AdipoRonAdipoR1 and AdipoR2 agonist, first orally active CAS# 924416-43-3 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 924416-43-3 | SDF | Download SDF |
| PubChem ID | 16307093 | Appearance | Powder |
| Formula | C27H28N2O3 | M.Wt | 428.52 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Solubility | DMSO : ≥ 44 mg/mL (102.68 mM) H2O : < 0.1 mg/mL (insoluble) *"≥" means soluble, but saturation unknown. | ||
| Chemical Name | 2-(4-benzoylphenoxy)-N-(1-benzylpiperidin-4-yl)acetamide | ||
| SMILES | C1CN(CCC1NC(=O)COC2=CC=C(C=C2)C(=O)C3=CC=CC=C3)CC4=CC=CC=C4 | ||
| Standard InChIKey | SHHUPGSHGSNPDB-UHFFFAOYSA-N | ||
| Standard InChI | InChI=1S/C27H28N2O3/c30-26(28-24-15-17-29(18-16-24)19-21-7-3-1-4-8-21)20-32-25-13-11-23(12-14-25)27(31)22-9-5-2-6-10-22/h1-14,24H,15-20H2,(H,28,30) | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| Description | AdipoRon is a novel AdipoR agonist, binding to both AdipoR1 (Kd=1.8 μM) and AdipoR2 (Kd=3.1 μM).In Vitro:AdipoRon (50 μM) attenuates the expression of TNF-α and TGF-β1, apparently in a dose-dependent manner in the L02 cells. AdipoRon exhibits significant and dosage-dependent growth suppression on macrophages[1]. AdipoRon treatment significantly improves cardiac functional recovery after reperfusion, and inhibits post-MI apoptosis[2]. AdipoRon exerts vasodilation by mechanisms distinct to adiponectin. AdipoRon induces vasorelaxation without a marked decrease in VSMC [Ca2+]i[3].In Vivo:AdipoRon (0.02, 0.1, and 0.5 mg/kg, i.g.) alleviates D-GalN induced hepatotoxicity in mice. AdipoRon dose-dependently 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)[1]. 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[2]. References: | |||||
AdipoRon Dilution Calculator
AdipoRon Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.3336 mL | 11.6681 mL | 23.3361 mL | 46.6723 mL | 58.3403 mL |
| 5 mM | 0.4667 mL | 2.3336 mL | 4.6672 mL | 9.3345 mL | 11.6681 mL |
| 10 mM | 0.2334 mL | 1.1668 mL | 2.3336 mL | 4.6672 mL | 5.834 mL |
| 50 mM | 0.0467 mL | 0.2334 mL | 0.4667 mL | 0.9334 mL | 1.1668 mL |
| 100 mM | 0.0233 mL | 0.1167 mL | 0.2334 mL | 0.4667 mL | 0.5834 mL |
| * Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
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AdipoRon is an agonist of AdipoR1 and AdipoR2 with Kd values of 1.8 and 3.1 μM, respectively [1].
Adiponectin receptor (AdipoR) is a receptor for adiponectin, which is a protein and plays an important role in regulating glucose levels and fatty acid breakdown.
AdipoRon is the first orally active AdipoR1 and AdipoR2 agonist. AdipoRon (5-50 μM) increased AMPK phosphorylation via AdipoR1 in a dose-dependent way. Also, AdipoRon replenished adiponectin-stimulated AMPK phosphorylation. In C2C12 myotubes, AdipoRon increased PGC-1α expression and mitochondrial DNA content in a Ca2+- and dose-dependent way [1].
In wild-type mice, AdipoRon (50mg/kg) significantly induced AMPK phosphorylation in liver and skeletal muscle. Also, AdipoRon (50mg/kg) significantly reduced fasting plasma insulin and glucose levels. In wild-type mice fed a high-fat diet, AdipoRon increased the expression levels of
PPAR-α via AdipoR2 and reduced plasma levels of free fatty acid (FFA) and triglycerides. Also, AdipoRon reduced the expression levels of pro-inflammatory cytokines such as TNF-α and MCP-1 in the liver. In db/db obese mice, AdipoRon significantly reduced plasma glucose levels and ameliorated insulin resistance, glucose intolerance and dyslipidaemia [1]. In wild type mice, AdipoRon significantly improved cardiac function and inhibited myocardial ischemia/reperfusion (MI/R)-induced apoptosis [2].
References:
[1]. Okada-Iwabu M, Yamauchi T, Iwabu M, et al. A small-molecule AdipoR agonist for type 2 diabetes and short life in obesity. Nature, 2013, 503(7477): 493-499.
[2]. Zhang Y, Zhao J, Li R, et al. AdipoRon, the First Orally Active Adiponectin Receptor Activator, Attenuates Post-Ischemic Myocardial Apoptosis. Am J Physiol Endocrinol Metab, 2015, ajpendo.00577.2014.
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AdipoRon may be benefit for atherosclerosis prevention.[Pubmed:28293385]
Iran J Basic Med Sci. 2017 Feb;20(2):107-109.
Atherosclerosis has serious role in coronary arteries disease, so it is important to establish effective strategies for prevention or even treatment of atherosclerosis. Adiponectin, as one of the most abundant adipokines, has insulin sensitivity, anti-inflammatory and anti-atherogenic properties. Disturbed adiponectin actions through its receptor, (AdipoR1 and AdipoR2) may be involved in atherosclerosis development. Some adiponectin effects are mediated by AMPK and PPAR-alpha signaling. AdipoRon is an orally active synthetic molecule which can bind to AdipoR1, Adipo R2 and activate them. AdipoRon can activate AdipoR1-AMPK- PGC-1alpha pathway and AdipoR2-PPAR-alpha pathway. Some studies indicated insulin sensitivity, anti-apoptotic and anti-oxidative effect of AdipoRon. We hypothesize that AdipoRon has anti atherosclerotic effect and may suppress atherosclerosis processes. With confirmation the benefit role of AdipoRon on atherosclerosis, it may be used in patients at risk of atherosclerotic development.
