IKK 16

"目录号: HY-13687

NF-κB-

IKK 16 是一种选择性的 IκB 激酶 (IKK) 抑制剂，作用于IKK-2，IKK complex和IKK-1，IC50分别为 40 nM，70 nM 和 200 nM。

IKK

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生物活性

Description

IKK 16 is a selective IκB kinase (IKK) inhibitor forIKK-2,IKK complexandIKK-1withIC50s of 40 nM, 70 nM and 200 nM, respectively.

IC50& Target

IC50: 40 nM (IKK-2), 70 nM (IKK complex), 200 nM (IKK-1)[1]

In Vitro

IKK 16 is a potent inhibitor of IKK2 with IC50value of 40 nM[1]. IKK 16 increases the expression of Nrf2 but it has no effect on TGF-β1-induced endothelial-mesenchymal transition (EndMT). IKK-16 has the ability to enhance the expression of IκBα and Nrf2. IKK 16 (10 μmol/mL) has the ability to enhance the expression of IκBα and Nrf2 but it has no effect on Smad7 expression. In addition, the AT-RvD1 can also enhance the expression of IκBα[2].

In Vivo

IKK 16 also demonstrates significant in vivo activity in an acute model of cytokine release. Both routes of administration of IKK 16 (30 mg/kg, sc) or orally (30 mg/kg, p.o) at the indicated dose results in a significant inhibition of 86% (sc) and 75% (p.o.).IKK 16(10 mg/kg, sc) is also active in the thioglycollate-induced peritonitis model in the mouse. The maximal inhibition of neutrophil extravasation in this model is about 50%[1]. Treatment of septic mice with IKK 16 (1 mg/kg body weight i.v.) results in a significantly increased degree of phosphorylation (P<0.05) of serine residues on Akt and eNOS in the liver[3].

References

[1].Waelchli R, et al. Design and preparation of 2-benzamido-pyrimidines as inhibitors of IKK. Bioorg Med Chem Lett. Bioorg Med Chem Lett. 2006 Jan 1;16(1):108-12.

[2].Shu Y, et al. Aspirin-Triggered Resolvin D1 Inhibits TGF-β1-Induced EndMT through Increasing the Expression of Smad7 and Is Closely Related to Oxidative Stress. Biomol Ther (Seoul). 2016 Mar 1;24(2):132-9.

[3].Coldewey SM, et al. Inhibition of IκB kinase reduces the multiple organ dysfunction caused by sepsis in the mouse. Dis Model Mech. 2013 Jul;6(4):1031-42.