Paclitaxel (Taxol)
(Synonyms: 紫杉醇) 目录号 : GC12511
紫杉醇是从短叶红豆杉的树皮和针叶中提取出来的三环二萜化合物。
Cas No.:33069-62-4
Sample solution is provided at 25 µL, 10mM.
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Related Biological Data
PTX damages mitochondria and generates ROS. (b) DCFH-DA fluorescent probe was used to detect the ROS content in PC3M cells under PTX treatment. Bar, 50 μm.
1 × 104 PC3M cells were cultured in 35 mm glass-bottom cell culture dishes for 24 h and added medium containing DMSO (3 μL/mL), PTX (2μM,GLPBIO), and/or NAC (5 mM) to treat cells in different groups for another 24h.
Talanta, 2023: 125355. PMID: 37952317 IF: 6.1004 -
Related Biological Data
WP1066 rescues paclitaxel-enhanced STAT3-Stathmin interaction and causes microtubule morphological change in ovarian cancer cells. (G). WP1066 promoted microtubule to be more instable while paclitaxel facilitated microtubule to be more stable in SKOV3 cells.
Paclitaxel-resistant SKOV3/PTX and A2780/PTX cells were established by a stepwise increase in paclitaxel (PTX), and maintained in the culture medium containing 10 ng/ml PTX(GLPBIO), while the parental cell lines were passaged in the absence of PTX.
Biochemical Pharmacology (2024): 116040. PMID: 38311257 IF: 5.8000 -
Related Biological Data
Downregulation of TRAF3 reduces the sensitivity of LUAD cells to paclitaxel (A) CCK-8 assay was applied to evaluate the effect of different concentrations of paclitaxel on the cell viability of A549 cells after transfection.
After incubating for 24 h, cells were adhered and grown in the wells. Then, 10 ul of paclitaxel (GlpBio, USA) was added at different concentrations and incubated for 48 h.
BMC cancer, 2023, 23(1): 1-9. PMID: 37798663 IF: 3.8001 -
Related Biological Data
Inhibition of MUC1 promoted apoptosis of A549/PR cells in treatment of paclitaxel. (B) Quantified results of A were presented.
Paclitaxel‑resistant NSCLC cell lines A549/PR were treated with 0.5 μM of paclitaxel (Glpbio) in the culture for 3 months.
Mol Med Rep 22.4 (2020): 2966-2972. PMID: 32945387 IF: 2.9500
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| Cell experiment [1]: | |
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Cell lines |
MCF-7 and MDA-MB-231 human breast carcinoma cell lines |
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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 . |
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Reaction Conditions |
20 nM; 12h |
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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 experiment [2]: | |
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Animal models |
Specific pathogen free nude mice |
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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). |
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Dosage form |
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Applications |
Paclitaxel (1 mg/kg, i.p.) induces changes in estrogen metabolism in liver that facilitate the formation of breast cancer metastases. |
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References: [1]. [1]Choi YH, Yoo YH. Taxol-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]. 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. |
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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 IC50 value 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:
[1]Zhu L, Chen L. Progress in research on paclitaxel and tumor immunotherapy. Cell Mol Biol Lett. 2019 Jun 13;24:40.
[2]Chen S, et al. Recent Development of Copolymeric Nano-Drug Delivery System for Paclitaxel. Anticancer Agents Med Chem. 2020;20(18):2169-2189.?
[3]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.?
[4]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.
[5]Saari H, et al. Microvesicle- and exosome-mediated drug delivery enhances the cytotoxicity of Paclitaxel in autologous prostate cancer cells. J Control Release. 2015 Dec 28;220(Pt B):727-37.?
[6]Jing C, et al. Lenvatinib enhances the antitumor effects of paclitaxel in anaplastic thyroid cancer. Am J Cancer Res. 2017 Apr 1;7(4):903-912.
