Intravenous administration of 300 mg. Triton/kg. to rats increased only the free cholesterol fraction in the blood within 18 hrs. of administration, without altering the liver lipids; free cholesterol increased from 8 to 105 mg./100 ml.Simultaneous administration of nicotinic acid (I) (0.50 g./kg. given orally) antagonized the effects of Triton on cholesteremia; free cholesterol levels reached 64 mg./100 ml. after the combined treatment.However, I itself increased liver fatty acids from 16.5 to 22.66 g./100 g. fresh weight; this increase was not reflected in a decrease in hepatic chromagogue function.None of 14 I derivatives were more active than the parent compound as a hypocholesteremic or as a clarifying factor.N-Oxynicotinic acid, 4-acetylaminophenyl nicotinate, nicotinoylaminophenol, and nicotinamide (0.565, 1.042, 0.87, and 0.5 g./kg., resp.) were as effective as 0.5 g. I/kg. against serum cholesterol in Triton-treated rats, while 2-chloronicotinic acid, 2-iodonicotinic acid, and quinolinic acid (0.644, 1.012, and 0.783 g./kg., resp.) were inactive.The 4 compounds active against cholesterolemia plus 2-chloronicotinic acid were effective in reducing serum turbidity, while 2-methyl-5-phenylnicotinic acid increased this.4-Acetyl-aminophenol nicotinate, nicotinoylglycolic acid, mannitol hexanicotinate, sorbitol hexanicotinate, nicotinoylaminophenol, nicotinoylphenylisopropylamine, nicotinamide, and N-oxynicotinic acid (doses equivalent to 100 mg. I/kg.) showed a vasodilatory effect on the guinea pig ear which was 94, 50, 44, 40, 40, 18, 10, and 3%, resp., that of I (100 mg./kg.).A dissociation is therefore shown between hypocholesteremic, clarifying, and vasodilatory properties.