AdipoRon hydrochloride is an orally active and specificAdipoRagonist, binding to AdipoR1 and AdipoR2, withK_ds 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 K_ds 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].

464.98

C₂₇H₂₉ClN₂O₃

1781835-20-8

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.