Docetaxel (hydrate)
(Synonyms: 多烯紫杉醇三水合物(非药典标准品)) 目录号 : GC48968
A microtubule-stabilizing agent
Cas No.:700367-34-6
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Docetaxel is a semisynthetic analog of taxol that inhibits microtubule disassembly (IC50 = 0.2 μM) and inhibits cell replication (IC50 = 0.13 μM).1 It has proven more effective than taxol in preventing the proliferation of cancer cells.1,2 Docetaxel has applications in breast cancer and hormone-
1.Bissery, M.C., Guenard, D., Gueritte-Voegelein, F., et al.Experimental antitumor activity of taxotere (RP 56976, NSC 628503), a taxol analogueCancer Research514845-4852(1991) 2.Pazdur, R., Kudelka, A.P., Kavanagh, J.J., et al.The taxoids: Paclitaxel (Taxolr) and docetaxel (Taxoterer)Cancer Treatment Reviews19351-386(1993) 3.Mahon, K.L., Henshall, S.M., Sutherland, R.L., et al.Pathways of chemotherapy resistance in castration-resistant prostate cancerEndocrine-Related Cancer18R103-R123(2011) 4.Yao, X., Hosenpud, J., Chitambar, C.R., et al.A phase II study of concurrent docetaxel, epirubicin and cyclophospha-mide as a neoadjuvant chemotherapy regimen in patients with locally advanced breast cancerJournal of Cancer3145-151(2012)
| Cas No. | 700367-34-6 | SDF | |
| 别名 | 多烯紫杉醇三水合物(非药典标准品) | ||
| Canonical SMILES | CC(C1=C(C)[C@@H](OC([C@H](O)[C@@H](NC(OC(C)(C)C)=O)C2=CC=CC=C2)=O)C3)(C)[C@]3(O)[C@@H](OC(C4=CC=CC=C4)=O)[C@@]([C@@](CO5)(OC(C)=O)[C@@]5([H])C[C@@H]6O)([H])[C@]6(C)C([C@@H]1O)=O.O | ||
| 分子式 | C43H53NO14·XH2O | 分子量 | 807.9 |
| 溶解度 | DMF: 5 mg/ml,DMSO: 5 mg/ml,DMSO:PBS (pH 7.2) (1:10): 0.1 mg/ml,Ethanol: 1.5 mg/ml | 储存条件 | -20°C |
| 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 | 1.2378 mL | 6.1889 mL | 12.3778 mL |
| 5 mM | 0.2476 mL | 1.2378 mL | 2.4756 mL |
| 10 mM | 0.1238 mL | 0.6189 mL | 1.2378 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。
Systemic therapies for metastatic hormone-sensitive prostate cancer: network meta-analysis
BJU Int 2022 Apr;129(4):423-433.PMID:34171173DOI:10.1111/bju.15507.
Objectives: To perform a systematic review and network meta-analysis to compare the efficacy and safety of currently available treatments for the management of metastatic hormone-sensitive prostate cancer (mHSPC), as there has been a paradigm shift with the use of next-generation androgen receptor inhibitors (ARIs) and Docetaxel. Methods: Multiple databases were searched for articles published before May 2020 according to the Preferred Reporting Items for Systematic Review and Meta-analysis extension statement for network meta-analysis. Studies comparing overall/progression-free survival (OS/PFS) and/or adverse events (AEs) in patients with mHSPC were eligible. Results: Nine studies (N = 9960) were selected, and formal network meta-analyses were conducted. Abiraterone (hazard ratio [HR] 0.83, 95% credible interval [CrI] 0.76-0.90), Docetaxel (HR 0.90, 95% CrI 0.82-0.98), and enzalutamide (HR 0.85, 95% CrI 0.73-0.99) were associated with significantly better OS than androgen-deprivation therapy (ADT), and abiraterone emerged as the best option. Abiraterone (HR 0.71, 95% CrI 0.67-0.76), apalutamide (HR 0.73, 95% CrI 0.65-0.81), Docetaxel (HR 0.84, 95% CrI 0.78-0.90), and enzalutamide (HR 0.67, 95% CrI 0.63-0.71) were associated with significantly better PFS than ADT, and enzalutamide emerged as the best option. Abiraterone (HR 0.85, 95% CrI 0.78-0.93), apalutamide (HR 0.87, 95% CrI 0.77-0.98), and enzalutamide (HR 0.80, 95% CrI 0.73-0.88) were significantly more effective than Docetaxel. Regarding AEs, apalutamide was the likely best option among the three ARIs. In patients with low-volume mHSPC, enzalutamide was the best option in terms of OS and PFS. Conclusions: All three ARIs are effective therapies for mHSPC; apalutamide was the best tolerated. All three seemed more effective than Docetaxel. These findings may facilitate individualised treatment strategies and inform future comparative trials.
