SMU-L11 is a potent, selecitve small-molecule TLR7 agonist with EC50 of 24 nM (hTLR7).
SMU-L11 effectively promoted SEAP signals in HEK-Blue hTLR7 cells, also exhibited TLR8 activation with increasing dose (EC50=4.5 uM).
SMU-L11 shows negligible activation of HEK-Blue hTLR2, hTLR3, or hTLR4.
SMU-L11 induced significant phosphorylation of IKK α/β, p65, p38, JNK, ERK1/2, and IRF7 in bone marrow-derived DCs (BMDCs).
SMU-L11 activated conventional TLR7 downstream signaling pathways via the MyD88 adaptor protein, including the NF-κB, MAPK, and IFN signaling pathways.
SMU-L11 induces cytokine secretion and gene expression in mouse and human cells.
SMU-L11 (0, 0.1, 1, 5, and 10 μM) promotes M1-like polarization of macrophages.
SMU-L11 induced strong antitumor response, especially by upregulating NK cells, macrophages, DCs, and cytotoxic CD8+ T lymphocytes, which in turn contributed to significant antitumor responses in B16-F10 melanoma model.