α-NETA is a potent choline acetyltransferase (ChA) inhibitor and an ALDH1A1 and chemokine-like receptor 1 (CMKLR1) antagonist.Anti-cancer activity,Cholinesterase and acetylcholinesterase (AChE) inhibition,Dose-dependent reduction of body weight and fasting blood glucose levels in STZ-induced diabetic mice,Significantly reduced expression of renal injury markers,May be CEP-9722 can be used for the study of diabetic nephropathy.

ChE:84 μM, ALDH1A1:0.04 μM, chemokine-like receptor 1:0.38 μM, ChAT:9 μM, AChE:300 μM

α-NETA is a potent, non-competitive inhibitor of choline acetyltransferase (ChAT) with an IC50 of 9 μM. α-NETA is also a potent inhibitor of aldehyde dehydrogenase 1A1 (ALDH1A1) with an IC50 of 0.04 μM, and acts as a chemokine-like receptor 1 (CMKLR1) antagonist with an IC50 of 0.38 μM. α-NETA inhibits both ChE and AChE less than they do, with IC50s of 84 μM and 300 μM, respectively.[3] α-NETA is also a potent, non-competitive inhibitor of ChAT. Compared to cholinesterase (ChE) and acetylcholinesterase (AChE), α-NETA has a weaker inhibitory effect on these two enzymes, with IC50s of 84 μM and 300 μM, respectively.[2]
In cellular experiments, α-NETA (50-150 nM, 24 h) reduced the viability of several cell lines in a dose-dependent manner. At doses of 2.5-10.0 μg/mL and a treatment time of 24 hours, it resulted in epithelial ovarian cancer (EOC) cell death, which was associated with cell membrane blistering and cytoplasmic leakage. In addition, α-NETA treatment significantly increased the expression levels of focal death-related proteins in EOC cells. [3]
α-NETA has unique fluorescence properties with naphthalene-based fluorescence excitation spectra with maxima at 255 nm and 297 nm, and an emission spectrum with a maximum at 437 nm.[1]

In in vivo studies, α-NETA (intraperitoneal injection, 0.125 mg/kg every other day for 20 days) was able to significantly reduce the volume and weight of tumors in mice.[3]
In an experimental autoimmune encephalomyelitis (EAE) model, α-NETA (subcutaneous injection, 3 mg/kg or 10 mg/kg once daily for 30 days) significantly delayed the onset of EAE at a dose of 3 mg/kg, whereas a dose of 10 mg/kg completely suppressed the clinical signs of EAE in female C57BL/6 mice up to 9 days after its onset. [2]