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Last Updated: November 22, 2024

CLINICAL TRIALS PROFILE FOR REGITINE


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All Clinical Trials for REGITINE

Trial ID Title Status Sponsor Phase Start Date Summary
NCT02966665 ↗ : Vascular Function in Health and Disease Recruiting Russell Richardson Phase 1 2008-09-01 Many control mechanisms exist which successfully match the supply of blood with the metabolic demand of various tissues under wide-ranging conditions. One primary regulator of vasomotion and thus perfusion to the muscle tissue is the host of chemical factors originating from the vascular endothelium and the muscle tissue, which collectively sets the level of vascular tone. With advancing age and in many disease states, deleterious adaptations in the production and sensitivity of these vasodilator and vasoconstrictor substances may be observed, leading to a reduction in skeletal muscle blood flow and compromised perfusion to the muscle tissue. Adequate perfusion is particularly important during exercise to meet the increased metabolic demand of the exercising tissue, and thus any condition that reduces tissue perfusion may limit the capacity for physical activity. As it is now well established that regular physical activity is a key component in maintaining cardiovascular health with advancing age, there is a clear need for further studies in populations where vascular dysfunction is compromised, with the goal of identifying the mechanisms responsible for the dysfunction and exploring whether these maladaptations may be remediable. Thus, to better understand the etiology of these vascular adaptations in health and disease, the current proposal is designed to study changes in vascular function with advancing age, and also examine peripheral vascular changes in patients suffering from chronic obstructive pulmonary disease (COPD), Sepsis, Pulmonary Hypertension, and cardiovascular disease. While there are clearly a host of vasoactive substances which collectively act to govern vasoconstriction both at rest and during exercise, four specific pathways that may be implicated have been identified in these populations: Angiotensin-II (ANG-II), Endothelin-1 (ET-1), Nitric Oxide (NO), and oxidative stress.
NCT03079921 ↗ Adrenergic System in Islet Transplantation Active, not recruiting National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Early Phase 1 2017-01-20 To determine the effect of sympathetic neural and hormonal (epinephrine) input on islet cell hormonal responses to insulin-induced hypoglycemia in type 1 diabetic recipients of intrahepatic islet transplantation. We hypothesize that α-adrenergic (neural) blockage will abolish insulin-mediated suppression of C-peptide, attenuating α-cell glucagon secretion during hypoglycemia, and that β-adrenergic (hormonal) blockage will have no effect. Glucose counterregulatory responses will be measured during hyperinsulinemic euglycemic-hypoglycemic clamps on three occasions with randomized, double-blind administration of the α-adrenergic blocker phentolamine, the β-adrenergic blocker propranolol, or placebo. The demonstration of neural rather than hormonal regulation of the transplanted islet cell response to hypoglycemia is critical for understanding the mechanism for protection from hypoglycemia afforded by intrahepatically transplanted.
NCT03079921 ↗ Adrenergic System in Islet Transplantation Active, not recruiting National Institutes of Health (NIH) Early Phase 1 2017-01-20 To determine the effect of sympathetic neural and hormonal (epinephrine) input on islet cell hormonal responses to insulin-induced hypoglycemia in type 1 diabetic recipients of intrahepatic islet transplantation. We hypothesize that α-adrenergic (neural) blockage will abolish insulin-mediated suppression of C-peptide, attenuating α-cell glucagon secretion during hypoglycemia, and that β-adrenergic (hormonal) blockage will have no effect. Glucose counterregulatory responses will be measured during hyperinsulinemic euglycemic-hypoglycemic clamps on three occasions with randomized, double-blind administration of the α-adrenergic blocker phentolamine, the β-adrenergic blocker propranolol, or placebo. The demonstration of neural rather than hormonal regulation of the transplanted islet cell response to hypoglycemia is critical for understanding the mechanism for protection from hypoglycemia afforded by intrahepatically transplanted.
>Trial ID >Title >Status >Phase >Start Date >Summary

Clinical Trial Conditions for REGITINE

Condition Name

Condition Name for REGITINE
Intervention Trials
Islet Cell Transplantation 1
Pulmonary Artery Hypertension 1
Type1diabetes 1
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Condition MeSH

Condition MeSH for REGITINE
Intervention Trials
Pulmonary Disease, Chronic Obstructive 1
Pulmonary Arterial Hypertension 1
Lung Diseases, Obstructive 1
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Clinical Trial Locations for REGITINE

Trials by Country

Trials by Country for REGITINE
Location Trials
United States 2
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Trials by US State

Trials by US State for REGITINE
Location Trials
Pennsylvania 1
Utah 1
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Clinical Trial Progress for REGITINE

Clinical Trial Phase

Clinical Trial Phase for REGITINE
Clinical Trial Phase Trials
Phase 1 1
Early Phase 1 1
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Clinical Trial Status

Clinical Trial Status for REGITINE
Clinical Trial Phase Trials
Active, not recruiting 1
Recruiting 1
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Clinical Trial Sponsors for REGITINE

Sponsor Name

Sponsor Name for REGITINE
Sponsor Trials
Russell Richardson 1
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) 1
National Institutes of Health (NIH) 1
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Sponsor Type

Sponsor Type for REGITINE
Sponsor Trials
Other 2
NIH 2
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