Gemcitabine HCI

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Chemical Structure| 122111-03-9 同义名 : 吉西他滨盐酸盐 ;LY 188011 hydrochloride;Gemcitabine(hydrochloride);Gemcitabine HCl;LY 188011(hydrochloride)
CAS号 : 122111-03-9
货号 : A309564
分子式 : C9H12ClF2N3O4
纯度 : 97%
分子量 : 299.659
MDL号 : MFCD01735988
存储条件:

Pure form Keep in dark place,Inert atmosphere,Room temperature

In solvent -20°C:3-6个月-80°C:12个月

溶解度 :

DMSO: 60 mg/mL(200.23 mM),配合低频超声,并水浴加热至45℃助溶,注意:DMSO长时间开封后,会吸水并导致溶解能力下降,请避免使用长期开封的DMSO

H2O: 25 mg/mL(83.43 mM),配合低频超声助溶

DMF: 2 mg/mL(6.67 mM),配合低频超声助溶

动物实验配方:

PO 0.5% CMC-Na 32 mg/mL suspension

生物活性
描述 Gemcitabine hydrochloride is the hydrochloride form of Gemcitabine. Gemcitabine (dFdCTP, LY-188011, NSC 613327, (+)-2'-Deoxy-2',2'-difluorocytidine) is a deoxycytidine analogue that has a spectrum of activity against solid tumors[1]. Gemcitabine can inhibit DNA synthesis through a combination of two actions. The first, gemcitabine can inhibit ribonucleotide reductase (RR) and then cause the decrease of the deoxynucleotide pool sizes for DNA repair and synthesis[2][3]. The second, gemcitabine inhibit DNA synthesis through competition with dCTP and incorporation into DNA[4][4]. Gemcitabine can induce S-phase arrest and cell growth inhibition[6].
作用机制 Gemcitabine, as nucleoside analogue, can inhibit DNA synthesis through inhibition of ribonucleotide reductase and incorporation into DNA.[2][3]
细胞研究
细胞系 浓度 检测类型 检测时间 活性说明 数据源
CCRF-CEM Growth Inhibition Assay IC50=2.9 ± 1.8 nM 22425885
CCRF-CEM Growth Inhibition Assay IC50=2.9 ± 1.8 nM 22425885
CCRF-CEM Growth Inhibition Assay 72 h IC50=2.0 ± 0.6 nM 21851843
实验方案
1mg 5mg 10mg

1 mM

5 mM

10 mM

3.34mL

0.67mL

0.33mL

16.69mL

3.34mL

1.67mL

33.37mL

6.67mL

3.34mL

参考文献

[1]Hertel LW, Boder GB, et al. Evaluation of the antitumor activity of gemcitabine (2',2'-difluoro-2'-deoxycytidine). Cancer Res. 1990 Jul 15;50(14):4417-22.

[2]Pereira S, Fernandes PA, et al. Mechanism for ribonucleotide reductase inactivation by the anticancer drug gemcitabine. J Comput Chem. 2004 Jul 30;25(10):1286-94.

[3]Heinemann V, Xu YZ, et al. Cellular elimination of 2',2'-difluorodeoxycytidine 5'-triphosphate: a mechanism of self-potentiation. Cancer Res. 1992 Feb 1;52(3):533-9.

[4]Huang P, Chubb S, et al. Action of 2',2'-difluorodeoxycytidine on DNA synthesis. Cancer Res. 1991 Nov 15;51(22):6110-7.

[5]Huang P, Chubb S, et al. Action of 2',2'-difluorodeoxycytidine on DNA synthesis. Cancer Res. 1991 Nov 15;51(22):6110-7.

[6]Shi Z, Azuma A, et al. S-Phase arrest by nucleoside analogues and abrogation of survival without cell cycle progression by 7-hydroxystaurosporine. Cancer Res. 2001 Feb 1;61(3):1065-72.

[7]Turk J, Bemis K, et al. General pharmacology of gemcitabine hydrochloride in animals. Arzneimittelforschung. 1994 Sep;44(9):1089-92.

[8]Freise KJ, Martín-Jiménez T, et al. Pharmacokinetics of gemcitabine and its primary metabolite in dogs after intravenous bolus dosing and its in vitro pharmacodynamics. J Vet Pharmacol Ther. 2006 Apr;29(2):137-45.

[9]Gemcitabine