IC50: 9 μM (ChAT); 0.04 μM (ALDH1A1); CMKLR1; 84 μM (ChE); 300 μM (AChE)

α-NETA (50-150 nM; 24 hours) decreases all cell lines viability in a dose-dependent manner.
α-NETA (2.5-10.0 μg/mL; 24 hours) leads to epithelial ovarian cancer (EOC) cell death associated with membrane blistering and cytoplasm leakage.
α-NETA treatment increases EOC cell expression of pyroptosis-associated proteins.
α-NETA is most potent in inhibiting aldehyde dehydrogenase 1 family, member A1 (ALDH1A1; IC ₅₀ =0.04 μM; purified enzymes assay), followed by CMKLR1 (IC ₅₀ =0.375 μM for β-ARR2 recruitment; Cell-based assay) and G9a histone lysine methyltransferase (IC ₅₀ =0.50 μM; purified enzymes assay). α-NETA selectively inhibits chemerin-stimulated CMKLR1 association with β-arrestin2.
α-NETA possesses fluorescent characteristics (excitation spectrum: maxima 255 and 297 nm; emission spectrum: maximum 437 nm) of naphthyl moiety.

α-NETA (i.p.; 0.125 mg/kg; once every other day for 20 days) significantly decreases tumor volume and tumor weight.
α-NETA (s.c. injection; 3 mg/kg or 10 mg/kg; daily; for 30 days) significantly delays the onset of EAE with 3 mg/kg, and completely suppresses clinical signs for an average of nine days with 10 mg/kg beyond the first appearance of disease in control female C57BL/6 mice.