Anisomycin

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Anisomycin

本产品不向个人销售，仅用作科学研究，不用于任何人体实验及非科研性质的动物实验。

CAS NO:

22862-76-6

包装与价格：

包装	价格(元)
10mM (in 1mL DMSO)	电议
10mg	电议
50mg	电议

产品介绍

化学性质

Physical Appearance	A solid
Storage	Store at -20°C
M.Wt	265.31
Cas No.	22862-76-6
Formula	C₁₄H₁₉NO₄
Solubility	≥26.5 mg/mL in DMSO; insoluble in H2O; ≥30.55 mg/mL in EtOH
Chemical Name	(2R,3S,4S)-4-hydroxy-2-(4-methoxybenzyl)pyrrolidin-3-yl acetate
Canonical SMILES	O[C@@H]1[C@H]([C@@H](CC(C=C2)=CC=C2OC)NC1)OC(C)=O
运输条件	蓝冰运输或根据您的需求运输。
一般建议	为了使其更好的溶解，请用37℃加热试管并在超声波水浴中震动片刻。不同厂家不同批次产品溶解度各有差异，仅做参考。若实验所需浓度过大至产品溶解极限，请添加助溶剂助溶或自行调整浓度。溶液形式一般不宜长期储存，请尽快用完。

资料参考

Anisomycin是JNK特异性的激动剂，作用浓度为25 ng / ml[1]。

JNK是c-Jun N端激酶的缩写，作为促凋亡激酶，在许多细胞进程例如细胞周期、增殖、凋亡和细胞应激中起重要作用。研究表明，JNK在UV诱导的细胞凋亡中发挥重要作用，JNK途径的激活可以加强TNF-α介导的细胞凋亡，因此，JNK被认为是临床的重要靶标[2,3]。

Anisomycin是一种强效的JNK激动剂。在细胞系DU145（对Fas介导的凋亡具有较高抗性）中，250 ng/ml anisomysin和Fas (200 ng/ml)共同作用通过激活JNK，诱导DU145细胞凋亡[4]。在HL-60细胞中，使用anisomysin活化JNK途径可以诱导细胞凋亡[5]。在原代鼠胚胎成纤维细胞中，anisomycin通过激活JNK的表达诱导细胞凋亡[6]。

参考文献：
[1].Jiang, J., et al., Spermassociated antigen 9 promotes astrocytoma cell invasion through the upregulation of podocalyxin. Mol Med Rep, 2014. 10(1): p. 417-22.
[2].Lin, A., Activation of the JNK signaling pathway: breaking the brake on apoptosis. Bioessays, 2003. 25(1): p. 17-24.
[3].Liu, J. and A. Lin, Role of JNK activation in apoptosis: a double-edged sword. Cell Res, 2005. 15(1): p. 36-42.
[4].Curtin, J.F. and T.G. Cotter, Anisomycin activates JNK and sensitises DU 145 prostate carcinoma cells to Fas mediated apoptosis. Br J Cancer, 2002. 87(10): p. 1188-94.
[5].Stadheim, T.A. and G.L. Kucera, c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK) is required for mitoxantrone- and anisomycin-induced apoptosis in HL-60 cells. Leuk Res, 2002. 26(1): p. 55-65.
[6].Tournier, C., et al., Requirement of JNK for stress-induced activation of the cytochrome c-mediated death pathway. Science, 2000. 288(5467): p. 870-4.

试验操作

Cell experiment:[1]
Cell lines	Hormone refractory cell line DU 145
Reaction Conditions	250 ng/ml anisomycin for 8 h incubation
Applications	In DU 145 cells, anisomycin activated JNK, and acted in synergy with anti-Fas IgM to induce apoptosis. Furthermore, anisomycin was found to activate JNK activation over a prolonged period, whilst anti-Fas IgM was unable to induce transient (1 h) or prolonged (8 h) JNK activation in DU 145 cells.
Animal experiment:[2]
Animal models	Ehrlich ascites carcinoma (EAC)-bearing mice
Dosage form	5 mg/kg Injected peritumorally every other day for 7 times
Applications	Peritumoral administration of anisomycin (5 mg/kg) significantly suppressed EAC growth, resulting in the survival of approximately 60% of the mice 90 days after EAC inoculation. Enhancement of infiltrating lymphocytes was noted in the tumor tissue, which was dramatically superior to adriamycin.
Note	The technical data provided above is for reference only.
	References: 1. Curtin JF, Cotter TG. Anisomycin activates JNK and sensitises DU 145 prostate carcinoma cells to Fas mediated apoptosis. British Journal of Cancer, 2002, 87(10): 1188-1194. 2. You P, Xing F, Huo J, et al. In vitro and in vivo evaluation of anisomycin against Ehrlich ascites carcinoma. Oncology Reports, 2013, 29(6): 2227-2236.