| Description |
IQZ23 inhibits adipocyte differentiation via AMPK pathway activation. IQZ23 exerts a high efficacy in decreasing the triglyceride level (EC50=0.033 μM) in 3T3-L1 adipocytes. IQZ23 could be used for the research of obesity and related metabolic disorders[1].
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| Related Catalog |
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| Target |
AMPK
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| In Vitro |
IQZ23 activates AMPK pathway by modulating ATP synthase activity[1]. IQZ23 (0.3 and 1.0 μM) markedly decreases the protein level of adipogenic factors C/EBPα, PPARγ, and sterol regulatory element-binding protein 1c (SREBP-1c)) after 24 h treatment as well as the level of fatty acid synthesis related proteins fatty acid synthase (FAS), acetyl CoA carboxylase (ACC), stearoyl-CoA desaturase 1 (SCD1) after 6 days of treatment in 3T3-L1 adipocytes[1]. Western Blot Analysis[1] Cell Line: 3T3-L1 adipocytes Concentration: 0.3 and 1.0 μM Incubation Time: 24 hours Result: Decreased the protein level of adipogenic factors C/EBPα, PPARγ, and SREBP-1c.
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| In Vivo |
IQZ23 (20 mg/kg, i.p.) treatment significantly reverses high fat and cholesterol diet (HFC)- induced body weight increases and accompanying clinical symptoms of obesity in mice but without indicative toxicity[1]. IQZ23 exhibits moderate terminal elimination half-lives (rat 4.2±0.3 h) and Cmax (rat 37.1±7.0 ng/mL) following oral administration (rat 5 mg/kg)[1]. IQZ23 exhibits terminal elimination half-lives (rat 4.4±0.4 h) following intravenous administration (rat 2 mg/kg)[1].
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| References |
[1]. Yong Rao, et al. Discovery of a Promising Agent IQZ23 for the Treatment of Obesity and Related Metabolic Disorders. Eur J Med Chem. 2020 Apr 15;192:112172.
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