688009-09-8

Basic information

• Product Name: DTBS-GEMCITABINE
• Synonyms: DTBS-GEMCITABINE;3',5'-Bis-O-tert-butyldimethylsilyl-2'-deoxy-2',2'-difluorocytidine
• CAS NO: 688009-09-8
• Molecular Formula: C₂₁H₃₉F₂N₃O₄Si₂
• Molecular Weight: 491.72
• Mol File: 688009-09-8.mol
• Article Data: 24

Chemical Properties

• Appearance: /
• CAS DataBase Reference: DTBS-GEMCITABINE(CAS DataBase Reference)
• NIST Chemistry Reference: DTBS-GEMCITABINE(688009-09-8)
• EPA Substance Registry System: DTBS-GEMCITABINE(688009-09-8)

Safety Data

• Hazardous Substances Data: 688009-09-8(Hazardous Substances Data)

Upstream product

• 18162-48-6 tert-butyldimethylsilyl chloride 
• 122111-03-9 gemcitabine hydrochloride 
• 95058-81-4 gemcitabine 
• 69739-34-0 t-butyldimethylsiyl triflate 

Downstream Products

• 95058-81-4 gemcitabine 

Relevant articles and documents

Enhancing efficacy of gemcitabine in pancreatic patient-derived xenograft mouse models

Gemcitabine (Gem), a nucleoside analog, is a preferred choice of treatment for pancreatic cancer (PCa) and often used in combination therapy against wide range of solid tumors. It is known to be rapidly inactivated in blood by cytidine deaminase. The objective of the study was to improve the systemic stability and anticancer activity of modified Gem termed 4-N-stearoylGem (4NSG) In this study, the IC50 values of 4NSG treated MiaPaCa-2 and primary pancreatic cancer (PPCL-46) cultures were significantly lower when compared with gemcitabine hydrochloride (GemHCl) treated cultures. In acute toxicity study, liver enzyme level of aspartate aminotransferase (AST) of the control mice was not significantly different from AST levels of 4NSG and GemHCl treated mice. However, alanine aminotransferase (ALT) level of control mice (67 ± 5 mUnits/mL) was significantly lower compared with ALT levels of GemHCl (232 ± 28 mUnits/mL) and that of 4NSG (172 ± 22 mUnits/mL) (p a remarkable tumor growth inhibition and revealed significant antiangiogenic activity in 4GSN treated pancreatic PDX tumor.

Enhanced anti-tumor efficiency of gemcitabine prodrug by FAPα-mediated activation

Gemcitabine (Gem) as an anti-cancer agent has been limited by its short circulation time and rapid metabolism that reflects in low tumor uptake and low therapeutic efficiency. To improve its anti-tumor activity, a novel FAPα enzyme-activated prodrug of Z-

Single Diastereomers of the Clinical Anticancer ProTide Agents NUC-1031 and NUC-3373 Preferentially Target Cancer Stem CellsIn Vitro

A 3′-protected route toward the synthesis of the diastereomers of clinically active ProTides, NUC-1031 and NUC-3373, is described. Thein vitrocytotoxic activities of the individual diastereomers were found to be similar to their diastereomeric mixtures. In the KG1a cell line, NUC-1031 and NUC-3373 have preferential cytotoxic effects on leukemic stem cells (LSCs). These effects were not diastereomer-specific and were not observed with the parental nucleoside analogues gemcitabine and FUDR, respectively. In addition, NUC-1031 preferentially targeted LSCs in primary AML samples and cancer stem cells in the prostate cancer cell line, LNCaP. Although the mechanism for this remains incompletely resolved, NUC-1031-treated cells showed increased levels of triphosphate in both LSC and bulk tumor fractions. As ProTides are not dependent on nucleoside transporters, it seems possible that the LSC targeting observed with ProTides may be caused, at least in part, by preferential accumulation of metabolized nucleos(t)ide analogues.

Prodrug based on gemcitabine structure as well as preparation method and application of prodrug

The invention discloses a prodrug based on a gemcitabine structure. The prodrug has a structure of general formula I. The prodrug has certain inhibitory activity on tumors. The invention further discloses a preparation method of the prodrug. According to the preparation method, lipid solubility of the prodrug is improved by modifying N4 site of the gemcitabine structure, and membrane permeabilityof the compound is improved. The invention further discloses application of the prodrug in antitumor drugs. The fat-soluble prodrug can enter tumors through passive diffusion and active transport, thereby inhibiting tumor growth, overcoming tumor drug resistance, and improving tumor targeting of gemcitabine. The invention further discloses a pharmaceutical composition containing the prodrug. The pharmaceutical composition is administrated in an oral administration mode, and after the prodrug is absorbed, the prodrug can be rapidly broken into gemcitabine in vivo, thereby exerting a therapeuticeffect in time and increasing oral bioavailability of gemcitabine.