Toll-like receptor (TLR) family proteins play a crucial role in the initiation of the hosts' immune responses, which can trigger the proinflammatory signaling cascades that result in activation of nuclear factor (NF)-κB and upregulation of inflammatory cytokines and chemokines. This TLR response is crucial for helping to eliminate the pathogen and establishing long lasting adaptive responses, but also can cause various autoimmune diseases and inflammatory disorders[1]. CU-CPT-9a is a specific TLR8 antagonist, with an IC50 of 0.5 ± 0.1 nM. The elevation of the downstream protein levels induced by R848 in both THP-1 and HEK-Blue TLR8 cells can be reversed by CU-CPT-9a in a dose-dependent manner. Immunoblot analysis results support the notion that the inhibitory effects of CU-CPT-9a occur specifically through TLR8 in cells. Moreover, CU-CPT-9a significantly suppresses the TNF-α level in a dose-dependent manner[1]. Results of this proof-of-concept study show that CU-CPT-9a treatment exerts potent anti-inflammatory effects in the specimens of OA (osteoarthritis), RA (rheumatoid arthritis), and AOSD (adult-onset Still's disease) patients[1].
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