CL097, a potent TLR7 and TLR8 agonist, induces pro-inflammatory cytokines in macrophages CL097 induces NADPH oxidase priming, resulting in an increase of the fMLF-stimulated ROS production . In Vitro CL097 induces activation of NF-κB at 0.1 μM in TLR7 transfected HEK293 cells and at 4 μM in TLR8-transfected HEK293 cells. CL097 induces hyperactivation of the NADPH oxidase by stimulating the phosphorylation of p47phox on selective sites in human neutrophils and suggest that p38 MAPK, ERK1/2, protein kinase C, and Pin1 control this process. CL097 induces the phosphorylation of p47phox on specific sites and enhances fMLF-induced p47phox phosphorylation. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Western Blot AnalysisCell Line: Neutrophils Concentration: 0, 0.5, 2.5, 5, and 10 μg/mL Incubation Time: Pretreated for 30 minutes Result: Induced phosphorylation of p47phox on specific sites in a concentration-dependent manner. In Vivo CL097 and CD40 agonist stimulation induces efficient diabetogenic Cytotoxic T lymphocyte (CTL) function in NOD mice. CL097 (5 mg/kg, s.c.) alone causes a modest specific lysis of the target peptide (∼25%). However, treatment with a combination of CL097 and CD40 agonist (10 mg/kg, i.p.) results in an increase of approximately twofold in the specific lysis of the IGRP-peptide-coated targets compared with CL097 treatment alone. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: Female 8.3 NOD mice (5-6 weeks old)Dosage: 5 mg/kg Administration: Injected s.c. Result: Caused a modest specific lysis of the target peptide (∼25%). Form:Solid IC50& Target:TLR7 TLR8