IKKγ NBD Inhibitory Peptide TFA

IKKγ NBD Inhibitory Peptide TFA is a highly specific inhibitor NF-κB inhibitor. IKKγ NBD Inhibitory Peptide TFA acts by disrupting the interaction between IKKγ/NEMO-binding domain (NBD) with IKKα and IKKβ, thus blocking TNF-α-induced NF-kB activation. IKKγ NBD Inhibitory Peptide TFA could significantly suppresses inflammation and ameliorate the cerebral ischemia-induced neurological deficits ^{[1] [2] [3]}.

In Vivo, IKKγ NBD Inhibitory Peptide TFA (40 μg/4 μL; ICV; single dose; 2 h before MCAO) exhibits neuroprotective effect with reduction in DNA fragmentation, and its ischemic brain damage reduction mechanism be attributed to reduction in inflammation following ischemic injury in middle cerebral artery occlusion (MCAO) rats model^[3].

In Vitro, In a canonical pathway, NF kappa B activation depends on the IKK complex activity, which is formed by three subunits (IKKκ and IKKβ and IKKγ/NEMO), thus the KKγ NBD Inhibitory Peptide TFA inhibits TNF-α-induced NF-kB activation^[2]. IKKγ NBD Inhibitory Peptide TFA (10 μM; 90 min) prevents Doxorubicin -induced (15 μM; 4 h) p65 phosphorylation in BT-474 cells^[2]. IKKγ NBD Inhibitory Peptide TFA (10 μM; 48 h) slightly inhibits BT-474 cell viability while it markedly enhances the effects on Doxorubicin^[2].

References:
[1]. Zhao J, et al. Development of novel NEMO-binding domain mimetics for inhibiting IKK/NF-κB activation. PLoS Biol. 2018 Jun 11;16(6):e2004663.
[2]. Tapia MA, et al. Inhibition of the canonical IKK/NF kappa B pathway sensitizes human cancer cells to doxorubicin. Cell Cycle. 2007 Sep 15;6(18):2284-92.
[3]. Desai A, et al. Neuroprotective potential of the NF-κB inhibitor peptide IKK-NBD in cerebral ischemia-reperfusion injury. Neurochem Int. 2010 Dec;57(8):876-83.