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Search results for "Drug or Chemical by Structure[C1913]|Organic Chemical[C718]|Glycoside Compound[C45653]" in comments (approximate match)
Showing 1 - 3 of 3 results
Status:
US Approved Rx
(2002)
Source:
ANDA076268
(2002)
Source URL:
First approved in 1954
Source:
NDA009330
Source URL:
Class (Stereo):
CHEMICAL (ABSOLUTE)
Targets:
Conditions:
Digoxin, a cardiac glycoside similar to digitoxin, is used to treat congestive heart failure and supraventricular arrhythmias due to reentry mechanisms, and to control ventricular rate in the treatment of chronic atrial fibrillation. Digoxin inhibits the Na-K-ATPase membrane pump, resulting in an increase in intracellular sodium. The sodium calcium exchanger (NCX) in turn tries to extrude the sodium and in so doing, pumps in more calcium. Increased intracellular concentrations of calcium may promote activation of contractile proteins (e.g., actin, myosin). Digoxin also acts on the electrical activity of the heart, increasing the slope of phase 4 depolarization, shortening the action potential duration, and decreasing the maximal diastolic potential.
Status:
Investigational
Class (Stereo):
CHEMICAL (ABSOLUTE)
Conditions:
PYM50018 (also known as Myogane or SARSAGENIN) has demonstrated neuroprotective effects in several preclinical models. It was observed that PYM50018 protects against neuronal damage, increases neurite outgrowth, reverses oxidative damage and reversed neuronal apoptosis. PYM50018 is in phase I clinical study for the treatment of amyotrophic lateral sclerosis (ALS).
Status:
Investigational
Class (Stereo):
CHEMICAL (ABSOLUTE)
Tiqueside is the synthetic spirostane-based steroid glycoside. It precipitates cholesterol from micellar solution in vitro and reduces plasma cholesterol absorption in rats through a mechanism that is currently thought to be independent of either association of the saponin with the intestinal mucosal surface or absorption of the saponin molecule. As a consequence of this inhibition, tiqueside has been shown to reduce plasma cholesterol concentrations in cynomolgus monkeys. Inhibition of cholesterol absorption by tiqueside produces profound effects on cholesterol metabolism without affecting bile acid metabolism, and these changes lead to reductions primarily in plasma non-HDL cholesterol concentrations. Tiqueside produced a dose-dependent reduction in plasma LDL cholesterol levels in the hypercholesterolemic patients. In the mechanistic study, it decreased fractional cholesterol absorption rates and increased fecal neutral sterol excretion rates, changes associated with trends toward lower LDL cholesterol levels. Other lipoprotein levels were unaffected, as were fecal fat and bile acid excretion and fat-soluble vitamin absorption. Thus tiquesidedose-dependently inhibits cholesterol absorption in humans, resulting in a reduction in serum LDL cholesterol levels.