Docetaxel - CAS 114977-28-5
Catalog number: B0084-081971
Category: Inhibitor
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Docetaxel, also called Taxoltere metro, a semisynthetic side-chain analogue of taxol differing at two positions in its chemical structure, is an inhibitior of microtubule disassembly (IC50 = 0.2 μM). And it inhibits cell replication (IC50 = 0.13 μM).
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B0084-081971 5 g $499 In stock
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Brife Description:
An inhibitior of microtubule disassembly (IC50 = 0.2 μM); Inhibits cell replication (IC50 = 0.13 μM)
White solid
docetaxel; docetaxel anhydrous; docetaxel hydrate; docetaxel trihydrate; docetaxol; N-debenzoyl-N-tert-butoxycarbonyl-10-deacetyltaxol; NSC 628503; RP 56976; RP-56976; Taxoltere metro; 114977-28-5
Soluble to 100 mM in DMSO and to 100 mM in ethanol
Store in a cool and dry place and at 0 - 4℃ for short term (days to weeks) or -55℃ for long term (months to years).
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1.Oridonin inhibits gefitinib-resistant lung cancer cells by suppressing EGFR/ERK/MMP-12 and CIP2A/Akt signaling pathways.
Xiao X1, He Z1, Cao W2, Cai F1, Zhang L1, Huang Q1, Fan C1, Duan C1, Wang X3, Wang J4, Liu Y1. Int J Oncol. 2016 Apr 15. doi: 10.3892/ijo.2016.3488. [Epub ahead of print]
Oridonin (Ori), a diterpenoid compound extracted from traditional medicinal herbs, elicits antitumor effects on many cancer types. However, whether Ori can be used in gefitinib-resistant non-small cell lung cancer (NSCLC) cells remains unclear. This study investigated the antitumor activity and underlying mechanisms of Ori. Results demonstrated that this compound dose-dependently inhibited the proliferation, invasion, and migration of the gefitinib-resistant NSCLC cells in vitro. Ori also significantly downregulated the phosphorylation of EGFR, ERK, Akt, expression levels of matrix metalloproteinase-12 (MMP-12), and the cancerous inhibitor of protein phosphatase 2A (CIP2A). In addition, Ori upregulated protein phosphatase 2A (PP2A) activity of gefitinib-resistant NSCLC cells. Ori combined with docetaxel synergistically inhibited these cells. Ori also inhibited tumor growth in murine models. Immunohistochemistry results further revealed that Ori downregulated phospho-EGFR, MMP-12, and CIP2A in vivo.
2.Expression of BRCA1, a factor closely associated with relapse-free survival, in patients who underwent neoadjuvant chemotherapy with docetaxel, cisplatin, and fluorouracil for squamous cell carcinoma of the esophagus.
Ojima T1, Nakamori M1, Nakamura M1, Katsuda M1, Hayata K1, Nakamura Y2, Yamaue H3. Surg Today. 2016 Apr 29. [Epub ahead of print]
PURPOSE: The aim of this study was to identify the biomarkers associated with chemotherapeutic efficacy and long-term survival for patients with advanced squamous cell carcinoma of the esophagus (SCCE) who had received neoadjuvant chemotherapy with docetaxel and cisplatin plus 5-fluorouracil (NAC-DCF).
3.Docetaxel induces Bcl-2- and pro-apoptotic caspase-independent death of human prostate cancer DU145 cells.
Ogura T1, Tanaka Y1, Tamaki H2, Harada M3. Int J Oncol. 2016 Apr 8. doi: 10.3892/ijo.2016.3482. [Epub ahead of print]
Docetaxel is a useful chemotherapeutic agent for the first-line treatment of hormone-refractory prostate cancer. Abnormal expression of Bcl-2 is commonly found in cancer cells, which increases their anti-apoptotic potency and chemoresistance. We investigated the effects of Bcl-2 expression status on the susceptibility of DU145 cells, an androgen-independent human prostate cancer cell line, to docetaxel and other anticancer agents. A panel of Bcl-2-expressing DU145 cell lines was established. Bcl-2 expression levels were unrelated to the susceptibility of DU145 cells to docetaxel. The sensitivity of DU145 cells to cisplatin fluctuated, and the sensitivity to tumor necrosis factor (TNF)-α was decreased by Bcl-2 overexpression. In a xenograft mouse model, overexpression of Bcl-2 drastically decreased the sensitivity of DU145 cells to cisplatin and TNF-α; however, there was no change in the response to docetaxel. Fluorescent microscopy revealed that Bcl-2-overexpression had no effect on the docetaxel-induced death of DU145 cells, but significantly decreased DU145 cell death induced by cisplatin or TNF-α.
4.Docetaxel combined with intraperitoneal hyperthermic perfusion chemotherapy and hyperthermia in the treatment of advanced ovarian cancer.
Zhang T1, Pan Q1, Xiao S1, Li L1, Xue M1. Oncol Lett. 2016 May;11(5):3287-3292. Epub 2016 Apr 5.
Ovarian cancer is a clinical type of gynecological malignant tumor with poor prognosis and a high mortality rate. At present, the primary treatment method used is surgery, with chemotherapy as an ajdunctive therapy. Thus, new short-term treatments should be identified. The aim of the present study was to investigate the short-term curative effects and safety of docetaxel combined with intraperitoneal cisplatin chemotherapy and hyperthermia treatment of advanced ovarian cancer. A total of 112 cases of advanced (stage III-IV) ovarian cancer patients confirmed by clinical diagnosis between October 2014 and December 2015 were included in the study. The patients were randomly divided into the study and control groups (n=56 cases). The control group was treated with docetaxel and intraperitoneal cisplatin hyperthermic perfusion chemotherapy, while the study group was treated with docetaxel venous chemotherapy and intraperitoneal cisplatin cyclical hyperthermic perfusion chemotherapy with BR-TRG-1 body cavity hyperthermic perfusion treatment system.
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CAS 114977-28-5 Docetaxel

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