AdipoRon hydrochloride

Cas No.:	1781835-20-8
SMILES:	O=C(C1=CC=CC=C1)C2=CC=C(OCC(NC3CCN(CC4=CC=CC=C4)CC3)=O)C=C2.Cl
Formula:	C₂₇H₂₉ClN₂O₃
M.Wt:	464.98
Purity:	>98%
Sotrage:	2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO

Description:

In Vitro 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. 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 exerts vasodilation by mechanisms distinct to adiponectin and induces vasorelaxation without a marked decrease in VSMC [Ca2+]i. 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. 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). 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.

MSDS

COA

LOT NO.	DOWNLOAD

2018-0101

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