AdipoRon | Adiponectin agonist
NMR (Conforms)
Available Options
| size : | Price | Quantity | |
|---|---|---|---|
| 10 mg | $50.00 | ||
| 50 mg | $200.00 |
AdipoRon (924416-43-3) is a novel potent and selective adiponectin (AdipoR1 and AdipoR2) receptor agonist, Kd=1.8 and 3.1 μM respectively.1 Displayed similar effects to adiponectin in muscle and liver such as activation of PPARα and AMPK signaling pathways. It also reversed insulin resistance and glucose intolerance in mice on a high-fat diet. AdipoRon ameliorated diabetes in a genetically obese mouse model and prolonged the shortened lifespan of db/db mice on a high-fat diet.1 Attenuates PDGF-induced VSMC proliferation via inhibition of mTPR signaling in an AMPK independent manner.2 Active in vivo.
References/Citations:
1) Okada-Iwabu et al. (2013), A small-molecule AdipoR agonist for type 2 diabetes and short life obesity; Nature 503 493
2) Fairaq et al. (2017), AdipoRon, an adiponectin receptor agonist, attenuates PDGF-induced VSMC proliferation through inhibition of mTOR signaling independent of AMPK: Implications toward suppression of neointimal hyperplasia; Pharmacol. Res. 119 289
NMR (Conforms)
Safety Data Sheet:
Product Data Sheet:
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AdipoRon (924416-43-3) is a novel potent and selective adiponectin (AdipoR1 and AdipoR2) receptor agonist, Kd=1.8 and 3.1 μM respectively.1 Displayed similar effects to adiponectin in muscle and liver such as activation of PPARα and AMPK signaling pathways. It also reversed insulin resistance and glucose intolerance in mice on a high-fat diet. AdipoRon ameliorated diabetes in a genetically obese mouse model and prolonged the shortened lifespan of db/db mice on a high-fat diet.1 Attenuates PDGF-induced VSMC proliferation via inhibition of mTPR signaling in an AMPK independent manner.2 Active in vivo.
References/Citations:
1) Okada-Iwabu et al. (2013), A small-molecule AdipoR agonist for type 2 diabetes and short life obesity; Nature 503 493
2) Fairaq et al. (2017), AdipoRon, an adiponectin receptor agonist, attenuates PDGF-induced VSMC proliferation through inhibition of mTOR signaling independent of AMPK: Implications toward suppression of neointimal hyperplasia; Pharmacol. Res. 119 289
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