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Home / Drugs / Starting with P / Paclitaxel

A cyclodecane isolated from the bark of the Pacific yew tree, TAXUS brevifolia. It stabilizes microtubules in their polymerized form leading to cell death. [PubChem] ABI-007 (Abraxane) is the latest attempt to improve upon paclitaxel, one of the leading chemotherapy treatments. Both drugs contain the same active agent, but Abraxane is delivered by a nanoparticle technology that binds to albumin, a natural protein, rather than the toxic solvent known as Cremophor. It is thought that delivering paclitaxel with this technology will cause fewer hypersensitivity reactions and possibly lead to greater drug uptake in tumors.
Taxol A
Vascular Wrap
CategoriesAntineoplastic Agents
Antineoplastic Agents, Phytogenic
Tubulin Modulators
ManufacturersAbraxis bioscience llc
Accord healthcare inc usa
Actavis totowa llc
Bedford laboratories div ben venue laboratories inc
Ebewe pharma ges mbh nfg kg
Fresenius kabi oncology plc
Hospira inc
Mylan pharmaceuticals inc
Pliva lachema as
Teva parenteral medicines inc
Bristol myers squibb co pharmaceutical research institute
PackagersAbraxis BioScience Inc.
Accord Healthcare
APP Pharmaceuticals
Barr Pharmaceuticals
Bedford Labs
Ben Venue Laboratories Inc.
Bristol-Myers Squibb Co.
Ebewe Pharma
Ethex Corp.
Fresenius Kabi AB
Hospira Inc.
Intas Pharmaceuticals Ltd.
Ivax Pharmaceuticals
Mead Johnson and Co.
Pharmachemie BV
Pliva Inc.
Teva Pharmaceutical Industries Ltd.
UDL Laboratories


Used in the treatment of Kaposi's sarcoma and cancer of the lung, ovarian, and breast.


Paclitaxel is a taxoid antineoplastic agent indicated as first-line and subsequent therapy for the treatment of advanced carcinoma of the ovary, and other various cancers including breast cancer. Paclitaxel is a novel antimicrotubule agent that promotes the assembly of microtubules from tubulin dimers and stabilizes microtubules by preventing depolymerization. This stability results in the inhibition of the normal dynamic reorganization of the microtubule network that is essential for vital interphase and mitotic cellular functions. In addition, paclitaxel induces abnormal arrays or "bundles" of microtubules throughout the cell cycle and multiple asters of microtubules during mitosis.

mechanism of action

Paclitaxel interferes with the normal function of microtubule growth. Whereas drugs like colchicine cause the depolymerization of microtubules in vivo, paclitaxel arrests their function by having the opposite effect; it hyper-stabilizes their structure. This destroys the cell's ability to use its cytoskeleton in a flexible manner. Specifically, paclitaxel binds to the β subunit of tubulin. Tubulin is the "building block" of mictotubules, and the binding of paclitaxel locks these building blocks in place. The resulting microtubule/paclitaxel complex does not have the ability to disassemble. This adversely affects cell function because the shortening and lengthening of microtubules (termed dynamic instability) is necessary for their function as a transportation highway for the cell. Chromosomes, for example, rely upon this property of microtubules during mitosis. Further research has indicated that paclitaxel induces programmed cell death (apoptosis) in cancer cells by binding to an apoptosis stopping protein called Bcl-2 (B-cell leukemia 2) and thus arresting its function.


Rat (ipr) LD50=32530 µg/kg. Symptoms of overdose include bone marrow suppression, peripheral neurotoxicity, and mucositis. Overdoses in pediatric patients may be associated with acute ethanol toxicity.


Hepatic. In vitro studies with human liver microsomes and tissue slices showed that paclitaxel was metabolized primarily to 6a-hydrox-ypaclitaxel by the cytochrome P450 isozyme CYP2C8; and to two minor metabolites, 3’-p-hydroxypaclitaxel and 6a, 3’-p-dihydroxypaclitaxel, by CYP3A4.


I.V injected

half life

Average distribution half-life of 0.34 hours and an average elimination half-life of 5.8 hours.

route of elimination

In 5 patients administered a 225 or 250 mg/m2 dose of radiolabeled paclitaxel as a 3-hour infusion, a mean of 71% of the radioactivity was excreted in the feces in 120 hours, and 14% was recovered in the urine.

drug interactions

Aprepitant: Aprepitant may change levels of the chemotherapy agent, paclitaxel.

Carboplatin: Platinum derivatives such as carboplatin may enhance the myelosuppressive effect of taxane derivatives such as paclitaxel. Administer taxane derivative before platinum derivative when given as sequential infusions to limit toxicity. Administering the taxane derivative before the platinum derivative seems prudent.

Cisplatin: Cisplatin increases the effect and toxicity of paclitaxel

Gemcitabine: Paclitaxel increases the effect/toxicity of gemcitabine

Quinupristin: This combination presents an increased risk of toxicity

Telithromycin: Telithromycin may reduce clearance of Paclitaxel. Consider alternate therapy or monitor for changes in the therapeutic/adverse effects of Paclitaxel if Telithromycin is initiated, discontinued or dose changed.

Tolbutamide: Tolbutamide, a strong CYP2C9 inhibitor, may decrease the metabolism and clearance of Paclitaxel. Consider alternate therapy or monitor for changes in Paclitaxel therapeutic and adverse effects if Tolbutamide is initiated, discontinued or dose changed.

Trastuzumab: Trastuzumab may increase the risk of neutropenia and anemia. Concomitant therapy may also increase Trastuzumab serum concentration and decrease Paclitaxel serum concentrations. Monitor closely for adverse events and therapeutic response.

Valrubicin: The taxane derivative, Paclitaxel, may increase Valrubicin toxicity. Consider alternate therapy or monitor for toxic effects.

Voriconazole: Voriconazole, a strong CYP3A4 inhibitor, may increase the serum concentration of paclitaxel by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of paclitaxel if voriconazole is initiated, discontinued or dose changed.