紫杉醇是从短叶红豆杉的树皮和针叶中提取出来的三环二萜化合物。它可以促进微管蛋白聚集成微管，并防止微管解离，从而阻碍细胞周期进展、预防有丝分裂并抑制癌细胞生长。[1]
在体外实验中，紫杉醇以剂量依赖的方式显著抑制了ATC细胞的增殖；IC50值范围为1.99至9.97纳摩尔。将紫杉醇封装到纳米药物载体中可以提高其水溶性、选择性地传递给癌细胞、组织毒性、控制释放和药代动力学特性，从而改善其对人体的毒性，保持或增强其活性并改善其药代动力学特性。在 vitro 实验中，在短时间内接触紫杉醇可诱导 IkappaB-alpha 的磷酸化和降解，进而导致 NF-kappaB 在人乳腺癌BCap37和人表皮样癌KB细胞中被激活。此外，通过将紫杉醇加载到自体前列腺癌细胞衍生的EVs上可以增强其细胞毒作用。
在体内实验中，使用1毫克/千克和20毫克/千克紫杉醇治疗后，低剂量紫杉醇处理的小鼠肝脏中浅色斑点转移显著增加，而高剂量紫杉醇组的转移明显减少。在体内，C643细胞来源的异种移植瘤在接受5毫克/千克口服利妥昔单抗和5毫克/千克腹腔注射紫杉醇处理组中生长速度较缓慢，比对照组要慢。
| Cas No. | 33069-62-4 | SDF | |
| 别名 | 紫杉醇 | ||
| Canonical SMILES | O=C(N[C@H]([C@H](C(O[C@H]1C[C@]2(O)C(C)(C)C([C@@H](OC(C)=O)C([C@@]3(C)[C@]([C@@](CO4)(OC(C)=O)[C@H]4C[C@@H]3O)([H])[C@@H]2OC(C5=CC=CC=C5)=O)=O)=C1C)=O)O)C6=CC=CC=C6)C7=CC=CC=C7 | ||
| 分子式 | C47H51NO14 | 分子量 | 853.91 |
| 溶解度 | ≥ 42.6955mg/mL in DMSO, ≥ 31.6 mg/mL in EtOH with ultrasonic | 储存条件 | 4°C, protect from light |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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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 |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
How Taxol/paclitaxel kills cancer cells
Taxol (generic name paclitaxel) is a microtubule-stabilizing drug that is approved by the Food and Drug Administration for the treatment of ovarian, breast, and lung cancer, as well as Kaposi's sarcoma. It is used off-label to treat gastroesophageal, endometrial, cervical, prostate, and head and neck cancers, in addition to sarcoma, lymphoma, and leukemia. Paclitaxel has long been recognized to induce mitotic arrest, which leads to cell death in a subset of the arrested population. However, recent evidence demonstrates that intratumoral concentrations of paclitaxel are too low to cause mitotic arrest and result in multipolar divisions instead. It is hoped that this insight can now be used to develop a biomarker to identify the ?50% of patients that will benefit from paclitaxel therapy. Here I discuss the history of paclitaxel and our recently evolved understanding of its mechanism of action.
Paclitaxel (Taxol) and docetaxel (Taxotere): not simply two of a kind
Paclitaxel and docetaxel are the two presently clinically available representatives of the new class of taxane drugs. They share major parts of their structures and mechanisms of action, but differ in several other aspects. For instance, there is a difference in their tubulin polymer generation, and docetaxel appears twice as active in depolymerization inhibition. In vitro docetaxel also tends to be more potent in different cell lines and investigational models. While in vitro and in vivo studies suggest that prolonged exposure to paclitaxel is better than a brief exposure, no such tendency is seen for docetaxel, indicating it to be a schedule-independent drug. Clinical studies have not confirmed an advantage for prolonged exposure to paclitaxel; but do show differences in the toxicity profiles of the two drugs. These topics will be addressed in detail.
Paclitaxel (taxol)
Paclitaxel is a novel antineoplastic that effects cytotoxicity by promoting intracellular tubulin polymerization and stabilizes abnormal microtubule structures against depolymerization. Although its clinical development had been hampered by misconceptions about its pharmacology, its scarcity, difficulties extracting it from its natural source, formulation problems, and frequent severe hypersensitivity reactions, paclitaxel recently was approved for treatment-refractory ovarian cancer. Two major adverse effects are dosage- and schedule-related myelosuppression and mucositis. Neurotoxicity is directly related to both the individual and cumulative doses. Other relevant toxicities are hypersensitivity reactions, effects on cardiac rate and rhythm, arthralgias and myalgias, generalized hair loss, and mild nausea and emesis. Continuing clinical studies will evaluate paclitaxel as initial therapy for ovarian cancer and its utility in other malignancies. In addition, major efforts are under way to develop alternative sources to increase the availability of taxene analogs and reduce our dependence on yew species.
Taxol?: The First Microtubule Stabilizing Agent
Taxol?, an antitumor drug with significant activity, is the first microtubule stabilizing agent described in the literature. This short review of the mechanism of action of Taxol? emphasizes the research done in the Horwitz' laboratory. It discusses the contribution of photoaffinity labeled analogues of Taxol? toward our understanding of the binding site of the drug on the microtubule. The importance of hydrogen/deuterium exchange experiments to further our insights into the stabilization of microtubules by Taxol? is addressed. The development of drug resistance, a major problem that arises in the clinic, is discussed. Studies describing differential drug binding to distinct β-tubulin isotypes are presented. Looking forward, it is suggested that the β-tubulin isotype content of a tumor may influence its responses to Taxol?.