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Purity: ≥98%
Paclitaxel (also known as NSC-125973; BMS-181339-01; trade name taxol; Anzatax; Asotax; Bristaxol) is a highly potent microtubule polymer stabilizer (mitotic inhibitor that stabilizes the polymerization of tubulin) with an IC50 of 0.1 pM in human endothelial cells. Paclitaxel has shown potent and a broad spectrum of antineoplastic activities, and has been extensively used in the treatment of various cancers. It is a natural product isolated from the Pacific yew tree Taxus brevifolia that has anticancer activity. Paclitaxel binds to tubulin and inhibits the disassembly of microtubules, thereby resulting in the inhibition of cell division. This agent also induces apoptosis by binding to and blocking the function of the apoptosis inhibitor protein Bcl-2.
ln Vitro |
In the G2/M phase of the cell cycle, paclitaxel (20 nM; 48 h) causes programmed cell death and arrest [1]. A prolonged rise in p53 levels is induced by paclitaxel (20 nM; 48 hours) [1].
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ln Vivo |
In the low-paclitaxel group, paclitaxel (1–20 mg/kg; intraperitoneal injection; once every two days, 5 cycles total) significantly increased the risk of liver metastasis while having minimal influence on the growth of the underlying tumor [3].
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Cell Assay |
Apoptosis Analysis[1]
Cell Types: MCF-7, MDA-MB-231 cells Tested Concentrations: 20 nM Incubation Duration: 48 hrs (hours) Experimental Results: Induced programmed cell death. Cell Cycle Analysis[1] Cell Types: MCF-7, MDA-MB -231 cells Tested Concentrations: 20 nM Incubation Duration: 48 hrs (hours) Experimental Results: >60% of MCF-7 cells and 50% of MDA-MB-231 cells were in the G2/M phase following 24 h treament. Western Blot Analysis[1] Cell Types: MCF-7 cells (harboring wild-type p53) Tested Concentrations: 20 nM Incubation Duration: 48 hrs (hours) Experimental Results: Induced a consistent increase in the level of p53. |
Animal Protocol |
Animal/Disease Models: MDA-231 xenograft-bearing mice[3]
Doses: 1, 20 mg/kg Route of Administration: intraperitoneal (ip)injection; five cycles (1 time/2 days) Experimental Results: Liver metastases were obviously induced in the low-PTX (1 mg /kg) group with little influence on primary tumor growth compared with high-PTX group. |
References |
[1]. Choi YH, et al. Paclitaxel-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]. 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. [3]. 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. [4]. Pan Z, et al. Paclitaxel attenuates Bcl-2 resistance to apoptosis in breast cancer cells through an endoplasmic reticulum-mediated calciumrelease in a dosage dependent manner. Biochem Biophys Res Commun. 2013 Feb 13. pii: S0006-291X(13)00259-3. [5]. Cadamuro M, et al. Low dose paclitaxel reduces S100A4 nuclear import to inhibit invasion and hematogenous metastasis of cholangiocarcinoma. Cancer Res. 2016 Jun 21. [6]. Li Q, et al. Low doses of paclitaxel enhance liver metastasis of breast cancer cells in the mouse model. FEBS J. 2016 Jun 16. [7]. Yilmaz E, et al. Sensory neuron subpopulation-specific dysregulation of intracellular calcium in a rat model of chemotherapy-induced peripheral neuropathy. Neuroscience. 2015 Aug 6;300:210-8. [8]. Jing C, et al. E7080 enhances the antitumor effects of paclitaxel in anaplastic thyroid cancer. Am J Cancer Res. 2017 Apr 1;7(4):903-912. |
Molecular Formula |
C47H51NO14
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Molecular Weight |
853.91
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CAS # |
33069-62-4
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SMILES |
O=C1[C@H](OC(C)=O)C(C2(C)C)=C(C)[C@@H](OC([C@H](O)[C@@H](NC(C3=CC=CC=C3)=O)C4=CC=CC=C4)=O)C[C@@]2(O)[C@@H](OC(C5=CC=CC=C5)=O)[C@@]6([H])[C@@]1(C)[C@@H](O)C[C@@]7([H])OC[C@]76OC(C)=O
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Chemical Name |
(2aR,4S,4aS,6R,9S,11S,12S,12aR,12bS)-9-(((2R,3S)-3-benzamido-2-hydroxy-3-phenylpropanoyl)oxy)-12-(benzoyloxy)-4,11-dihydroxy-4a,8,13,13-tetramethyl-5-oxo-2a,3,4,4a,5,6,9,10,11,12,12a,12b-dodecahydro-1H-7,11-methanocyclodeca[3,4]benzo[1,2-b]oxete-6,12b-diyl diacetate
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Synonyms |
NSC 125973; BMS 181339-01; NSC-125973; BMS181339-01; NSC125973; BMS-181339-01; Trade name: Taxol; Taxol Konzentrat; Anzatax; Asotax; Bristaxol; Praxel; TAX.
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Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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Solubility (In Vitro) |
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Solubility (In Vivo) |
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Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
1 mM | 1.1711 mL | 5.8554 mL | 11.7108 mL | |
5 mM | 0.2342 mL | 1.1711 mL | 2.3422 mL | |
10 mM | 0.1171 mL | 0.5855 mL | 1.1711 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration: mg/mL;
Method for preparing DMSO stock solution: mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation::Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O,mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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