NF-κB-IN-8 is a competitive antagonist of LPS for MD-2 binding, and it impedes the expression of inflammatory factors by engaging MD-2. Additionally, it inhibits ALP activity and is usable in inflammation research, including acute lung injury (ALI) [1].

NF-κB-IN-8 (compound L26) at a concentration of 10 μM inhibits 64.30% of ALP activity [1]. Additionally, within a range of 1-10 μM for 24 hours, NF-κB-IN-8 suppresses the expression of IL-6 and TNF-α in RAW 264.7 cells [1]. At concentrations spanning from 0 to 50 μM, NF-κB-IN-8 hinders the binding of LPS to MD-2, as detected by ELISA [1]. At 50 μM, administered overnight, the compound prevents the formation of the LPS/MD-2/TLR4 complex in RAW264.7 cells [1].

NF-κB-IN-8 (Compound L26), administered orally at a dose of 5 mg/kg, mitigated LPS-induced acute lung injury in mice [1]. At higher doses of 1000 and 1500 mg/kg, NF-κB-IN-8 demonstrated low toxicity and was deemed safe in mice [1]. In rats, with an administered dose of 0 mg/kg, NF-κB-IN-8 exhibited a half-life (T 1/2) of 4.2 hours and a maximum concentration (C max) of 163.288 μg/L [1].