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10-Deacetyl-7-xylosyl paclitaxel

10-Deacetyl-7-xylosyl paclitaxel

Catalog No. BCN2947
Size Price Stock
20mg $268 In stock
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Quality Control of 10-Deacetyl-7-xylosyl paclitaxel

Chemical structure

10-Deacetyl-7-xylosyl paclitaxel

10-Deacetyl-7-xylosyl paclitaxel Dilution Calculator

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10-Deacetyl-7-xylosyl paclitaxel Molarity Calculator



Chemical Properties of 10-Deacetyl-7-xylosyl paclitaxel

Cas No. 90332-63-1 SDF Download SDF
Standard InChI InChI=1S/C50H57NO17/c1-25-31(65-45(61)38(56)35(27-15-9-6-10-16-27)51-43(59)28-17-11-7-12-18-28)22-50(62)42(67-44(60)29-19-13-8-14-20-29)40-48(5,41(58)37(55)34(25)47(50,3)4)32(21-33-49(40,24-64-33)68-26(2)52)66-46-39(57)36(54)30(53)23-63-46/h6-20,30-33,35-40,42,46,53-57,62H,21-24H2,1-5H3,(H,51,59)/t30-,31+,32+,33-,35+,36+,37-,38-,39-,40-,42+,46+,48-,49+,50-/m1/s1
Type of Compound Diterpenoids Appearance Powder
Formula C50H57NO17 M.Wt 944.0
Solubility Soluble in DMSO
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other courier with RT , or blue ice upon request.

Preparing Stock Solutions of 10-Deacetyl-7-xylosyl paclitaxel

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 1.0593 mL 5.2966 mL 10.5932 mL 21.1864 mL 26.4831 mL
5 mM 0.2119 mL 1.0593 mL 2.1186 mL 4.2373 mL 5.2966 mL
10 mM 0.1059 mL 0.5297 mL 1.0593 mL 2.1186 mL 2.6483 mL
50 mM 0.0212 mL 0.1059 mL 0.2119 mL 0.4237 mL 0.5297 mL
100 mM 0.0106 mL 0.053 mL 0.1059 mL 0.2119 mL 0.2648 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

Preparation of 10-Deacetyl-7-xylosyl paclitaxel

This product is isolated and purified from the barks of Taxus baccata

References on 10-Deacetyl-7-xylosyl paclitaxel

Mathematical deconvolution uncovers the genetic regulatory signal of cancer cellular heterogeneity on resistance to paclitaxel.[Pubmed: 28386641]

Drug resistance remains a major problem in combating malignancies, resulting critical the resistance to paclitaxel used in the treatment of many different cancers. Elucidating the cellular heterogeneity composition of tumours may be relevant to designing more effective treatment strategies on drug resistance. In particular, such heterogeneity correlates with the measurement of gene expression below the population level. However, experimental assays capturing differential response are limited and cannot discern the variation in gene expression specific to different cellular types in tumour populations. These limitations led us to consider a mathematical modelling approach, in which the gene expression of cellular subpopulations is recovered by deconvolution. Mathematically, the deconvolution is a multi-linear regression-based problem. We combined herein data on cellular subpopulation frequency composition with gene expression values from 16 tumour lines (8 resistant and 8 sensitive to paclitaxel treatment) to find genes that are differentially expressed between paclitaxel resistant and paclitaxel sensitive tumour lines in different cellular subpopulations. The results indicate that many genes differentially expressed between paclitaxel resistant and sensitive cancer lines are only detected when considering their heterogeneous cellular composition. Overall, our methodology is thought to keep in mind phenotypic heterogeneity improving our resolution in the identification of biomarkers on resistance to chemo-therapeutic agents.

2-Year Results of Paclitaxel-Coated Balloons for Long Femoropopliteal Artery Disease: Evidence From the SFA-Long Study.[Pubmed: 28385412]

The aim of this study was to appraise 2-year outcomes after percutaneous transluminal angioplasty of long femoropopliteal artery disease using paclitaxel-coated balloons (PCBs).

Prophylactic Administration of Aucubin Inhibits Paclitaxel-Induced Mechanical Allodynia via the Inhibition of Endoplasmic Reticulum Stress in Peripheral Schwann Cells.[Pubmed: 28381802]

Paclitaxel is a chemotherapeutic agent that causes peripheral neuropathy as its major dose-limiting side effect. However, the peripheral neuropathy is difficult to manage. A study we recently conducted showed that repetitive administration of aucubin as a prophylactic inhibits paclitaxel-induced mechanical allodynia. However, the mechanisms underlying the anti-allodynic activity of aucubin, which is a major component of Plantaginis Semen, was unclear. In addition to mechanical allodynia, aucubin inhibited spontaneous and mechanical stimuli-induced firing in spinal dorsal horn neurons; however, catalpol, a metabolite of aucubin, did not show these effects. Furthermore, paclitaxel induced the expression of CCAAT/enhancer-binding protein homologous protein, a marker of endoplasmic reticulum (ER) stress, in the sciatic nerve and a Schwann cell line (LY-PPB6 cells); however, this effect was inhibited by aucubin. These results suggest that aucubin inhibits paclitaxel-induced mechanical allodynia through the inhibition of ER stress in peripheral Schwann cells.

Antibody-targeted paclitaxel loaded nanoparticles for the treatment of CD20+ B-cell lymphoma.[Pubmed: 28378801]

We developed a nano-antibody targeted chemotherapy (nATC) delivery strategy in which tumor specific and clinically relevant antibodies (rituximab, anti-CD20) are non-covalently bound to the albumin scaffold of nab-paclitaxel (ABX). We define the nanoparticle formed when the 2 drugs are bound (AR160). The newly created nATC retains the cytotoxicity of ABX and CD20 affinity of rituximab in vitro. We describe the binding characteristics of the ABX and rituximab in AR160 using peptide mapping/Biacore approach. Flow-based methods, including ImageStream and nanoparticle tracking, were used to characterize the AR160 particles in vitro. A mouse model of human B-cell lymphoma was utilized to test in vivo efficacy of AR160 therapy, which suggested improved tumor targeting (biodistribution) as the most likely mechanism of AR160 therapeutic superiority over ABX or rituximab alone. These data suggest a novel platform for nATC delivery using a slight modification of existing cancer drugs with significantly improved treatment efficacy.


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