CU-T12-9 is a specific TLR1/2 agonist with an EC50 of 52.9 nM in the HEK-Blue hTLR2 SEAP assay. CU-T12-9 activates both the innate and adaptive immune systems. CU-T12-9 directly targets TLR1/2, initiating downstream signaling. By binding to TLR1 and TLR2, CU-T12-9 promotes the formation of TLR1/2 heterodimeric complexes (without acting on TLR2/6), thereby activating downstream signaling. CU-T12-9 causes an increase in the downstream effectors TNF-α, IL-10 and iNOS through NF-κB mediation. CU-T12-9 upregulates the mRNA levels of TLR1, TLR2, TNF, IL-10, and iNOS. In the concentration range of 0.1-10 μM, CU-T12-9 can activate TLR1 mRNA and iNOS mRNA after 24 hours of treatment on Raw 264.7 cells. In the concentration range of 0.1-10 μM, CU-T12-9 can activate TLR2 and IL-10 mRNA in Raw 264.7 cells after 2 hours of action, and activate TNF mRNA in Raw 264.7 cells after 8 hours of action[1].
CU-T12-9 细胞实验
Cell Line
Concentration
Treated Time
Description
References
U937 macrophage cells
5 µM
24 hours
Activates NF-κB signaling pathway
Sci Adv. 2015;1(3):e1400139.
Raw 264.7 macrophage cells
60.46 ± 16.99 nM (EC50)
24 hours
Activates TNF-α signaling pathway, upregulates downstream effectors via NF-κB pathway
To evaluate the effect of CU-T12-9 on the NF-κB pathway, results showed that CU-T12-9 significantly increased p-P65 protein expression, reversing the protective effect of si-POSTN.
J Cell Commun Signal. 2024 May 7;18(2):e12030.
PANC-1
1 µM/ml
72 hours
Reverse the inhibitory effect of Robinin on PANC-1 cell proliferation
Cancer Cell Int. 2023 Dec 18;23(1):328.
Mia-PACA2
1 µM/ml
72 hours
Reverse the inhibitory effect of Robinin on Mia-PACA2 cell proliferation
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