Paclitaxel

Biochemical Physiological Actions : Antitumor and antileukemic agent which lowers the critical concentration for tubulin polymerization and reversibly binds to tubulin prohibiting depolymerization; binds to the N-terminal region of beta-tubulin and promotes the formation of highly stable microtubles that resist depolymerization, thus preventing normal cell division and arresting the cell cycle at the G2-M phase. The microtubule damage induces apoptosis through a JNK-dependent pathway in the early phase followed by a JNK-independent pathway, perhaps related to the activation of protein kinase A or of Raf-1 kinase, that results in phosphorylation of Bcl-2.