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33069-62-4 分子结构
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(1S,2S,4S,7R,9S,10S,12R,15S)-4,12-bis(acetyloxy)-1,9-dihydroxy-15-{[(2R,3S)-2-hydroxy-3-phenyl-3-(phenylformamido)propanoyl]oxy}-10,14,17,17-tetramethyl-11-oxo-6-oxatetracyclo[11.3.1.0^{3,10}.0^{4,7}]heptadec-13-en-2-yl benzoate

ChemBase编号:72546
分子式:C47H51NO14
平均质量:853.90614
单一同位素质量:853.33095532
SMILES和InChIs

SMILES:
c1cccc(c1)C(=O)N[C@H]([C@H](C(=O)O[C@H]1C[C@@]2(C(C(=C1C)[C@H](C(=O)[C@]1(C([C@]3([C@@H](C[C@@H]1O)OC3)OC(=O)C)[C@@H]2OC(=O)c1ccccc1)C)OC(=O)C)(C)C)O)O)c1ccccc1
Canonical SMILES:
CC(=O)O[C@H]1C(=O)[C@]2(C)[C@@H](O)C[C@@H]3[C@](C2[C@@H]([C@]2(C(C1=C(C)[C@@H](OC(=O)[C@@H]([C@H](c1ccccc1)NC(=O)c1ccccc1)O)C2)(C)C)O)OC(=O)c1ccccc1)(CO3)OC(=O)C
InChI:
InChI=1S/C47H51NO14/c1-25-31(60-43(56)36(52)35(28-16-10-7-11-17-28)48-41(54)29-18-12-8-13-19-29)23-47(57)40(61-42(55)30-20-14-9-15-21-30)38-45(6,32(51)22-33-46(38,24-58-33)62-27(3)50)39(53)37(59-26(2)49)34(25)44(47,4)5/h7-21,31-33,35-38,40,51-52,57H,22-24H2,1-6H3,(H,48,54)/t31-,32-,33+,35-,36+,37+,38?,40-,45+,46-,47+/m0/s1
InChIKey:
RCINICONZNJXQF-VAZQATRQSA-N

引用这个纪录

CBID:72546 http://www.chembase.cn/molecule-72546.html

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名称和登记号

名称和登记号

名称 登记号
IUPAC标准名
(1S,2S,4S,7R,9S,10S,12R,15S)-4,12-bis(acetyloxy)-1,9-dihydroxy-15-{[(2R,3S)-2-hydroxy-3-phenyl-3-(phenylformamido)propanoyl]oxy}-10,14,17,17-tetramethyl-11-oxo-6-oxatetracyclo[11.3.1.0^{3,10}.0^{4,7}]heptadec-13-en-2-yl benzoate
IUPAC传统名
@paclitaxel
别名
Onxol
Taxol
Nov-Onxol
Paclitaxel(Taxol)
CAS号
33069-62-4
PubChem SID
162037471
PubChem CID
441276

数据来源

数据来源

所有数据来源 商品来源 非商品来源
数据来源 数据ID 价格
Selleck Chemicals
S1150 external link 加入购物车 请登录
数据来源 数据ID
PubChem 441276 external link

理论计算性质

理论计算性质

JChem
质子受体 10  质子供体
LogD (pH = 5.5) 3.5388339  LogD (pH = 7.4) 3.538369 
Log P 3.53884  摩尔折射率 218.2945 cm3
极化性 86.54275 Å3 极化表面积 221.29 Å2
可自由旋转的化学键 14  里宾斯基五规则 false 
Acid pKa 10.364198 

分子性质

分子性质

理化性质 安全信息 药理学性质 产品相关信息 生物活性(PubChem)
溶解度
DMSO expand 查看数据来源
保存条件
-20°C expand 查看数据来源
作用靶点
Microtubule Formation expand 查看数据来源
成盐信息
Free Base expand 查看数据来源

