AdipoRon hydrochloride |
| Catalog No.GC35251 |
Le chlorhydrate d'AdipoRon est un agoniste AdipoR actif et spécifique par voie orale, se liant À AdipoR1 et AdipoR2, avec des Kd de 1,8 et 3,1 μM, respectivement.
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 1781835-20-8
Sample solution is provided at 25 µL, 10mM.
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AdipoRon hydrochloride is an orally active and specific AdipoR agonist, binding to AdipoR1 and AdipoR2, with Kds of 1.8 and 3.1 μM, respectively. Kd: 1.8 μM (AdipoR1), 3.1 μM (AdipoR2)[1]
AdipoRon hydrochloride is an orally active and specific AdipoR agonist, binds to AdipoR1 and AdipoR2, with Kds of 1.8 and 3.1 μM. AdipoRon (50 nM-50 μM) increases AMPK phosphorylation via AdipoR1[1]. AdipoRon (50 μM) dose-dependently attenuates the expression of TNF-α and TGF-β1 in the L02 cells. AdipoRon exhibits significant and dosage-dependent growth suppression on macrophages[2]. AdipoRon treatment significantly improves cardiac functional recovery after reperfusion, and inhibits post-MI apoptosis[3]. AdipoRon exerts vasodilation by mechanisms distinct to adiponectin and induces vasorelaxation without a marked decrease in VSMC [Ca2+]i[4].
AdipoRon (50 mg/kg, i.v.) cuases significant phosphorylation of AMPK in skeletal muscle and liver of wild-type mice but not Adipor1-/- Adipor2-/- double-knockout mice[1]. AdipoRon (0.02, 0.1, and 0.5 mg/kg, i.g.) alleviates D-GalN induced hepatotoxicity in mice, and prevents hepatic architecture distortion against D-GalN challenge. The hepatoprotective potential of AdipoRon is particularly evident in higher dosages (0.1 and 0.5 mg/kg)[2]. Enhanced cardiomyocyte apoptosis in APN-deficient mice is rescued by AdipoRon (50 mg/kg, p.o.) administration. Antiapoptotic effect of AdipoRon is attenuated but not lost in AMPK-DN mice[3].
[1]. Okada-Iwabu M, et al. A small-molecule AdipoR agonist for type 2 diabetes and short life in obesity. Nature. 2013 Nov 28;503(7477):493-9. [2]. Wang Y, et al. Hepatoprotective effects of AdipoRon against d-galactosamine-induced liver injury in mice. Eur J Pharm Sci. 2016 Aug 9;93:123-131. [3]. Zhang Y, et al. AdipoRon, the first orally active adiponectin receptor activator, attenuates postischemic myocardial apoptosis through both AMPK-mediated and AMPK-independent signalings. Am J Physiol Endocrinol Metab. 2015 Aug 1;309(3):E275-82. [4]. Hong K, et al. Adiponectin Receptor Agonist, AdipoRon, Causes Vasorelaxation Predominantly Via a Direct Smooth Muscle Action. Microcirculation. 2016 Apr;23(3):207-20.
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