Biological activity of the hypolipidemic agent, N2-n-butylindazolone.
Previously, a series of N-substituted indazolone derivatives proved to be effective hypolipidemic agents in rodents. The most effective agent, N2-n-butylindazolone, at 20 mg/kg/d was shown to suppress the levels of cytoplasm acetyl coenzyme A required for cholesterol and fatty acid synthesis as well as sn-glycerol-3-phosphate acyl transferase and phosphatidate phosphohydrolase activities. Lipid content of the liver, small intestine, and serum lipoprotein fractions was lowered, whereas lipid content was increased in fecal excretions by drug treatment for 14 d. The absorption of orally administered cholesterol from the intestine was severely reduced after drug administration. The mode of action of N2-n-butylindazolone appears to be similar to cyclic imides possessing hypolipidemic activity.
D000818:Animals; D002784:Cholesterol / Q000378:metabolism; D006949:Hyperlipidemias / Q000097:blood; D000960:Hypolipidemic Agents / Q000378:metabolism / Q000494:pharmacology*; D007191:Indazoles / Q000378:metabolism / Q000494:pharmacology*; D008055:Lipids / Q000096:biosynthesis*; D008074:Lipoproteins / Q000097:blood; D008099:Liver / Q000201:enzymology; D008297:Male; D051379:Mice; D011720:Pyrazoles / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D014018:Tissue Distribution
D000960:Hypolipidemic Agents; D007191:Indazoles; D008055:Lipids; D008074:Lipoproteins; D011720:Pyrazoles; C044800:2-butyl-1,2-dihydro-3H-indazol-3-one; D002784:Cholesterol