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Paclitaxel (Taxol)

Catalog No.GC12511

Paclitaxel (Taxol) Chemical Structure

Paclitaxel, from the bark and needles of Taxus brevifolia, is a tricyclic diterpenoid compound.

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10mM (in 1mL DMSO)
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Cell experiment [1]:

Cell lines

MCF-7 and MDA-MB-231 human breast carcinoma cell lines

Preparation Method

The cells were transiently transfected with p21 promoter-luciferase reporter constructs using Lipofectamine, as recommended by the manufacturer. Following transfection, the cells were incubated for 12 h, the medium was exchanged, and the cells were incubated for various periods of time in the presence of 20 nM Paclitaxel .

Reaction Conditions

20 nM; 12h


The untreated control cells displayed exponential growth during the 48-h incubation, whereas paclitaxel (taxol) treatment resulted in a dramatic decrease in the number of viable cells.

Animal experiment [2]:

Animal models

Specific pathogen free nude mice

Preparation Method

MDA-231 cells (1 × 106) were subcutaneously transplanted. After the formation of primary tumors (diameter > 5 mm), the mice were randomly grouped (10 mice per group) and 1 mg/kg paclitaxel were diluted with normal saline and administrated by intraperitoneal injection (1 time/2 days).

Dosage form


Paclitaxel (1 mg/kg, i.p.) induces changes in estrogen metabolism in liver that facilitate the formation of breast cancer metastases.


[1]. [1]Choi YH, Yoo YH. Taxol-induced growth arrest and apoptosis is associated with the upregulation of the Cdk inhibitor, p21WAF1/CIP1, in human breast cancer cells. Oncol Rep. 2012 Dec;28(6):2163-9. 

[2]. Li Q, et al. Low doses of paclitaxel enhance liver metastasis of breast cancer cells in the mouse model. FEBS J. 2016 Aug;283(15):2836-52.


Paclitaxel, from the bark and needles of Taxus brevifolia, is a tricyclic diterpenoid compound. Paclitaxel can promote the assembly of tubulin into microtubules and prevent the dissociation of microtubules, blocking cell cycle progression, preventing mitosis, and inhibiting the growth of cancer cells.[1]

In vitro, paclitaxel significantly inhibited the proliferation of ATC cells in a dose-dependent manner; the IC50 value ranged from 1.99 to 9.97 nM.[6] Encapsulating paclitaxel into nano-drug carriers, the water-solubility, selective delivery to cancers, tissue toxicity, controlled release and pharmacokinetic property of paclitaxel are improved, can improve its toxicity to human, keep or enhance its activity and improve its pharmacokinetic property.[2] In vitro, in a short time, exposures to paclitaxel induced the phosphorylation and degradation of IkappaB-alpha, which in turn caused the activation of NF-kappaB in both human breast cancer BCap37 and human epidermoid carcinoma KB cells. [3] In addition, Paclitaxel can increase its cytotoxic effect by the loading of Paclitaxel to autologous prostate cancer cell-derived EVs.[5]

In vivo experiment it shown that treatment with 1 mg/kg and 20 mg/kg paclitaxel, the light-colored spotted metastases were dramatically increased in livers from the low-dose paclitaxel-treated mice and the metastasis was substantially reduced in the high-dose paclitaxel group.[4] In vivo, the growth of C643 cell-derived xenograft tumors in the lenvatinib-treated (5 mg/kg; p.o.) and paclitaxel-treated (5 mg/kg;i.p.) groups was slower than that in control group.[6]

[1]Zhu L, Chen L. Progress in research on paclitaxel and tumor immunotherapy. Cell Mol Biol Lett. 2019 Jun 13;24:40.
[2]Chen S, et al. Recent Development of Copolymeric Nano-Drug Delivery System for Paclitaxel. Anticancer Agents Med Chem. 2020;20(18):2169-2189. 
[3]Dziadyk JM, et al. Paclitaxel-induced apoptosis may occur without a prior G2/M-phase arrest. Anticancer Res. 2004 Jan-Feb;24(1):27-36. 
[4]Li Q, et al. Low doses of paclitaxel enhance liver metastasis of breast cancer cells in the mouse model. FEBS J. 2016 Aug;283(15):2836-52.
[5]Saari H, et al. Microvesicle- and exosome-mediated drug delivery enhances the cytotoxicity of Paclitaxel in autologous prostate cancer cells. J Control Release. 2015 Dec 28;220(Pt B):727-37. 
[6]Jing C, et al. Lenvatinib enhances the antitumor effects of paclitaxel in anaplastic thyroid cancer. Am J Cancer Res. 2017 Apr 1;7(4):903-912.

