irf-3

KIN101 (3-(4-Bromophenyl)-7-[(methylsulfonyl)oxy]-4-oxo-4H-chromene), an isoflavone agonist of IRF-3 dependent signaling, induces IRF-3 nuclear translocation. KIN101 has antiviral activity against RNA viruses, HCV, and RSV.

SU0268 is a potent and specific 8-Oxoguanine DNA glycosylase 1 (OGG1) inhibitor that regulates inflammatory responses during Pseudomonas aeruginosa infection.

ChX710 activates the type I interferon response to cytosolic DNA by priming specific Interferon-Stimulated Genes (ISGs), inducing the ISRE promoter sequence, and facilitating the phosphorylation of Interferon Regulatory Factor (IRF) 3.

cAIMP acts as a STING agonist and has been shown to more effectively activate STING-dependent IRF and NF-κB signaling pathways in mammalian cells in vitro when compared to standard murine (DMXAA) and human (2',3'-cGAMP) STING agonists. In ex vivo experiments with human blood, cAIMP analogs can induce the production of type I interferons (IFNs) and pro-inflammatory cytokines.

KIN1148 is a novel small-molecule adjuvant that acts through the RIG-I pathway and IRF-3 transcription factor to stimulate inN/Ate immunity and protection following viral infection. The adjuvant will be developed for an FDA-approved avian inluenza virus v

STING modulator-3 is a STING inhibitor with a Ki value of 43.1 nM in scintillation proximity assays, specifically targeting R232 STING. It does not affect IRF-3 activation or TNF-β induction in THP-1 cells.

Interferon alfa, a type I interferon, activates new genes, displaying strong antiviral and antiproliferative effects on target cells. It signals through receptor-mediated activation of Stat1 and Stat2, which heterodimerize into a STAT complex binding with the DNA-binding protein IRF-9 (p48) to form ISGF-3 (IFN-stimulated gene factor 3). This complex further activates driver genes to fulfill its antiviral role [1].

8-Prenylkaempferol is an effective agent for attenuating pro-inflammatory NO induction, it may be an anti-inflammatory agent for suppressing influenza A virus-induced RANTES production acts by blocking PI3K-mediated transcriptional activation of NF-κB and

Cyclo(Phe-Pro) (A-64863) known as a secondary metabolite of some bacteria and fungi, is also produced by Vibrio vulnificus.