antimitotics share obvious structural similarities and have been collectively referred to as colchicinoids.2b Their potent antimitotic activity is attributed to microtubule-destabilization through inhibition of tubulin polymerization, acting at a site distinct from the vinca-alkaloid tubulin destabilizing agents (vinblastine, vincristine etc.). Disruption of the microtubule assembly process results in the induction of apoptosis in actively dividing cells. The combretastatins are distinct in their mode of activity from other tubulin-active agents, such as paclitaxel (taxol) 5, that act directly on assembled microtubules enhancing tubulin polymerization. Both classes of tubulin-interactive compounds ultimately interfere with the normal cellular vascalature2d resulting in apoptosis induction. The combretastatins are also highly distinctive in comparison to paclitaxel and other taxoids in view of their relative structural simplicity.