CU-T12-9 is a potent TLR1/2 agonist(EC50 of 52.9 nM in HEK-Blue hTLR2 SEAP assay). It acts by activating the NFkB pathway, upregulating proinflammatory cytokines, and enhancing TLR1 and TLR2 dimerization.CU-T12-9 activates both the innate and the adaptive immune systems. CU-T12-9 selectively activates the TLR1/2 heterodimer, not TLR2/6. CU-T12-9 signals through NF-κB and invokes an elevation of the downstream effectors TNF-α, IL-10, and iNOS.

TLR1:52.9 nM （EC50）（in HEK-Blue cells), TLR2:52.9 nM （EC50）（in HEK-Blue cells)

CU-T12-9 直接针对 TLR1/2 以启动下游信号传导。它特异性激活 TLR1/2，此过程可以通过抗-hTLR1 或抗-hTLR2 抗体阻断，但抗-hTLR6 抗体则无法阻断。CU-T12-9 通过同时结合 TLR1 和 TLR2，促进了 TLR1/2 异二聚体复合物的形成，进一步激活下游信号传导。荧光偏振实验揭示了 CU-T12-9 与 Pam3CSK4 之间对 TLR1/2 复合物的竞争性结合，半最大抑制浓度（IC50）为 54.4 nM。CU-T12-9 通过核因子 κB (NF-κB) 传递信号，并引发下游效应器肿瘤坏死因子-α (TNF-α)、白细胞介素-10 (IL-10) 和诱导型一氧化氮合酶 (iNOS)[1] 的上升。