Modifications of the potent anticancer agent taxol were carried out in order to gain an understanding of the chemical reactivity of the drug and the factors which contribute to its biological activity. The C-2' and/or the C-7 hydroxyl groups of taxol were substituted with acetyl, ßalanyl, silyl, succinyl, trichloroethyloxycarbonyl or carbonate linked dibenzylidene protected glucosyl groups. The C-7 position was selectively epimerized under free radical conditions and a 2'-epiacetyltaxol was produced via base catalysed epimerization. The C-2' amide became nucleophilic in the presence of base and could attack a C-2; acyl substituent. The C-13 ester side chain was selectively reduced by borohydride. The 7 position of taxol was selectively oxidized by Jones reagent and longer reaction times also oxidized the 2' position. The D rings of the 7 oxotaxols were readily opened via beta elimination; hydrogenation of the double bond in the enone of the D seco products produced a product in which the C ring was opened. The D ring was also susceptible to electrophilic attack. Reaction of taxol with triethyloxonium tetrafluoroborate or acetyl chloride/HC1 produced D seco taxols. C-7 deoxygenation was not achieved due to steric hindrance at C-7 and the instability of taxol under free radical conditions. Biological testing of modified taxols showed that substitution of the C-2' hydroxyl removed biological activity but that C-2' acyl groups were readily removed vivo. The water soluble 2'-βalanyItaxol possessed in vivo activity equal to that of taxol. Substitution of the C-7 hydroxyl did not inhibit the ability of a taxol derivative to polymerize tubulin but did decrease in vivo activity; epimerization of C-7 decreased in vivo activity slightly. A 2'-oxotaxol was found to be less active than, but still comparable to, its nonoxidized analogue. All taxol derivatives having a 7-oxo group and/or not possessing a D ring lost almost all biological activity. / Ph. D.