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<p>Namodenoson—a selective A3 adenosine receptor (A3AR) agonist—is currently in clinical trials for hepatocellular carcinoma and metabolic dysfunction-associated steatotic liver disease. This preclinical study investigated its potential utility as a weight-loss drug. In 3T3-L1 adipocyte cells, namodenoson exhibited a dose-dependent inhibitory effect on the proliferation and accumulation of lipid droplets. Compared to vehicle, 5 and 10 nM of namodenoson inhibited adipocyte proliferation (determined using <sup>3</sup>H-thymidine incorporation assay) by 26 ± 12% (<i>P</i> &lt; 0.05) and 54 ± 5% (<i>P</i> &lt; 0.001), respectively, and lipid accumulation (determined by Oil-Red-O staining) by 22 ± 8% (<i>P</i> &lt; 0.05) and 41 ± 9% (<i>P</i> &lt; 0.001), respectively. Western blot analyses using 3T3-L1 adipocyte cells demonstrated that namodenoson led to downregulation of A3AR, PPAR<i>γ</i>, C/EBP<i>α</i>, C/EBPβ, p-AKT, PI3K, NF-kB, and β-catenin, and upregulation of adiponectin. In-vivo experiments in a murine model of diet-induced obesity demonstrated that administering daily namodenoson (100 μg/kg) to high-fat-fed mice led to a significant difference in weight after 4 weeks of treatment compared to high-fat-fed mice without namodenoson (44.3 ± 2.2 vs 47.2 ± 3.4 g, respectively, <i>P</i> = 0.001), representing a difference in weight of 6.1%. The same experiment on mice fed a lean diet demonstrated no namodenoson effect (mean weight: 33.5 ± 3.9 vs 33.0 ± 0.6 g, respectively). In conclusion, our findings support continued investigation of namodenoson as a weight-loss drug candidate.</p>

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The anti-obesity effect of namodenoson, an A3 adenosine receptor agonist

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月15日

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  • Pnina Fishman,
  • Inbal Itzhak,
  • Rifaat Safadi,
  • Johnny Amer,
  • Ahmad Salhab,
  • Avital Bareket-Samish

摘要

Namodenoson—a selective A3 adenosine receptor (A3AR) agonist—is currently in clinical trials for hepatocellular carcinoma and metabolic dysfunction-associated steatotic liver disease. This preclinical study investigated its potential utility as a weight-loss drug. In 3T3-L1 adipocyte cells, namodenoson exhibited a dose-dependent inhibitory effect on the proliferation and accumulation of lipid droplets. Compared to vehicle, 5 and 10 nM of namodenoson inhibited adipocyte proliferation (determined using 3H-thymidine incorporation assay) by 26 ± 12% (P < 0.05) and 54 ± 5% (P < 0.001), respectively, and lipid accumulation (determined by Oil-Red-O staining) by 22 ± 8% (P < 0.05) and 41 ± 9% (P < 0.001), respectively. Western blot analyses using 3T3-L1 adipocyte cells demonstrated that namodenoson led to downregulation of A3AR, PPARγ, C/EBPα, C/EBPβ, p-AKT, PI3K, NF-kB, and β-catenin, and upregulation of adiponectin. In-vivo experiments in a murine model of diet-induced obesity demonstrated that administering daily namodenoson (100 μg/kg) to high-fat-fed mice led to a significant difference in weight after 4 weeks of treatment compared to high-fat-fed mice without namodenoson (44.3 ± 2.2 vs 47.2 ± 3.4 g, respectively, P = 0.001), representing a difference in weight of 6.1%. The same experiment on mice fed a lean diet demonstrated no namodenoson effect (mean weight: 33.5 ± 3.9 vs 33.0 ± 0.6 g, respectively). In conclusion, our findings support continued investigation of namodenoson as a weight-loss drug candidate.