Description
Product Description
Docetaxel is a potent chemotherapeutic agent derived from the European yew tree (Taxus baccata) and semi-synthesized to enhance solubility and stability for laboratory use. It exerts its antitumor effects primarily through stabilization of microtubules, thereby preventing their normal dynamic reorganization necessary for mitotic progression. This stabilization leads to G2/M phase cell cycle arrest, inhibition of cell proliferation, and induction of programmed cell death.
Docetaxel has demonstrated activity across multiple tumor models, including breast, lung, prostate, and ovarian cancers. In vitro studies show that it disrupts microtubule dynamics by binding to the β-subunit of tubulin, suppressing microtubule depolymerization. This interference results in mitotic spindle dysfunction, prolonged mitotic arrest, and activation of apoptosis pathways through caspase signaling.
Preclinical research highlights Docetaxel’s ability to enhance tumor cell sensitivity to combination therapies, including radiation and targeted agents. Its biochemical properties also allow investigation of mechanisms of multidrug resistance (MDR) mediated by P-glycoprotein and related transporters. Researchers have explored Docetaxel’s impact on tumor microenvironment, angiogenesis, and signaling pathways such as PI3K/Akt and MAPK/ERK, making it a versatile compound in oncology research.
Additionally, Docetaxel exhibits unique pharmacokinetic features, including high plasma protein binding, slow elimination, and extensive hepatic metabolism predominantly through CYP3A4. These characteristics are critical for experimental design in in vitro and in vivo studies, influencing dose selection, administration schedules, and toxicity evaluation.
Its applications extend beyond cancer cell cytotoxicity, serving as a molecular probe to study microtubule dynamics, spindle checkpoint regulation, and apoptosis mechanisms. Researchers also employ Docetaxel in exploring synergistic effects with novel anticancer compounds, immunotherapies, and gene-targeted approaches.
Product Specifications
| Item | Details |
|---|---|
| Product Name | Docetaxel |
| CAS Number | 148408-61-6 |
| Synonyms | Taxotere, RP 56976 |
| Molecular Formula | C43H53NO14 |
| Molecular Weight | 807.88 g/mol |
| Purity | ≥99% |
| Appearance | White to off-white crystalline powder |
| Solubility | Soluble in DMSO, ethanol, and polysorbate 80 |
| Storage Temperature | 2–8 °C |
| Category | Anticancer agent |
| Applications | Tumor research, microtubule studies, apoptosis research |
| Formulation | Suitable for in vitro cell culture studies and preclinical models |
| Stability | Stable under recommended storage conditions |
| Shelf Life | 24 months |
| Supplier Type | Research chemical supplier |
| Intended Use | For laboratory research use only |
Mechanism of Action
Docetaxel exerts its biological effects primarily through microtubule stabilization. The detailed mechanisms include:
1. Microtubule Stabilization
Docetaxel binds to the β-tubulin subunit, promoting tubulin polymerization and inhibiting microtubule depolymerization. This stabilization impairs normal spindle function during mitosis, causing prolonged mitotic arrest.
2. G2/M Cell Cycle Arrest
Interference with spindle dynamics triggers activation of the spindle assembly checkpoint (SAC). Cells are unable to progress past the G2/M phase, leading to inhibition of cell proliferation and accumulation of cells in mitosis.
3. Apoptosis Induction
Prolonged mitotic arrest activates intrinsic apoptosis pathways, including mitochondrial membrane potential disruption, cytochrome c release, and caspase cascade activation. Docetaxel-mediated apoptosis involves both caspase-dependent and -independent pathways.
4. Anti-Angiogenic Effects
Preclinical studies demonstrate Docetaxel can inhibit tumor-associated angiogenesis by disrupting endothelial cell microtubules, reducing vascular network formation, and suppressing VEGF-mediated signaling.
5. Modulation of Multidrug Resistance
Docetaxel research provides insight into MDR mechanisms, particularly P-glycoprotein-mediated efflux. Experimental models using Docetaxel help explore chemosensitization strategies and MDR reversal approaches.
6. Signaling Pathway Regulation
Docetaxel impacts multiple signaling pathways, including PI3K/Akt, MAPK/ERK, and NF-κB. These interactions influence cell survival, apoptosis, and tumor progression in preclinical studies.

Side Effects
In controlled research settings, Docetaxel may induce cytotoxicity in tumor and normal cells. Observed in vitro and in vivo effects include:
Apoptotic cell death at high concentrations
Microtubule bundle formation disrupting normal cell architecture
Cell cycle perturbations leading to mitotic arrest
Dose-dependent cytotoxicity in non-tumor cell lines
Researchers must carefully titrate concentrations in cell-based assays to balance efficacy and biocompatibility. Protective measures such as proper PPE, biosafety cabinets, and adherence to institutional protocols are mandatory.
Docetaxel is for laboratory research use only and is not intended for human or veterinary administration. Its handling requires awareness of potential cytotoxic effects and environmental precautions.
Keywords
Docetaxel, CAS 148408-61-6, taxane derivative, microtubule stabilizer, tumor research, anticancer agent, apoptosis induction, cell cycle arrest, high-purity chemical, research chemical supplier
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We ensure product authenticity, verified ≥99% purity, and compliance with analytical standards (HPLC, MS, and NMR). Each batch is supplied with a Certificate of Analysis (CoA). Our trade assurance policy guarantees replacement or refund for any deviation from listed specifications.
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Disclaimer
All products listed are intended for laboratory research use only and not for human or veterinary use. They are not drugs, medical devices, or diagnostics and should not be administered to humans or animals. Researchers must handle all materials in accordance with institutional biosafety and chemical safety guidelines. The information provided is for scientific reference only and does not imply therapeutic efficacy, safety, or regulatory approval.



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