3M-011 is a potent dual toll-like receptor TLR7/8 agonist and a cytokine inducer, it is also a potent adjuvant to radiotherapy that induces local and profound systemic immune responses during radiotherapy. 3M-011 significantly inhibits H3N2 influenza viral replication in the nasal cavity and it strongly has antitumor action[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).

642473-62-9

C18H25N5O3S

391.49

(< 1 mg/ml refers to the product slightly soluble or insoluble )
Powder: -20°C for 3 years
In solvent: -80°C for 2 years