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TIC10

现货
Catalog No.
A8619
Akt/ERK抑制剂
组合的产品项目
规格价格库存 数量
10mM (in 1mL DMSO)
¥ 800.00
Ship with 10-15 days
10mg
¥ 840.00
现货
20mg
¥ 1,400.00
Ship with 10-15 days
50mg
¥ 2,520.00
Ship with 10-15 days
100mg
¥ 4,200.00
Ship with 10-15 days

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Background

TIC10 (TRAIL-inducing compound 10) is a potent and stable small molecule that is orally active. It induces TRAIL transcriptionally independent of p53 and crosses the blood-brain barrier. [1]

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is an apoptosis inducer in a variety of human cancer cell lines. It also acts as a tumor suppressor during immune surveillance but the function is lost in cancer progression. [1]

TIC10 caused a prominent and long-lasting production of TRAIL on cell surface of tumor cell.

TIC10 also led to TRAIL-mediated apoptosis in HCT116 p53-/- cells. In addition, TIC10 inactivated Akt and ERK cooperatively lead to the nuclear translocation of Foxo3a and ensuing TRAIL up-regulation. [1]

In mouse caner xenograft, TIC10 showed TRAIL-dependent antitumor effect. It caused tumor-specific cell death by RAIL-mediated direct and bystander effects. TIC10 is also an effective antitumor agent for orthotopic human glioblastoma multiforme tumors. [1]

Reference:
1. Allen JE, Krigsfeld G, Mayes PA et al.  Dual inactivation of Akt and ERK by TIC10 signals Foxo3a nuclear translocation, TRAIL gene induction, and potent antitumor effects. Sci Transl Med. 2013 Feb 6;5(171):171ra17.

Chemical Properties

Physical AppearanceA solid
StorageStore at -20°C
M.Wt386.49
Cas No.41276-02-2
FormulaC24H26N4O
Solubility≥6.43mg/mL in DMSO with gentle warming
Chemical Name7-benzyl-10-(2-methylbenzyl)-2,3,6,7,8,9-hexahydroimidazo[1,2-a]pyrido[4,3-d]pyrimidin-5(10H)-one
SDFDownload SDF
Canonical SMILESO=C1N2C(N(C([H])([H])C3=C([H])C([H])=C([H])C([H])=C3C([H])([H])[H])C4=C1C([H])([H])N(C([H])([H])C5=C([H])C([H])=C([H])C([H])=C5[H])C([H])([H])C4([H])[H])=NC([H])([H])C2([H])[H]
运输条件试用装:蓝冰运输。 其他可选规格:常温运输或根据您的要求用蓝冰运输。
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。

试验操作

细胞实验[1]:

细胞系

HCT116 Bax-/-和HCT116 p53-/-细胞

溶解方法

在DMSO中的溶解度>10 mM。为了获得更高的浓度,可以将离心管在37℃加热10分钟和/或在超声波浴中震荡一段时间。原液可以在-20℃以下储存几个月。

反应条件

1.25, 2.5, 5和10 μM; 24, 48或72小时

应用

在TRAIL敏感的HCT116 p53 - / - 细胞中,TIC10以p53非依赖性和Bax依赖性方式诱导提示细胞死亡的亚G1 DNA含量增加。在TRAIL抗性Bax-null HCT116人结肠癌细胞中,TIC10(10μM,72小时)以p53非依赖性方式剂量依赖性地增加TRAIL mRNA并诱导TRAIL蛋白的细胞表面定位。

动物实验[2]:

动物模型

皮下移植HCT116 p53 - / - 肿瘤和MDA-MB-231人类三阴性乳腺癌的雌性无胸腺nu / nu小鼠。

剂量

50, 80或100 mg/kg; 腹腔注射;在第0,3和6天给药

应用

在携带HCT116 p53 - / - 异种移植物的小鼠中,TIC10引起肿瘤消退。TIC10还诱导MDA-MB-231人三阴性乳腺癌异种移植物的消退。

注意事项

请测试所有化合物在室内的溶解度,实际溶解度和理论值可能略有不同,这是由实验系统的误差引起的,属于正常现象。

References:

[1] Allen JE, Krigsfeld G, Mayes PA et al. Dual inactivation of Akt and ERK by TIC10 signals Foxo3a nuclear translocation, TRAIL gene induction, and potent antitumor effects. Sci Transl Med. 2013 Feb 6;5(171):171ra17.

生物活性

描述 TIC10是Akt和ERK的抑制剂。
靶点 Akt ERK        
IC50            

质量控制

质量控制和MSDS

批次:

化学结构

TIC10