Hepatoprotective effects of AdipoRon against d-galactosamine-induced liver injury in mice.[Pubmed:27516150]
Eur J Pharm Sci. 2016 Oct 10;93:123-31.
Adiponectin is an antidiabetic and antiatherogenic adipokine, which plays distinct roles in the balance of energy homoeostasis. As an insulin sensitizing hormone, adiponectin exerts multiple biological effects by the specific receptors (AdipoR1 and AdipoR2), through activation of AMP-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor (PPAR)alpha pathways. AdipoRon, an orally active synthetic small-molecule AdipoR agonist, shows very similar effects to adiponectin in vitro and in vivo, which could be a promising therapeutic approach for obesity-related disorders. In view of the regulatory effects of adiponectin or AdipoRon on inflammatory response and energy metabolism, they might be endowed a curative potential for tissue damage. Hence, its effects and possible mechanism were investigated. In vitro studies on hepatocytes (L02) and macrophages (RAW264.7) suggested a protective and anti-inflammatory potential of AdipoRon. The effects were verified in acute hepatic injury mice induced by d-galactosamine (D-GalN): hepatic lesions were restored by AdipoRon or bicyclol (positive reference drug) pretreatment, which were characterized by a significant increase in serological and hepatic biomarkers (AST, ALT, MDA and NOSs). Besides, AdipoRon attenuated the inflammation in the liver, characterized by the dwindling proinflammatory macrophage infiltration, as well as the shrinkage of tumor necrosis factor-alpha (TNF-alpha), transforming growth factor beta 1 (TGF-beta1), interleukin-1 beta (IL-1beta) and interleukin-6 (IL-6); meanwhile conversely promoted AMPK activation by phosphorylation. Combined with liver histopathology, these results demonstrated the hepatoprotective effects of AdipoRon against D-GalN-induced damage, which might be ascribed to the attenuation of inflammation, inhibition of free radical reactions, as well as enhancement of liver energy metabolism.
Promigratory and proangiogenic effects of AdipoRon on bone marrow-derived mesenchymal stem cells: an in vitro study.[Pubmed:27627895]
Biotechnol Lett. 2017 Jan;39(1):39-44.
OBJECTIVES: To investigate the effect of AdipoRon on major factors involved in survival, migration and neovascularization of rat bone marrow-derived mesenchymal stem cells. RESULTS: AdipoRon promoted the MSCs viability. Real-time PCR indicated that the expression of cyclooxygenase-2 (COX-2), hypoxia-inducible factor-1 (HIF-1) C-X-C chemokine receptor type 4 (CXCR4), C-C chemokine receptor type 2 (CCR2), vascular endothelial growth factor matrix metalloproteinase-2 (MMP-2) and MMP-9 were upregulated in AdipoRon-treated MSCs compared to control groups. Prostaglandin E2 (PGE2) level, as well as migration ability of MSCs (scratch assay) was enhanced by AdipoRon preconditioning. CONCLUSION: Preconditioning of MSCs with AdipoRon prior to transplantation could enhance cell survival, angiogenesis and migration via activating the COX-2/PGE2/HIF-1 pathway and other contributing factors.
AdipoRon, an adiponectin receptor agonist, attenuates PDGF-induced VSMC proliferation through inhibition of mTOR signaling independent of AMPK: Implications toward suppression of neointimal hyperplasia.[Pubmed:28237515]
Pharmacol Res. 2017 May;119:289-302.
Hypoadiponectinemia is associated with an increased risk of coronary artery disease. Although adiponectin replenishment mitigates neointimal hyperplasia and atherosclerosis in mouse models, adiponectin therapy has been hampered in a clinical setting due to its large molecular size. Recent studies demonstrate that AdipoRon (a small-molecule adiponectin receptor agonist) improves glycemic control in type 2 diabetic mice and attenuates postischemic cardiac injury in adiponectin-deficient mice, in part, through activation of AMP-activated protein kinase (AMPK). To date, it remains unknown as to whether AdipoRon regulates vascular smooth muscle cell (VSMC) proliferation, which plays a major role in neointima formation. In the present study, oral administration of AdipoRon (50mg/kg) in C57BL/6J mice significantly diminished arterial injury-induced neointima formation by approximately 57%. Under in vitro conditions, AdipoRon treatment led to significant inhibition of platelet-derived growth factor (PDGF)-induced VSMC proliferation, DNA synthesis, and cyclin D1 expression. While AdipoRon induced a rapid and sustained activation of AMPK, it also diminished basal and PDGF-induced phosphorylation of mTOR and its downstream targets, including p70S6K/S6 and 4E-BP1. However, siRNA-mediated AMPK downregulation showed persistent inhibition of p70S6K/S6 and 4E-BP1 phosphorylation, indicating AMPK-independent effects for AdipoRon inhibition of mTOR signaling. In addition, AdipoRon treatment resulted in a sustained and transient decrease in PDGF-induced phosphorylation of Akt and ERK, respectively. Furthermore, PDGF receptor-beta tyrosine phosphorylation, which controls the phosphorylation state of Akt and ERK, was diminished upon AdipoRon treatment. Together, the present findings suggest that orally-administered AdipoRon has the potential to limit restenosis after angioplasty by targeting mTOR signaling independent of AMPK activation.