Chemical Properties

Cas No. 33069-62-4 SDF
Synonyms Taxol
Chemical Name N/A
Canonical SMILES O=C(N[C@H]([C@H](C(O[C@H]1C[C@]2(O)C(C)(C)C([C@@H](OC(C)=O)C([C@@]3(C)[C@]([C@@](CO4)(OC(C)=O)[C@H]4C[C@@H]3O)([H])[C@@H]2OC(C5=CC=CC=C5)=O)=O)=C1C)=O)O)C6=CC=CC=C6)C7=CC=CC=C7
Formula C47H51NO14 M.Wt 853.91
Solubility ≥ 42.6955mg/mL in DMSO, ≥ 31.6 mg/mL in EtOH with ultrasonic Storage 4°C, protect from light
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
Shipping Condition Evaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request

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Research Update

How Taxol/Paclitaxel kills cancer cells

Mol Biol Cell2014 Sep 15;25(18):2677-81.PMID: 25213191DOI: 10.1091/mbc.E14-04-0916

Taxol (generic name Paclitaxel) is a microtubule-stabilizing drug that is approved by the Food and Drug Administration for the treatment of ovarian, breast, and lung cancer, as well as Kaposi's sarcoma. It is used off-label to treat gastroesophageal, endometrial, cervical, prostate, and head and neck cancers, in addition to sarcoma, lymphoma, and leukemia. Paclitaxel has long been recognized to induce mitotic arrest, which leads to cell death in a subset of the arrested population. However, recent evidence demonstrates that intratumoral concentrations of Paclitaxel are too low to cause mitotic arrest and result in multipolar divisions instead. It is hoped that this insight can now be used to develop a biomarker to identify the ∼50% of patients that will benefit from Paclitaxel therapy. Here I discuss the history of Paclitaxel and our recently evolved understanding of its mechanism of action.

Paclitaxel (Taxol) and docetaxel (Taxotere): not simply two of a kind

Ann Oncol1994 Jul;5(6):495-505.PMID: 7918121DOI: 10.1093/oxfordjournals.annonc.a058903

Paclitaxel and docetaxel are the two presently clinically available representatives of the new class of taxane drugs. They share major parts of their structures and mechanisms of action, but differ in several other aspects. For instance, there is a difference in their tubulin polymer generation, and docetaxel appears twice as active in depolymerization inhibition. In vitro docetaxel also tends to be more potent in different cell lines and investigational models. While in vitro and in vivo studies suggest that prolonged exposure to Paclitaxel is better than a brief exposure, no such tendency is seen for docetaxel, indicating it to be a schedule-independent drug. Clinical studies have not confirmed an advantage for prolonged exposure to Paclitaxel; but do show differences in the toxicity profiles of the two drugs. These topics will be addressed in detail.

[Paclitaxel (Taxol)]

Cas Lek Cesk1996 Jun 12;135(12):393-6.PMID: 8706079DOI: 10.3390/ijms18081733

The Paclitaxel (TAXOL); Bristol-Myers Squibb Company) represents first agent from novel class of antineoplastic drugs--taxanes to enter routine clinical practice. Paclitaxel interferes with microtubular polymerization by promoting abnormal assembly of microtubules and inhibiting their subsequent disassembly. Pharmacokinetics of Paclitaxel has been intensively studied. There are indications for nonlinear pharmacokinetics when Paclitaxel is administered as a short infusion and at higher doses. Neurotoxicity, mucositis, and leukopenia correlate with some pharmacokinetic parameters. The clinical development of Paclitaxel was initially hampered by hypersensitivity reactions. Current dosage regiments with premedication reduced the incidence of these events to 3%. The major dose-limiting adverse effect of Paclitaxel is neutropenia. Significant activities were reported especially in patients with advanced ovarian, breast, non-small cell lung cancer (NSCLC), head and neck cancer and in other types of tumours. Long-term follow-up will also allow the effects of the drug on patient survival to be determined. At present combination of Taxol (Paclitaxel) with cisplatin clearly improves the duration of progression-free survival and of overall survival compared with cyclophosphamide and cisplatin in women ovarian cancer. Recently was TAXOL (Paclitaxel) registered in Czech republic for treatment of patients with advanced metastatic ovarian carcinoma and in patients with metastatic breast cancer after failure of the standard therapy.


Pharmacotherapy1994 Jan-Feb;14(1):3-34.PMID: 7909150DOI: 10.1002/j.1875-9114.1994.tb02785.x

Paclitaxel is a novel antineoplastic that effects cytotoxicity by promoting intracellular tubulin polymerization and stabilizes abnormal microtubule structures against depolymerization. Although its clinical development had been hampered by misconceptions about its pharmacology, its scarcity, difficulties extracting it from its natural source, formulation problems, and frequent severe hypersensitivity reactions, Paclitaxel recently was approved for treatment-refractory ovarian cancer. Two major adverse effects are dosage- and schedule-related myelosuppression and mucositis. Neurotoxicity is directly related to both the individual and cumulative doses. Other relevant toxicities are hypersensitivity reactions, effects on cardiac rate and rhythm, arthralgias and myalgias, generalized hair loss, and mild nausea and emesis. Continuing clinical studies will evaluate Paclitaxel as initial therapy for ovarian cancer and its utility in other malignancies. In addition, major efforts are under way to develop alternative sources to increase the availability of taxene analogs and reduce our dependence on yew species.


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Average Rating: 5 ★★★★★ (Based on Reviews and 21 reference(s) in Google Scholar.)

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