CL097 是一种有效的TLR7和TLR8激动剂，可在巨噬细胞中诱导促炎细胞因子。CL097 诱导 NADPH 氧化酶启动活性，导致 fMLF 刺激的ROS产生增加。

CL097, a potent TLR7 and TLR8 agonist, induces pro-inflammatory cytokines in macrophages [1]. CL097 induces NADPH oxidase priming, resulting in an increase of the fMLF-stimulated ROS production [2].

CL097 induces activation of NF-κB at 0.1 μM in TLR7 transfected HEK293 cells and at 4 μM in TLR8-transfected HEK293 cells [1]. 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 [2]. Western Blot Analysis [2] Cell 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.

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 [3]. Animal Model: Female 8.3 NOD mice (5-6 weeks old) [3] Dosage: 5 mg/kg Administration: Injected s.c. Result: Caused a modest specific lysis of the target peptide (～25%).

C13H15ClN4O

278.74

(< 1 mg/ml refers to the product slightly soluble or insoluble )
Powder: -20°C for 3 years
In solvent: -80°C for 2 years