| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 50mg | 电议 |
| 100mg | 电议 |
| 500mg | 电议 |
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 |
Applications | 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 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 | |
Applications | Paclitaxel (1 mg/kg, i.p.) induces changes in estrogen metabolism in liver that facilitate the formation of breast cancer metastases. |
| 文献引用 | |
| 产品描述 | 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 IC50value 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] References: |
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