详细说明

详细说明

Selleck Chemicals Selleck Chemicals
Selleck Chemicals -  S1150 external link
Research Area
Description Cancer
Biological Activity
Description Paclitaxel (Taxol, Onxol, Nov-Onxol) is a microtubule polymer stabilizer with IC50 of 0.1 pM in human endothelial cells.
Targets Microtubule (human endothelial cells)
IC50 0.1 pM [1]
In Vitro Paclitaxel inhibits non-endothelial type human cells at 104 - to 105 -fold higher concentrations, with IC50 of 1 nM-10 nM. The selectivity of Paclitaxel inhibition of cell proliferation is also species specific, as mouse ECs are not sensitive to Paclitaxel at ultra low concentrations. Inhibition of human ECs by Paclitaxel at ultra low concentrations does not affect the cellular microtubule structure, and the treated cells do not show G2/M cell cycle arrest and apoptosis, suggesting a novel but as yet unidentified mechanism of action. In an in vitro angiogenesis assay, Paclitaxel at ultra low concentrations blocks human ECs from forming sprouts and tubes in the three-dimensional fibrin matrix. [1] In the presence of SMF, the efficient concentration of Paclitaxel on K562 cells is decreased from 50 to 10 ng/mL. The cell cycle arrest effect of Paclitaxel with or without SMF on K562 cells is correlated with DNA damage. [2] Paclitaxel alone causes a time-dependent inhibition of CDK1 in four cell lines including A549 cells, H358, H1395 cells and H1666 cells. [3]
In Vivo The inhibition rations of Paclitaxel alone on BC-V and BC-ER tumors are 49.78% and 51.23%, respectively. Treatment of six cycles of 20 mg/kg Paclitaxel significantly reduces the percentages of Ki-67-positive cells to 20.4% in BC-V tumors and 25.1% in BC-ER tumors, respectively. [5]
Clinical Trials Paclitaxel has entered in a Phase III clinical trial for the treatment of tubular breast cancer stage II, mucinous breast cancer stage II, breast cancer female NOS and invasive ductal breast cancer.
Features
Combination Therapy
Description K562 cells treated with SMF plus Paclitaxel are arrested at the G2 phase, which is mainly induced by Paclitaxel. The potency of the combination of SMF and Paclitaxel is greater than that of SMF or Paclitaxel alone on K562 cells, and these effects are correlated with DNA damage induced by SMF and Paclitaxel. [2] The combination of Lobaplatin with antitubulin agents, especially with Paclitaxel, leads to significantly enhanced activity, which is superior to that of Cisplatin combined with antitubulin agents. [4] Paclitaxel in combination with Carboplatin, BIBW 2992, and Bevacizumab or BIBW2992 is currently under investigation in a Phase I clinical trial for the treatment of neoplasms.
Protocol
Cell Assay [1]
Cell Lines Cells including human neonatal dermal microvascular ECs (HMVECs), human umbilical vein ECs (HUVECs), human umbilical artery ECs (HUAVECs), normal human astrocytes (NHAs), normal human dermal fibroblasts (NHDFs), normal human epidermal keratinocytes (NHEKs), human mammary epithelial cells (HMEpCs), human prostate epithelial cells (PrEpCs) and human umbilical artery smooth muscle cells (UASMCs)
Concentrations 0.1-100 pM
Incubation Time 72 hours
Methods Cells including human neonatal dermal microvascular ECs (HMVECs), human umbilical vein ECs (HUVECs), human umbilical artery ECs (HUAVECs), normal human astrocytes (NHAs), normal human dermal fibroblasts (NHDFs), normal human epidermal keratinocytes (NHEKs), human mammary epithelial cells (HMEpCs), human prostate epithelial cells (PrEpCs) and human umbilical artery smooth muscle cells (UASMCs) are cultured. Cell proliferations are performed in 96-well plates using cells between passages 6 and 12. Cells are seeded at 3000–5000 cells/well and allowed to attach for 4 hours. Paclitaxel, diluted in culture medium, is added in quadruplicate wells and the cells ae incubated for 3 days before MTS reagents are added to quantitate the live cells in each well.
Animal Study [5]
Animal Models Female, 20-22 g homozygous nude athymic mice with BC-V and BC-ER tumors
Formulation Control
Doses 20 mg/kg
Administration Administered via i.v.
References
[1] Wang J, et al. Anticancer Drugs. 2003, 14(1), 13-19.
[2] Sun RG, et al. Gen Physiol Biophys. 2012, 31(1), 1-10.
[3] Zhang XH, et al. Cancer Lett. 2012, 322(2), 213-222.
[4] Xie CY, et al. Anticancer Drugs. 2012.
[5] Chang J, et al. Breast Cancer Res Treat. 2012.

参考文献

参考文献

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