Catalog No.S7787 Synonyms: RP56976 (NSC 628503) Trihydrate
Molecular Weight(MW): 861.93
Docetaxel, an analog of paclitaxel, is an inhibitor of depolymerisation of microtubules by binding to stabilized microtubules.
Cited by 8 Publications
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(B) Viability of cells after exposure to 0, 10, or 10,000 nM docetaxel, assessed by calcein-AM staining (green, left panels) and ethidium homodimer-1 (red, middle panels). Right panels show merged images. Scale bars = 100 μm.
Mol Pharm, 2014, 11(7):2040-50.. Docetaxel Trihydrate purchased from Selleck.
Polymerized and soluble tubulin fractions from docetaxel untreated and treated FOXM1-siRNA and pcDNA3, 1-FOXM1 transfected cell lines were generated by centrifugation. Western blot was used to assay α-tubulin and β-tubulin ratios in polymerized and soluble fractions. (A) Relative percentages are shown above western blot.
J Transl Med, 2013, 11:204.. Docetaxel Trihydrate purchased from Selleck.
Effect of siRNA-mediated knockdown for CDH1 in HCC4006ER cells. (A) Total cell lysates were harvested 72 hours after reverse-transfection of negative control siRNA (siNC) or validated siRNAs for CDH1 which encodes E-cadherin mixed with Lipofectamine RNAiMAX. (B-D) Tumor cells were reverse-transfected at the same time plating into 96-wells and then incubated for 24 hours. They were incubated with various concentrations of docetaxel, paclitaxel and vinorelbine for additional 72 hours. Percent growth relative to DMSO-treated controls was evaluated by Cell Counting Kit-8 assay.
PLoS One,2015, 10(4):e0123901. Docetaxel Trihydrate purchased from Selleck.
Purity & Quality Control
Choose Selective Microtubule Associated Inhibitors
|Description||Docetaxel, an analog of paclitaxel, is an inhibitor of depolymerisation of microtubules by binding to stabilized microtubules.|
Docetaxel is a cytotoxic agent, especially for proliferating cells, which is related to its ability to promote the formation of microtubule bundles and induce sustained mitotic arrest, followed by apoptosis of mitotically arrested cells or permanent mitotic block. Docetaxel suppresses microtubule dynamic instability as well as tread-milling, resulting in the failure of chromosomes to segregate to the daughter cells, which in turn triggers premature exit from mitosis rather than a block at this phase of the cell cycle.  Docetaxel inhibits the clonogenic survival of Human cancer cell Hs746T (stomach), AGS (stomach), HeLa (cervix), CaSki (cervix), BxPC3 (pancreas), Capan-1 (pancreas) with IC50 of 1 nM, 1 nM, 0.3 nM, 0.3 nM, 0.3 nM and 0.3 nM respectively.  Docetaxel inhibits endothelial cell migration that does not affects microtubule gross morphology or inhibit cell proliferation, although they does produce more subtle effects on microtubule dynamics. Docetaxel inhibits HUVEC migration with an observed IC50 of 1 pM. HUVEC chemotaxis stimulated by either of two angiogenic factors, thymidine phosphorylase or VEGF, is inhibited by Docetaxel with IC 50 of 10 pM and is ablated at 1 nM.  Docetaxel induces human monocytes, but not RAW 264.7 murine macrophages, Prostaglandin H Synthase-2m (PGHS-2) expression. 
|In vivo||Docetaxel (33 mg/kg/dose, given i.v. every 4 days for 3 injections) results in a tumor growth delay of 19.3 days in M2OL2 colon xenografts. Docetaxel also shows great antitumor activities in MX-1, SK-MEL-2, LX-1 and OVCAR-3 xenografts. Docetaxel inhibits the angiogenic response to fibroblast growth factor 2 with IC 50 of 5.4 mg/kg when injected twice weekly over a 14-day period, and angiogenesis is completely blocked in mice that receives 10 mg/kg Docetaxel. Docetaxel has selectivity for endothelial cell migration and/or microvessel formation because infiltration of inflammatory cells into the Matrigel plug is much less sensitive to inhibition by Docetaxel. |
-  Buey RM. Chem Biol, 2004, 11(2), 225-236.
-  Riou JF, et al. Biochem Biophys Res Commun, 1992, 187(1), 164-170.
-  Balcer-Kubiczek EK, et al. Chemotherapy, 2006, 52(5), 231-240.
|In vitro||DMSO||100 mg/mL (116.01 mM)|
|Ethanol||100 mg/mL (116.01 mM)|
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
|Synonyms||RP56976 (NSC 628503) Trihydrate|
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT02124902||Recruiting||Triple Negative Breast Neoplasms||Washington University School of Medicine||July 7, 2014||Phase 2|
|NCT01683994||Recruiting||Prostatic Neoplasms||National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC)||September 6, 2012||Phase 1|Phase 2|
|NCT02649855||Recruiting||Prostate Cancer|Prostate Neoplasms|Neoplasms, Prostatic||National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC)||January 4, 2016||Phase 2|
|NCT03041181||Recruiting||Non-Squamous Non-Small Cell Lung Cancer (NSCLC)|Adenocarcinoma of the Lung|Lung Cancer||Nasser Hanna, M.D.|Hoosier Cancer Research Network|Bristol-Myers Squibb||January 27, 2017||Phase 2|
|NCT00251433||Active, not recruiting||Neoplasms, Breast||Novartis Pharmaceuticals|Novartis||September 26, 2005||Phase 1|
|NCT01907529||Not yet recruiting||Stage III Breast Cancer||Hebei Medical University Fourth Hospital||August 2018||Phase 2|Phase 3|
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