U.S. Department of Health & Human Services Divider Arrow National Institutes of Health Divider Arrow NCATS

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Showing 71 - 80 of 477 results

Status:
Investigational
Source:
INN:beloxamide [INN]
Source URL:

Class (Stereo):
CHEMICAL (ACHIRAL)

Beloxamide, a hypolipidemic agent, produced regression of the lipid deposits that was shown during experiments with rodents.
Status:
Investigational
Source:
INN:tiopropamine
Source URL:

Class (Stereo):
CHEMICAL (ACHIRAL)

Tiopropamine is an anti-inflammatory agent. Tiopropamine hydrochloride has been used in the treatment of peptic ulcers.
Status:
Investigational
Source:
INN:octimibate
Source URL:

Class (Stereo):
CHEMICAL (ACHIRAL)

Octimibate is a non-prostanoid inhibitor of platelet aggregation that acts via the prostacyclin receptor.
Status:
Investigational
Source:
INN:gliamilide
Source URL:

Class (Stereo):
CHEMICAL (RACEMIC)

Gliamilide is a high-potency sulfamylurea hypoglycemic agent. It has been found to be well tolerated in humans and displays a very short plasma half-life. Like sulfonylureas, gliamilide can lower blood glucose levels by increasing the insulin release from pancreatic beta cells.
Status:
Investigational
Source:
INN:glyprothiazol
Source URL:

Class (Stereo):
CHEMICAL (ACHIRAL)

Glyprothiazol (VK 57 or RP 2254) is a sulfonamide derivative. This compound lowers blood glucose levels by increasing the release of insulin from the pancreas. It stimulates insulin secretion through a direct action on pancreatic islets. Glyprothiazol was the first of oral hypoglycemic sulfonamides used in the treatment of type 2 diabetes mellitus.
Status:
Investigational
Source:
NCT01057654: Phase 3 Interventional Completed Hypercholesterolemia
(1996)
Source URL:

Class (Stereo):
CHEMICAL (RACEMIC)

Lifibrol is a hypocholesterolemic compound. The effect of lifibrol on serum cholesterol levels has been examined in several animal models and clinical trials. The efficacy of lifibrol in lowering total cholesterol, LDL cholesterol, and apo B is comparable to the 3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, the most potent lipid-lowering drugs known so far. In addition, lifibrol reduces serum triglycerides, lipoprotein (a), and fibrinogen. lifibrol acts synergistically upon key regulatory processes of cholesterol homeostasis: it reduces cholesterol absorption from the intestine, moderately decreases hepatic cholesterol biosynthesis and stimulates the expression of low density lipoprotein receptors, presumably by a sterol-independent mechanism. Lifibrol had been in phase II clinical trials for the treatment of hypercholesterolaemia. However, this study was discontinued. It has the potential to accumulate in the liver and induce hepatic peroxisome proliferation.
Status:
Investigational
Source:
INN:urefibrate
Source URL:

Class (Stereo):
CHEMICAL (ACHIRAL)

Urefibrate, clofibrate derivative, is a peroxisome proliferator activated receptor-α (PPAR-α) agonist. It is an antihyperlipidaemic agent.
Status:
Investigational
Source:
NCT00080132: Phase 2 Interventional Terminated Hypertriglyceridemia
(2004)
Source URL:

Class (Stereo):
CHEMICAL (ABSOLUTE)

Implitapide is a microsomal triglyceride transfer protein (MTP) inhibitor with antihyperlipidemic activity. Microsomal triglyceride transfer protein (MTP) is essential for the synthesis of both chylomicron in the intestine and very low-density lipoprotein in the liver. In an animal model, inhibition of MTP by implitapide reduced both total cholesterol and triglyceride levels and suppressed progression of atherosclerotic lesions in apolipoprotein E knockout mice fed a Western-type diet.
Status:
Investigational
Source:
INN:ursulcholic acid [INN]
Source URL:

Class (Stereo):
CHEMICAL (ABSOLUTE)

Ursulcholic acid is a soluble form of ursodeoxycholic acid. It is an anticholinergic agent.
Status:
Investigational
Source:
INN:triletide
Source URL:

Class (Stereo):
CHEMICAL (ABSOLUTE)

Triletide is a tripeptide derivative which shows cytoprotective and antiulcerogenic activity. It is a thromboxane synthase inhibitor. Analysis of both individual and pooled data indicated that triletide was well absorbed after oral administration, with a lag time of 0.3 hours and the blood peak was reached after about 1.1 to 1.3 hours. Metabolization to desmethyl, desacetyl, desmethyl-desacetyl and hydroxylated derivatives plays a major role in the biotransformation of the drug and thus in its disappearance from blood, the distribution half-life being about 1 hour. A greater proportion of patients given the combination cimetidine and triletide was found to be endoscopically healed after treatment in comparison with those who had cimetidine alone (53% vs 40%). Intensity of symptoms decreased significantly faster and to a significantly greater extent in the same patients, as did antacid intake. Triletide appears to be equally well tolerated as, but significantly more effective than, aluminium hydroxide and magnesium hydroxide in relieving symptoms and promoting healing in patients with mild to moderate duodenal ulcer. There were no complaints of possible side-effects with either triletide treatment and no evidence of any significant changes in blood pressure, heart rate or routine haematology and haematochemistry investigations.