IC-87114

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Chemical Structure| 371242-69-2 同义名 : -
CAS号 : 371242-69-2
货号 : A937152
分子式 : C22H19N7O
纯度 : 99%+
分子量 : 397.433
MDL号 : MFCD09970845
存储条件：

Pure form Keep in dark place,Inert atmosphere,Store in freezer, under -20°C

In solvent -20°C:3-6个月-80°C:12个月
溶解度 :

DMSO: 9 mg/mL(22.65 mM)，配合低频超声助溶，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
动物实验配方：
生物活性
靶点

  • p110γ

    PI3Kγ, IC50:29 μM

  • p110δ

    PI3Kδ, IC50:0.5 μM
描述 IC-87114 has been synthesized to assess its selectivity for PI3Kδ relative to other class I PI3Ks. The IC50 for PI3Kδ inhibition by IC-87114 is 0.5μM, while the IC50 values for PI3Kα, PI3Kβ, and PI3Kγ are >100μM, 75μM, and 29μM, respectively. This demonstrates that IC-87114 is 58-fold more selective for PI3Kδ compared to PI3Kγ, and exhibits over 100-fold selectivity relative to PI3Kα and PI3Kβ. IC-87114 selectively antagonizes PI3Kδ over a concentration range of 0.3-10μM[1]. IC-87114, at a concentration of 10μM, is utilized to selectively target PI3Kδ catalytic function. This concentration of IC-87114 successfully deactivates Akt in macrophages after a 1-hour treatmen. Subsequently, the impact of IC-87114 on AP-1 DNA-binding activity is assessed. The electrophoretic mobility shift assay reveals that AP-1 DNA-binding activity significantly rises following TNF-α treatment (10/20 ng/mL). IC-87114 alone prompts AP-1 DNA-binding activity post 1-hour treatment. Moreover, the combination of IC-87114 (10μM) with TNF-α (0-20 ng/mL) results in stronger AP-1 DNA-binding activity than TNF-α alone. Additionally, IC-87114 (10μM) effectively curtails p110δ catalytic activities (Akt phosphorylation) in macrophages, irrespective of TNF-α treatment over 24 hours[2].
实验方案
1mg 5mg 10mg

1 mM

5 mM

10 mM

2.52mL

0.50mL

0.25mL

12.58mL

2.52mL

1.26mL

25.16mL

5.03mL

2.52mL
参考文献

[1]Sadhu C, et al. Essential role of phosphoinositide 3-kinase delta in neutrophil directional movement. J Immunol. 2003 Mar 1;170(5):2647-54.

[2]Zheng L, et al. Inactivation of PI3Kδ induces vascular injury and promotes aneurysm development by upregulating the AP-1/MMP-12 pathway in macrophages. Arterioscler Thromb Vasc Biol. 2015 Feb;35(2):368-77.

[3]El-Hashim AZ, et al. Src-dependent EGFR transactivation regulates lung inflammation via downstream signaling involving ERK1/2, PI3Kδ/Akt and NFκB induction in a murine asthma model. Sci Rep. 2017 Aug 30;7(1):9919.