Docetaxel remodels prostate cancer immune microenvironment and enhances checkpoint inhibitor-based immunotherapy
Theranostics 2022 Jun 27;12(11):4965-4979.PMID:35836810DOI:10.7150/thno.73152.
Background: Prostate cancer is usually considered as immune "cold" tumor with poor immunogenic response and low density of tumor-infiltrating immune cells, highlighting the need to explore clinically actionable strategies to sensitize prostate cancer to immunotherapy. In this study, we investigated whether docetaxel-based chemohormonal therapy induces immunologic changes and potentiates checkpoint blockade immunotherapy in prostate cancer. Methods: We performed transcriptome and histopathology analysis to characterize the changes of prostate cancer immune microenvironment before and after docetaxel-based chemohormonal therapy. Furthermore, we investigated the therapeutic benefits and underlying mechanisms of chemohormonal therapy combined with anti-PD1 blockade using cellular experiments and xenograft prostate cancer models. Finally, we performed a retrospective cohort analysis to evaluate the antitumor efficacy of anti-PD1 blockade alone or in combination with docetaxel-based chemotherapy. Results: Histopathology assessments on patient samples confirmed the enrichment of tumor-infiltrating T cells after chemohormonal therapy. Moreover, we found that Docetaxel activated the cGAS/STING pathway in prostate cancer, subsequently induced IFN signaling, resulting in lymphocytes infiltration. In a xenograft mouse model, docetaxel-based chemohormonal therapy prompted the intratumoral infiltration of T cells and upregulated the abundance of PD1 and PD-L1, thereby sensitizing mouse tumors to the anti-PD1 blockade. To determine the clinical significance of these results, we retrospectively analyzed a cohort of 30 metastatic castration-resistant prostate cancer patients and found that Docetaxel combined with anti-PD1 blockade resulted in better prostate-specific antigen progression-free survival when compared with anti-PD1 blockade alone. Conclusions: Our study demonstrates that Docetaxel activates the antitumoral immune response and facilitates T cell infiltration in a cGAS/STING-dependent manner, providing a combination immunotherapy strategy that would improve the clinical benefits of immunotherapy.
Treatments for Metastatic Hormone-sensitive Prostate Cancer: Systematic Review, Network Meta-analysis, and Benefit-harm assessment
Eur Urol Oncol 2022 Dec;5(6):605-616.PMID:35599144DOI:10.1016/j.euo.2022.04.007.
Context: Multiple treatments for metastatic, hormone-sensitive prostate cancer (mHSPC) are available, but their effects on health-related quality of life (HRQoL) and benefit-harm balance remain unclear. Objective: To assess clinical effectiveness regarding survival and HRQoL, safety, and benefit-harm balance of mHSPC treatments. Evidence acquisition: We searched MEDLINE, EMBASE, CENTRAL, and ClinicalTrials.gov until March 1, 2022. Randomized controlled trials (RCTs) comparing Docetaxel, abiraterone, enzalutamide, apalutamide, darolutamide, and radiotherapy combined with androgen deprivation therapy (ADT) mutually or with ADT alone were eligible. Three reviewers independently performed screening, data extraction, and risk of bias assessment in duplicate. Evidence synthesis: Across ten RCTs, we found relevant survival benefits for ADT + Docetaxel (high certainty according to the Grading of Recommendations, Assessment, Development and Evaluation [GRADE]), ADT + abiraterone (moderate certainty), ADT + enzalutamide (low certainty), ADT + apalutamide (high certainty), and ADT + Docetaxel + darolutamide (high certainty) compared with ADT alone. ADT + radiotherapy appeared effective only in low-volume de novo mHSPC. We found a short-term HRQoL decrease lasting 3-6 mo for ADT + Docetaxel (moderate certainty) and a potential HRQoL benefit for ADT + abiraterone up to 24 mo of follow-up (moderate certainty) compared with ADT alone. There was no difference in HRQoL for ADT + enzalutamide, ADT + apalutamide, or ADT + radiotherapy over ADT alone (low-high certainty). Grade 3-5 adverse effect rates were increased with all systemic combination treatments. A benefit-harm assessment showed high probabilities (>60%) for a net clinical benefit with ADT + abiraterone, ADT + enzalutamide, and ADT + apalutamide, while ADT + Docetaxel and ADT + Docetaxel + darolutamide appeared unlikely (<40%) to be beneficial. Conclusions: Despite substantial survival benefits, no systemic combination treatment showed a clear HRQoL improvement compared with ADT alone. We found evidence for a short-term HRQoL decline with ADT + Docetaxel and a higher net clinical benefit with ADT + abiraterone, ADT + apalutamide and ADT + enzalutamide. While individualized decision-making remains important and economic factors need to be considered, the evidence may support a general preference for the combination of ADT with androgen receptor axis-targeted therapies over docetaxel-containing strategies. Patient summary: We assessed different combination treatments for metastatic hormone-sensitive prostate cancer. While survival was better with all systemic combination treatments, there was no clear improvement in health-related quality of life compared with androgen deprivation therapy alone. Novel hormonal combination treatments had a more favorable benefit-harm balance than combination treatments that include chemotherapy.
