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[CAS NO. 924416-43-3] AdipoRon
| Ships within | Stock | Price | Qty | Total |
Please click "REQUEST A QUOTE" button if there is no stock, or you need other sizes or custom synthesis.
| Catalog: | HY-15848 |
| Brand: | MCE |
| CAS: | 924416-43-3 |
Overview
| MDL | MFCD08271060 |
|---|---|
| Molecular Weight | 428.52 |
| Molecular Formula | C27H28N2O3 |
| SMILES | O=C(NC1CCN(CC2=CC=CC=C2)CC1)COC3=CC=C(C(C4=CC=CC=C4)=O)C=C3 |
15 Publications Citing Use of MCE
- [1]Mol Psychiatry. 2020 Mar 4.
- [2]Redox Biol. August 2022, 102390.
- [3]Prog Neurobiol. 2021 Jul 29;102125.
- [4]Diabetes. 2021 Jun;70(6):1303-1316.
- [5]Acta Pharmacol Sin. 2022 Aug 2.
- [6]J Biol Chem. 2018 Apr 20;293(16):6064-6074.
- [7]J Cell Biochem. 2020 Jun;121(5-6):3333-3344.
- [8]Poult Sci. 5 November 2022, 102319.
- [9]Poult Sci. 10 January 2022, 101708.
- [10]J Neurotrauma. 2019 Mar 19;36(6):903-918.
- [11]Neurochem Res. 2019 May;44(5):1214-1227.
- [12]Diabetes Metab Syndr Obes. 2019 Oct 23;12:2165-2179.
- [13]Biomed Chromatogr. 2019 Nov;33(11):e4645.
- [14]Mol Biol Rep. 2020 Sep;47(9):6561-6572.
- [15]Research Square Preprint. 2022 May.
Summary
AdipoRon is an orally active adiponectin receptor (AdipoR) agonist, binding to AdipoR1 and AdipoR2 with K d s of 1.8 and 3.1 μM, respectively.
IC50 & Target
Kd: 1.8 μM (AdipoR1), 3.1 μM (AdipoR2) [1]
In Vitro
AdipoRon is an orally active and specific AdipoR agonist, binds to AdipoR1 and AdipoR2, with K d s 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 [Ca 2+ ] i [4] .
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
In Vivo
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] .
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Appearance
Solid
Shipping
Room temperature in continental US; may vary elsewhere.
Storage
| Powder | -20°C | 3 years |
|---|---|---|
| 4°C | 2 years | |
| In solvent | -80°C | 6 months |
| -20°C | 1 month |
Solvent & Solubility
DMSO : ≥ 44 mg/mL ( 102.68 mM )
H 2 O : < 0.1 mg/mL (insoluble)
* "≥" means soluble, but saturation unknown.
Stock Solutions
| Concentration Solvent Mass | 1 mg | 5 mg | 10 mg |
|---|
| 1 mM | 2.3336 mL | 11.6681 mL | 23.3361 mL |
| 5 mM | 0.4667 mL | 2.3336 mL | 4.6672 mL |
| 10 mM | 0.2334 mL | 1.1668 mL | 2.3336 mL |
References
- [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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