LSN3318839

LSN3318839 is a small-molecule compound and a positive allosteric modulator of the glucagon-like peptide-1 receptor (GLP-1R), featuring oral activity and selective enhancement of G protein-coupled signaling, which promotes glucose-dependent insulin secretion for blood glucose reduction.

Methods: The broth microdilution method was used to detect the in vitro antibacterial activity of LSN3318839. Strains including Staphylococcus aureus, MRSA, Streptococcus pneumoniae, and Haemophilus influenzae were selected. Serial concentration gradients were set, and MIC was determined after incubation at 37°C for 18–24 h.
Results: LSN3318839 showed strong inhibitory effects against Gram-positive bacteria and some Gram-negative bacteria, with low MIC values against MRSA and significant concentration-dependent bactericidal effects. [1]
Methods: The MTT assay was used to detect the in vitro antitumor activity of LSN3318839. Tumor cells HCT116, MCF7, HepG2, and A549, as well as normal cells L02 and HUVEC, were selected. Concentrations of 0–50 μM were set, and cells were incubated at 37°C with 5% CO₂ for 48 h.
Results: LSN3318839 showed the strongest inhibitory effect against A549 cells, with an IC₅₀ of 5.4 μM. It elevated ROS levels, induced S-phase arrest, and activated the mitochondrial apoptosis pathway, with low toxicity to normal cells. [2]

Methods: A C57BL/6 mouse LPS-induced systemic inflammation model was used. LSN3318839 was administered by oral gavage at doses of 50 and 100 mg/kg as a single dose, followed by intraperitoneal LPS injection 1 hour later to establish the model. The vehicle was conventional pharmaceutical excipients, with a vehicle control group and CA 4948 positive control group established.
Results: LSN3318839 significantly reduced serum TNF-α levels in mice, with the 100 mg/kg dose showing efficacy comparable to the positive control drug, demonstrating definite in vivo anti-inflammatory activity and rapid oral onset. [3]

DMSO: 255 mg/mL (530.82 mM), Sonication is recommended.