Managing the Neurotoxicity of Paclitaxel (Taxol®) and Docetaxel (Taxotere®) with Neurotrophic Factors

Publisher Website
Google Scholar
Abstract
Paclitaxel and the related compound docetaxel are diterpine alkaloids (taxoids) that have demonstrated significant efficacy against a variety of different tumors, including carcinomas of the ovary, breast, head and neck, and lung (1–5). Paclitaxel was originally isolated from the bark of the Pacific yew tree, Taxus brevifolia, during a screening program looking for natural antitumor agents sponsored by the National Cancer Institute in 1971 (6). Before 1993, paclitaxel was referred to as taxol. The Bristol-Myers Squibb Company (Princeton, NJ) registered the name Taxol®, and the generic name paclitaxel was approved. Paclitaxel binds to tubulin and promotes microtubule polymerization (7,8). In tissue culture, paclitaxel causes abnormal bundles of microtubules to form throughout the cytoplasm, disrupting normal cell functions such as proliferation (8). Docetaxel has a similar mechanism of action in that it also binds to the β-subunit of tubulin, inducing polymerization, but may be more potent than paclitaxel (9).