Ccl3 enhances Docetaxel chemosensitivity in breast cancer by triggering proinflammatory macrophage polarization
J Immunother Cancer 2022 May;10(5):e003793.PMID:35613826DOI:10.1136/jitc-2021-003793.
Background: Although the antitumor efficacy of Docetaxel (DTX) has long been attributed to the antimitotic activities, its impact on the tumor microenvironment (TME) has recently gained more attention. Macrophages are a major component of the TME and play a critical role in DTX efficacy; however, the underlying action mechanisms remain unclear. Methods: DTX chemotherapeutic efficacy was demonstrated via both macrophage depletion and C-C motif chemokine ligand 3 (Ccl3)-knockout transgenic allograft mouse model. Ccl3-knockdown and Ccl3-overexpressing breast cancer cell allografts were used for the in vivo study. Combination therapy was used to evaluate the effect of Ccl3 induction on DTX chemosensitivity. Vital regulatory molecules and pathways were identified using RNA sequencing. Macrophage phagocytosis of cancer cells and its influence on cancer cell proliferation under DTX treatment were assessed using an in vitro coculture assay. Serum and tumor samples from patients with breast cancer were used to demonstrate the clinical relevance of our study. Results: Our study revealed that Ccl3 induced by DTX in macrophages and cancer cells was indispensable for the chemotherapeutic efficacy of DTX. DTX-induced Ccl3 promoted proinflammatory macrophage polarization and subsequently facilitated phagocytosis of breast cancer cells and cancer stem cells. Ccl3 overexpression in cancer cells promoted proinflammatory macrophage polarization to suppress tumor progression and increase DTX chemosensitivity. Mechanistically, DTX induced Ccl3 by relieving the inhibition of cAMP-response element binding protein on Ccl3 via reactive oxygen species accumulation, and Ccl3 then promoted proinflammatory macrophage polarization via activation of the Ccl3-C-C motif chemokine receptor 5-p38/interferon regulatory factor 5 pathway. High CCL3 expression predicted better prognosis, and high CCL3 induction revealed better DTX chemosensitivity in patients with breast cancer. Furthermore, both the Creb inhibitor and recombinant mouse Ccl3 significantly enhanced DTX chemosensitivity. Conclusions: Our results indicate that Ccl3 induced by DTX triggers proinflammatory macrophage polarization and subsequently facilitates phagocytosis of cancer cells. Ccl3 induction in combination with DTX may provide a promising therapeutic rationale for increasing DTX chemosensitivity in breast cancer.
Mechanisms of Docetaxel resistance in prostate cancer: The key role played by miRNAs
Biochim Biophys Acta Rev Cancer 2021 Jan;1875(1):188481.PMID:33217485DOI:10.1016/j.bbcan.2020.188481.
One of the main problems with the treatment of metastatic prostate cancer is that, despite an initial positive response, the majority of patients develop resistance and progress. In particular, the resistance to Docetaxel, the gold standard therapy for metastatic prostate cancer since 2010, represents one of the main factors responsible for the failure of prostate cancer therapy. According to the present knowledge, different processes contribute to the appearance of Docetaxel resistance and non-coding RNA seems to play a relevant role in them. In this review, a comprehensive overview of the miRNA network involved in Docetaxel resistance is described, highlighting the pathway/s affected by their activity.