Paclitaxel [33069-62-4]
Katalog-Nummer HY-B0015-50mg
Size : 50mg
Marke : MedChemExpress
Paclitaxel est un agent antinéoplasique naturel et stabilise la polymérisation de la tubuline. Paclitaxel peut provoquer à la fois l'arrêt mitotique et la mort cellulaire apoptotique. Paclitaxel induit également l'autophagie.
Paclitaxel ist ein natürlich vorkommendes antineoplastisches Mittel und stabilisiert die tubulinpolymerisation. Paclitaxel kann sowohl einen mitotischen Stillstand als auch apoptotic Zelltod verursachen. Paclitaxel induziert auch autophagy.
Paclitaxel is a naturally occurring antineoplastic agent and stabilizes tubulin polymerization. Paclitaxel can cause both mitotic arrest and apoptotic cell death. Paclitaxel also induces autophagy.
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Paclitaxel Chemische Struktur
CAS. Nr. : 33069-62-4
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- Paclitaxel (PTX; 3.125, 6.25, 12.5, 25, 50, 100 nM; 48 h) reduces the viability of Hela, SiHa, and C33A cells in a dose-dependent manner.(3.125 nM for Hela cells, 100 nM for SiHa and C33A cells)
- Paclitaxel (PTX; 50 nM; 48 h) increases the expression of Cleaved-caspase-9 and Cleaved-caspase-3 in Hela cells.
- Paclitaxel (25, 50 μM; 24 h) significantly increases the expression of caspase-3 in PK-15 cells.
- Paclitaxel (PTX; 0‑100 nM; 72 h) inhibits the viability of MDA‑MB‑231cells.
- Paclitaxel (CPT; 10-6 -12-10 M; 72 h) demonstrates a strong antitumor activity and an inhibitory of proliferation (IC50 = 6.28 nM) in U937 cells.
- Western blot image and statistical analysis of phosphorylated γH2AX levels in HT-29 cells with different treatments after 48 h. Myricetin and PTX used are 32 μM and 100 nM, respectively.
- The effects of CS1 on polymerized microtubules are also investigated using a cellular tubulin polymer assay. Nocodazole (1 μM) and Paclitaxel (1.5 μM) are used as depolymerization and polymerization controls, respectively.
- Synergistic inhibition of colony formation of ATC cells by E7080 and Paclitaxel. Representative images of colony formation in C643 cells treated with vehicle control (DMSO) or E7080 and Paclitaxel at the indicated concentrations, individually or in combination, are shown in left panel. Quantitative analysis of colony numbers is shown in right panel.
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Paclitaxel is a naturally occurring antineoplastic agent and stabilizes tubulin polymerization. Paclitaxel can cause both mitotic arrest and apoptotic cell death. Paclitaxel also induces autophagy. | |||||||||||||||||||||||||
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In Vitro | Paclitaxel (20 nM; 48 hours) induces programmed cell death and exists a block at the G2/M phase of the cell cycle. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Apoptosis Analysis
Cell Cycle Analysis
Western Blot Analysis
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In Vivo | Paclitaxel (1-20 mg/kg; i.p.; 1 time/2 days for five cycles) obviously induces liver metastases at the low-Paclitaxel group with little influence on primary tumor growth. MCE has not independently confirmed the accuracy of these methods. They are for reference only.
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853.91 | |||||||||||||||||||||||||
Solid | |||||||||||||||||||||||||
C47H51NO14 | |||||||||||||||||||||||||
33069-62-4 | |||||||||||||||||||||||||
O=C(C1=CC=CC=C1)N[C@@H](C2=CC=CC=C2)[C@H](C(O[C@@H]3C(C)=C([C@@H](OC(C)=O)C([C@@]4(C)[C@]([C@@](CO5)(OC(C)=O)[C@@]5(03)C[C@@H]4O)(03)[C@@H]6OC(C7=CC=CC=C7)=O)=O)C(C)(C)[C@@]6(O)C3)=O)O | |||||||||||||||||||||||||
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Room temperature in continental US; may vary elsewhere. | |||||||||||||||||||||||||
4°C, protect from light *In solvent : -80°C, 6 months; -20°C, 1 month (protect from light) | |||||||||||||||||||||||||
In Vitro: DMSO : 100 mg/mL (117.11 mM; Need ultrasonic) H2O : < 0.1 mg/mL (insoluble) Preparing Stock Solutions
*Please refer to the solubility information to select the appropriate solvent. In Vivo:
*All of the co-solvents are available by MCE. | |||||||||||||||||||||||||
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[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.
- Cytoskeleton Cell Cycle/DNA Damage Antibody-drug Conjugate/ADC Related Apoptosis Autophagy
- Microtubule/Tubulin ADC Cytotoxin Apoptosis Autophagy
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Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.