IQZ23 is a chemical compound that effectively inhibits adipocyte differentiation by activating the AMPK pathway. It demonstrates high efficacy in reducing triglyceride levels (EC50=0.033 μM) in 3T3-L1 adipocytes. Given its properties, IQZ23 holds potential for research related to obesity and metabolic disorders.

IQZ23 enhances the AMPK pathway by altering ATP synthase activity, significantly reducing adipogenic factor proteins C/EBPα, PPARγ, and SREBP-1c (sterol regulatory element-binding protein 1c) levels after 24 hours of exposure at concentrations of 0.3 and 1.0 μM in 3T3-L1 adipocytes. This compound also lowers the levels of proteins associated with fatty acid synthesis, such as fatty acid synthase (FAS), acetyl CoA carboxylase (ACC), and stearoyl-CoA desaturase 1 (SCD1), following a 6-day treatment period. Western Blot Analysis confirms these findings, highlighting IQZ23's potential in modulating lipid metabolism-related proteins in 3T3-L1 adipocytes.

Treatment with IQZ23 (20 mg/kg, i.p.) significantly mitigates the increase in body weight and associated clinical signs of obesity in mice caused by a high fat and cholesterol diet (HFC), without showing signs of toxicity[1]. In terms of pharmacokinetics, IQZ23 demonstrates moderate terminal elimination half-lives (rat 4.2±0.3 h) and peak plasma concentrations (Cmax) (rat 37.1±7.0 ng/mL) after oral administration at a dose of 5 mg/kg[1]. Additionally, when administered intravenously at a dose of 2 mg/kg, IQZ23 shows similar elimination half-lives (rat 4.4±0.4 h)[1].