AdipoRon - CAS 924416-43-3
Not Intended for Therapeutic Use. For research use only.
Category:
Inhibitor
Product Name:
AdipoRon
Catalog Number:
B0084-463481
CAS Number:
924416-43-3
Description:
AdipoRon is a novel small-molecule AdipoR agonist, binding to both AdipoR1(Kd=1.8 μM) and AdipoR2(Kd=3.1 μM).
Molecular Weight:
428.52
Molecular Formula:
C27H28N2O3
COA:
Inquire
MSDS:
Inquire
Targets:
Adiponectin Receptor
Catalog Number Size Price Stock Quantity
B0084-463481 100 mg $198 In stock
Bulk Inquiry
Chemical Structure
CAS 924416-43-3 AdipoRon

Related Adiponectin Receptor Products


CAS 924416-43-3 AdipoRon

AdipoRon
(CAS: 924416-43-3)

AdipoRon is a novel small-molecule AdipoR agonist, binding to both AdipoR1(Kd=1.8 μM) and AdipoR2(Kd=3.1 μM).

Reference Reading


1.Adiponectin Receptor Agonist, AdipoRon, Causes Vasorelaxation Predominantly Via a Direct Smooth Muscle Action.
Hong K1,2, Lee S2,3, Li R2,4, Yang Y2, Tanner MA2, Wu J2,4, Hill MA1,2. Microcirculation. 2016 Apr;23(3):207-20. doi: 10.1111/micc.12266.
OBJECTIVE: AdipoRon, an adiponectin receptor agonist, was recently proposed for treating insulin resistance and hyperglycemia. As adiponectin is vasoprotective via NO-mediated signaling, it was hypothesized that adipoRon similarly exerts potentially beneficial vasodilator effects. We therefore examined if adipoRon induces vasorelaxation and via what contributing mechanisms.
2.Identification and characterization of in vitro and in vivo generated metabolites of the adiponectin receptor agonists AdipoRon and 112254.
Dib J1, Thomas A1, Delahaut P2, Fichant E2, Schänzer W1, Thevis M3. J Pharm Biomed Anal. 2016 Mar 14;125:68-76. doi: 10.1016/j.jpba.2016.03.027. [Epub ahead of print]
Peroxisome proliferator-activated receptors (PPARs), peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α), sirtuin 1 (SIRT1) and adenosine monophosphate-activated protein kinase (AMPK) are regulators of transcriptional processes and effects of exercise and pseudo-exercise situations. Compounds occasionally referred to as endurance exercise mimetics such as AdipoRon and 112254, both adiponectin receptor agonists, can be used to simulate the physiology of endurance exercise via pathways including these transcriptional regulators. Adiponectin supports fatty acid utilization and triglyceride-content reduction in cells and increases both the mitochondrial biogenesis and the oxidative metabolism in muscle cells. In routine doping control analysis, knowledge about phase-I and -II metabolic products of target analytes is essential. Hence, in vitro- and in vivo-metabolism experiments are frequently employed tools in preventive doping research to determine potential urinary metabolites for sports drug testing purposes, especially concerning new, (yet) unapproved compounds.
3.AdipoRon, the first orally active adiponectin receptor activator, attenuates postischemic myocardial apoptosis through both AMPK-mediated and AMPK-independent signalings.
Zhang Y1, Zhao J1, Li R2, Lau WB3, Yuan YX3, Liang B2, Li R3, Gao EH4, Koch WJ4, Ma XL3, Wang YJ5. Am J Physiol Endocrinol Metab. 2015 Aug 1;309(3):E275-82. doi: 10.1152/ajpendo.00577.2014. Epub 2015 Jun 2.
Adiponectin (APN) is a cardioprotective molecule. Its reduction in diabetes exacerbates myocardial ischemia/reperfusion (MI/R) injury. Although APN administration in animals attenuates MI/R injury, multiple factors limit its clinical application. The current study investigated whether AdipoRon, the first orally active molecule that binds APN receptors, may protect the heart against MI/R injury, and if so, to delineate the involved mechanisms. Wild-type (WT), APN knockout (APN-KO), and cardiomyocyte specific-AMPK dominant negative (AMPK-DN) mice were treated with vehicle or AdipoRon (50 mg/kg, 10 min prior to MI) and subjected to MI/R (30 min/3-24 h). Compared with vehicle, oral administration of AdipoRon to WT mice significantly improved cardiac function and attenuated postischemic cardiomyocyte apoptosis, determined by DNA ladder formation, TUNEL staining, and caspase-3 activation (all P < 0.01). MI/R-induced apoptotic cell death was significantly enhanced in mice deficient in either APN (APN-KO) or AMPK (AMPK-DN).
4.AdipoRon: a possible drug for colorectal cancer prevention?
Malih S1, Najafi R2. Tumour Biol. 2015 Sep;36(9):6673-5. doi: 10.1007/s13277-015-3911-3. Epub 2015 Aug 18.
Colorectal cancer (CRC) is in the third place of the most common cancers. Certain risk factors can increase the development of CRC, including diet and inheritance. Several studies have shown that there is a potential link between obesity and CRC. Adipose tissue is known to be a largest endocrine organ in the body, with the ability to produce various cytokines including adiponectin. Two types of adiponectin receptor, AdipoR1 and AdipoR2, have been detected in various cancer tissues such as CRC. There is mounting evidence that AdipoR1 signaling occurs mainly through 5' AMP-activated protein kinase (AMPK) and adiponectin inhibits colorectal cancer cell growth via activation of AMPK, thereby suppression of the mammalian target of rapamycin (mTOR) pathway. Thus, adiponectin replacement-based therapies may represent a novel approach in CRC cell growth inhibition in early stages. AdipoRon is an adiponectin-like synthetic small molecule that activated both adiponectin receptors 1 and 2.