PTERi is a selective inhibitor of PTER with selectivity towards HDACs. PTERi increases the level of N-acetyltaurine in both lean and obese mice, and reduces food intake in obese mice. PTERi can be used in the research of obesity [1].
In Vivo, PTERi (100 mg/kg; i.p.; daily/single administration) dose-dependently increases plasma N-acetyltaurine levels, reduces food intake and body weight, decreases fat mass, enhances the weight loss efficacy of Semaglutide, and prevents body weight rebound after discontinuation of GLP-1R agonists in obese mice[1].
In Vitro, PTERi (Compound 41) (1 h) potently and selectively inhibits recombinant mouse PTER-mediated N-acetyltaurine hydrolysis, with over 250-fold selectivity over HDAC enzymes[1]. PTERi exhibits only weak inhibitory activity against HDACs 1-11 and SIRTs 1-4, and shows high selectivity for PTER[1].
References:
[1]. Jonathan Z. Long, et al. Compounds, compositions, and methods for treating metabolic disorders. WO2026015683A1. 2026-01-15.
In Vivo, PTERi (100 mg/kg; i.p.; daily/single administration) dose-dependently increases plasma N-acetyltaurine levels, reduces food intake and body weight, decreases fat mass, enhances the weight loss efficacy of Semaglutide, and prevents body weight rebound after discontinuation of GLP-1R agonists in obese mice[1].
In Vitro, PTERi (Compound 41) (1 h) potently and selectively inhibits recombinant mouse PTER-mediated N-acetyltaurine hydrolysis, with over 250-fold selectivity over HDAC enzymes[1]. PTERi exhibits only weak inhibitory activity against HDACs 1-11 and SIRTs 1-4, and shows high selectivity for PTER[1].
References:
[1]. Jonathan Z. Long, et al. Compounds, compositions, and methods for treating metabolic disorders. WO2026015683A1. 2026-01-15.