T2M-010 is a potent TREM2 agonist capable of crossing the blood-brain barrier (Kd= 0.83 μM). It activates receptor proximal signaling pathways, induces SYK phosphorylation in TREM2-expressing cells, and enhances phagocytosis in microglia. T2M-010 is applicable for research on protective microglial responses associated with Alzheimer's disease (AD).

T2M-010, at 25 µM for 1 hour, significantly doubles the phosphorylation level of SYK in HEK-hTREM2/DAP12 cells. At 25 µM for 30 minutes, it markedly enhances microparticle uptake by BV2 cells, indicating a substantial increase in phagocytic activity. T2M-010 is non-cytotoxic to human fibroblasts (WI-38 and HS-27; IC50 > 100 µM), has a low hERG risk (IC50 > 60 µM), and exhibits minimal inhibition (≤ 11.2%) of major CYP isozymes at 10 µM. In the MDCK-MDR1 cell line, T2M-010 demonstrates strong A→B transport capability (Papp = 2.85 × 10⁻⁵ cm/s) and a low efflux ratio (ER = 1.07), indicating minimal P-gp-mediated efflux. The compound shows good gastrointestinal stability (greater than 88-86% remaining in simulated gastric and intestinal fluids after 2 hours) and a relatively long plasma half-life (167 minutes in mice and 214 minutes in humans).