Jack Mills
Eli Lilly and Company
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Featured researches published by Jack Mills.
Biochemical Pharmacology | 1965
Ray W. Fuller; C.W. Hines; Jack Mills
Abstract 4-Chloroamphetamine and several structurally similar compounds lowered serotonin level in the whole brain of rats without lowering the level of norepinephrine. Relationships between chemical structure of chloroamphetamines and their effects on brain serotonin level are presented. There was no difference between the effects of dextrorotatory and levorotatory isomers of 4-chloromethamphetamine. 4-Chloro-amphetamine lowered serotonin but not norepinephrine level in the septum-diencephalon-midbrain area of dog brain. 4-Chloroamphetamine did not inhibit tryptophan hydroxylation in rat liver or bacterial preparations nor did it inhibit the uptake of 14 C-5-hydroxytryptophan into rat brain. The lowering of brain serotonin level does not appear to be a result of decreased serotonin synthesis but may be due to an unusual type of release of serotonin.
Biochemical Pharmacology | 1978
Ray W. Fuller; Susan K. Hemrick; Jack Mills
Abstract N -phenacyl-cyclopropylamine hydrobromide (54761) was evaluated in vitro and in vivo as a monoamine oxidase (MAO) inhibitor in rats. In contrast to 51641, which has an o-chlorophenoxy group in place of the phenacyl group and which is a highly selective inhibitor of type A MAO, 54761 showed a slight preference as a type B MAO inhibitor, since it inhibited phenylethylamine oxidation at slightly lower concentrations than were required to inhibit serotonin oxidation in vitro by rat liver MAO. Twelve analogs of 54761 with various substituents on the phenyl ring were also studied, but none was substantially more selective than 54761 as a type B inhibitor and most were preferential type A inhibitors. When 51641 and 54761 were injected into rats and MAO activity was assayed in tissue homogenates, the oxidation of serotonin in brain, heart and liver was inhibited more by 51641 than by 54761. In contrast, the oxidation of phenylethylamine was inhibited more by 54761 than by 51641 in brain and liver. In heart, however, 51641 was a more effective inhibitor of phenylethylamine oxidation than was 54761, supporting earlier evidence that phenylethylamine is destroyed in heart mainly by type A MAO. The oxidation of exogenous [ 14 C]phenylethylamine was inhibited in vivo more effectively by 54761, whereas the oxidation of endogenous serotonin in brain was inhibited more by 51641. Although 54761 is not as selective an inhibitor of type B MAO as some other compounds such as deprenyl, it illustrates that a large range of selectivity in MAO inhibition can exist within the N -cyclopropylamine series. Further, selective type B inhibition could be achieved in vivo 24 hr after injection of 54761 by co-administration of harmaline. Harmaline selectively protected against the inactivation of type A MAO by 54761 but permitted the inactivation of type B MAO to occur.
Life Sciences | 1981
Walter Norman Shaw; Klaus Kurt Schmiegel; Terence T. Yen; Richard E. Toomey; Donald B. Meyers; Jack Mills
Abstract Compound LY79771 given subcutaneously reduced weight or decreased weight gain of genetically obese rats and mice, gold thioglucose obese mice, and obese beagles. The compound had no effect on body weight of lean rats. Food consumption was not decreased. Obese rats showed a transient rise in body temperature after each administration of the drug. The change in body weight was due mainly to a decrease in body fat mass.
Archive | 1979
Jack Mills; Klaus Kurt Schmiegel; Walter Norman Shaw
Journal of Medicinal Chemistry | 1968
Ray W. Fuller; Max M. Marsh; Jack Mills
Archive | 1979
Jack Mills; Klaus Kurt Schmiegel; Walter Norman Shaw
Archive | 1975
Ronald Ralph Tuttle; Jack Mills
Journal of Medicinal Chemistry | 1971
Ray W. Fuller; Jack Mills; Max M. Marsh
Journal of Medicinal Chemistry | 1969
Robert E. McMahon; Jack Mills; Hilman W. Culp; William R. Gibson; Warren M. Miller; Frederick J. Marshall
Journal of Medicinal Chemistry | 1968
Jack Mills; Richard W. Kattau; Irwin H. Slater; Ray W. Fuller