1. Metabolic Enzyme/Protease
  2. Adiponectin Receptor
  3. AdipoRon hydrochloride

AdipoRon hydrochloride is an orally active and specific AdipoR agonist, binding to AdipoR1 and AdipoR2, with Kds of 1.8 and 3.1 μM, respectively.

For research use only. We do not sell to patients.

AdipoRon hydrochloride Chemical Structure

AdipoRon hydrochloride Chemical Structure

CAS No. : 1781835-20-8

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Top Publications Citing Use of Products

    AdipoRon hydrochloride purchased from MedChemExpress. Usage Cited in: J Neurotrauma. 2019 Mar 19;36(6):903-918.  [Abstract]

    WT macrophages are incubated with myelin debris for 3 hours to obtain mye-MΦ, and further treated with AdipoRon for another 48 hours. ABCA1 and ABCG1 levels are assessed by western blot.

    AdipoRon hydrochloride purchased from MedChemExpress. Usage Cited in: J Biol Chem. 2018 Apr 20;293(16):6064-6074.  [Abstract]

    Interaction of APPL1sv with adiponectin receptors in cells. Mouse hepatocytes are serum-starved for 4 h and treated with or without 50 μM AdipoRon (Ad) for 0, 5, or 10 min.
    • Biological Activity

    • Protocol

    • Purity & Documentation

    • References

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    Description

    AdipoRon hydrochloride is an orally active and specific AdipoR agonist, binding to AdipoR1 and AdipoR2, with Kds of 1.8 and 3.1 μM, respectively.

    IC50 & Target

    Kd: 1.8 μM (AdipoR1), 3.1 μM (AdipoR2)[1]

    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[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].

    MedChemExpress (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].

    MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

    Molecular Weight

    464.98

    Formula

    C27H29ClN2O3

    CAS No.
    SMILES

    O=C(C1=CC=CC=C1)C2=CC=C(OCC(NC3CCN(CC4=CC=CC=C4)CC3)=O)C=C2.Cl

    Shipping

    Room temperature in continental US; may vary elsewhere.

    Storage

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

    Purity & Documentation
    References
    Cell Assay
    [2]

    The effects of AdipoRon on the proliferation of parenchymal and non-parenchymal hepatocytes are evaluated in vitro via L02 and RAW264.7, by MTT assay as described with slight modification: 100 μL cells suspension (6×104/mL) are seeded in a 96-well plate and incubated for 18 h. Fresh media with AdipoRon are added at specified concentrations, and the incubations continue for a further 24 h. Then cells are incubated for 4 h with 0.5 mg/mL of MTT, and analyzed in a microplate reader at 490 nm. Each group is performed in six replications. The mean absorbance values corrected for a blank (medium only) are calculated as percentages of survival[2].

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Animal Administration
    [2]

    Mice[2]
    After 3 days of acclimation, mice are randomLy divided into six groups (9 mice in each): control, model, bicyclol (20 mg/kg), AdipoRon (0.02 mg/kg, 0.1 mg/kg, 0.5 mg/kg). The synthetic AdipoRon and bicyclol are dissolved in DMSO and diluted by saline containing 0.5% sodium carboxymethyl cellulose (CMC-Na) [final vehicle: 5% DMSO (v/v) saline solution]. All test groups are administered with vehicle (control and model groups) or therapeutic agents (bicyclol or AdipoRon groups) at a dosing volume of 10 mL/kg, by intragastric (i.g.) gavage twice per day for three consecutive days prior to D-GalN administration. 2 h after last treatment, mice are challenged with a single intraperitoneal (i.p.) administration of D-GalN saline solution at a dose of 600 mg/kg to induce acute liver injury, while the control group mice receive saline instead. Then mice are fasted for 20 h before orbital blood collection. Finally, all animals are sacrificed by cervical dislocation, and livers are harvested for biochemical or histopathology analysis[2].

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    References
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    AdipoRon hydrochloride Related Classifications

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    • Do most proteins show cross-species activity?

      Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

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    Product Name:
    AdipoRon hydrochloride
    Cat. No.:
    HY-110164
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