The reduction of N-protected amino ketones can be carried stereoselectively to produce either the syn- or anti-amino alcohol diastereomer. Carbamate-protected amino ketones can be reduced predictably and selectively to anti-amino alcohols with LiAlH(O-t-Bu)3 in ethanol at -78 degrees C. N-Trityl-protected amino ketones can be reduced selectively to syn-amino alcohols with LiAlH(O-t-Bu)3 in THF at -5 degrees C.

Aromatic substrates were adsorbed on the surface of fly ash from a municipal incinerator. Treatment with gaseous hydrogen chloride gave aromatic chlorination. Relative yields and isomer distributions indicate that an electrophilic mechanism is likely for the chlorination reaction. Inverse addition experiments were used to show that a surface-bound chlorinating agent is produced by the interaction of hydrogen chloride with the fly ash surface.Recycling experiments indicate that the fly ash surface functions as a stoichiometric oxidant, and not a catalyst, in promoting aromatic chlorination by HC1. The yields of aromatic chlorination on three different fly ash samples were found to be quite different. A variety of physical and chemical characterizations revealed no simple relationship between properties and yields. It was noted that the reaction of hydrogen chloride with the fly ash surface led to release of metal ions from the surface upon solvent extraction. It was found that the release of iron from the surface corresponded to the changing yields noted. Based on the known chlorinating ability of iron(III) chloride, as well as other data from aromatic chlorinations on fly ash surfaces, reaction of HC1 with iron(III) sites on the fly ash surface could produce surface-bound iron(III) chloride species that are the actual chlorinating agents.

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A series of P2-modified, orally active peptidic inhibitors of human neutrophil elastase (HNE) are reported. These pentafluoroethyl ketone-based inhibitors were designed using pentafluoroethyl ketone 1 as a model. Rational structural modifications were made at the P3, P2, and activating group (AG) portions of 1 based on structure-activity relationships (SAR) developed from in vitro (measured Ki) data and information provided by modeling studies that docked inhibitor 1 into the active site of HNE. The modeling-based design was corroborated with X-ray crystallographic analysis of the complex between 1 and porcine pancreatic elastase (PPE) and subsequently the complex between 1 and HNE.

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