3M-011, a potent dual toll-like receptor TLR7/8 agonist and cytokine inducer, serves as a powerful adjuvant to radiotherapy, eliciting significant local and systemic immune responses. Additionally, it effectively inhibits H3N2 influenza viral replication in the nasal cavity and exhibits strong antitumor activity[1][2][3].

3M-011 (0-100 μg/mL; 24 hours; B16-F10 melanoma cells) treatment can decrease B16-F10 melanoma cell counts[1]. 3M-011 in humans activates both TLR7 and TLR8, whereas in mice, 3M011 activates only TLR7 and not TLR8[1]. The NF-κB reporter is stably integrated into HEK-293 cells that are subsequently transiently transfected with human or mouse TLR7 or TLR8. With all the TLRs tested, except mouse TLR8, stimulation with 3M-011 results in a dose-dependent induction of NF-κB-controlled luciferase activity. 3M-011 potentiates natural killer (NK) cells cytotoxicity[1].

3M-011 (1 mg/kg; intravenous injection; every other day with six doses; female scid/NOD mice) treatment shows antitumor effects in scid/NOD mice bearing B16-F10 cells[1]. 3M-011 induces a dose-dependent increase in serum concentrations of both TNF-α and IFN-α/β[1]. Wild-type C57BL/6 mice are injected subcutaneously with different doses of 3M-011 (0.01 mg/kg, 0.1 mg/kg, 1 mg/kg, or 10 mg/kg).