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AdipoRon is a novel, and orally bioavailable adiponectin receptor agonist with KD of 1.8 and 3.1 μM for AdipoR1 and AdipoR2, respectively.
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. AdipoRon treatment significantly improves cardiac functional recovery after reperfusion, and inhibits post-MI apoptosis.
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.
Cell Experiment | |
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Cell lines | DG granule cells |
Preparation method | A baseline recording of DG granule cells from WT mouse brain slices was first made followed by bath application of 15 μM AdipoRon, an AdipoR agonist that binds to both AdipoR1 and AdipoR2 with comparable high affinities. In response to depolarizing current injections (300 ms), AdipoRon treatment decreased the excitability of DG granule neurons, causing reduced number of action potentials elicited by current injections (60–90 pA), increased rheobase current and a more negative resting membrane potential without changing other membrane properties including input resistance, action potential threshold, fAHP and action potential waveforms. |
Concentrations | 15 μM |
Incubation time | 24 h |
Animal Experiment | |
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Animal models | Mice |
Formulation | DMSO |
Dosages | 50 mg/kg |
Administration | oral |
Molecular Weight | 428.52 |
Formula | C27H28N2O3 |
CAS Number | 924416-43-3 |
Solubility (25°C) | DMSO 55 mg/mL |
Storage |
Powder -20°C 3 years ; 4°C 2 years In solvent -80°C 6 months ; -20°C 1 month |
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