weight has little or no effect on weight unless given in doses 10-20 times what would be considered to be in the normal physiological range. This study examines the hypothesis that leptin is "read" by various systems regulating energy balance as an indicator of how much energy we have stored and that the body perceives the weight-reduced state as a condition of relative leptin insufficiency. Within this model, restoration of leptin to levels present prior to weight loss should relieve much of the metabolic opposition to keeping weight off. Preliminary studies support this hypothesis. |
| NCT00296686 ↗ | Sequential Tranylcypromine (TC), TC + Dextroamphetamine and TC + Triiodothyronine for Refractory Depression | Terminated | New York State Psychiatric Institute | Phase 4 | 2001-09-01 | This pilot study will assess the efficacy of several sequential pharmacological treatments for patients with Refractory Depression. |
| NCT00311987 ↗ | Study of 3,5-Diiodothyropropionic Acid (DITPA) in Hypercholesterolemic Patients | Terminated | Johns Hopkins University | Phase 1/Phase 2 | 2006-04-01 | The natural thyroid hormones, thyroxine (T4) and triiodothyronine (T3), are known to have a cholesterol-lowering effect. Their pharmacologic use for this purpose is limited, however, by their actions on other organs, including the heart, bone, and brain, where there can be side effects of excessive thyroid hormone action. 3,5-diiodothyropropionic acid (DITPA) is a thyroid hormone analog with relative selectivity for a form of the thyroid hormone receptor expressed in the liver, where it regulates several aspects of lipid metabolism, including the clearance of low-density lipoprotein (LDL) cholesterol. This study is designed to determine whether DITPA is safe and effective in achieving LDL cholesterol levels that are consistent with the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) guidelines in patients who have not achieved those levels on conventional therapy, due to drug-resistant disease, drug intolerance, or both. This is a single-center, randomized, double-blind, placebo-controlled study. Following a 4-week Pre-Randomization Phase with dietary counseling and a 2-week placebo run-in, eligible patients will be randomized (1:1:1) to receive DITPA (90 mg/day, 180 mg/day), or placebo for a total treatment duration of 12 weeks. Sixty (60) patients will be randomized to 1 of 3 treatment groups in a 1:1:1 ratio (i.e., 20 patients per treatment group): - DITPA at 90 mg/day (45 mg twice a day [BID] taken orally) - DITPA at 180 mg/day (90 mg BID taken orally) - Placebo (BID taken orally) Those patients randomized to receive DITPA at 90 mg/day will receive 45 mg/day for the first 2 weeks, followed by 90 mg/day for 10 weeks. Those patients randomized to receive DITPA at 180 mg/day will receive 45 mg/day for the first 2 weeks, followed by 90 mg/day for the next 2 weeks, and then 180 mg/day for 8 weeks. |
| >Trial ID | >Title | >Status | >Sponsor | >Phase | >Start Date | >Summary |
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