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Last update 08 May 2025

ADIPOR2

Last update 08 May 2025

Basic Info

Synonyms

ACDCR2, adiponectin receptor 2, Adiponectin receptor protein 2

+ [4]

Introduction

Receptor for ADIPOQ, an essential hormone secreted by adipocytes that regulates glucose and lipid metabolism (PubMed:12802337, PubMed:25855295). Required for normal body fat and glucose homeostasis. ADIPOQ-binding activates a signaling cascade that leads to increased PPARA activity, and ultimately to increased fatty acid oxidation and glucose uptake. Has intermediate affinity for globular and full-length adiponectin. Required for normal revascularization after chronic ischemia caused by severing of blood vessels (By similarity).

Drugs associated with ADIPOR2

BHD-1028

Target

ADIPOR1 x ADIPOR2

Mechanism

ADIPOR1 agonists [+1]

Active Org.

EncuraGen Co., Ltd.

Originator Org.

EncuraGen Co., Ltd.

Active Indication

Insulin Resistance [+4]

Inactive Indication-

Drug Highest PhasePhase 1

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

AdipoRon

Target

ADIPOR1 x ADIPOR2

Mechanism

ADIPOR1 agonists [+1]

Active Org.

The Catholic University of Korea [+2]

Originator Org.

University of Tokyo

Active Indication

Breast Cancer [+4]

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

AdipoRaMab(Mitsubishi Tanabe Pharma)

Target

ADIPOR1 x ADIPOR2

Mechanism

ADIPOR1 agonists [+1]

Active Org.

Mitsubishi Tanabe Pharma Corp.

Originator Org.

Mitsubishi Tanabe Pharma Corp.

Active Indication

Diabetes Mellitus, Type 2 [+1]

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with ADIPOR2

NCT06563115

/ CompletedPhase 1

A Randomized, Double-Blinded, Placebo-Controlled, Single and Multiple Ascending Dose Study in Overweight/Obese Subjects to Evaluate the Safety, Tolerability, Pharmacokinetics and Pharmacodynamics of (PEG)-BHD1028

Adiponectin has been known to play critical roles in various physio-regulatory processes, and adiponectin deficiency may contribute to insulin resistance. (PEG)-BHD1028 was developed as an agonist of adiponectin receptors.
This first-in-human study evaluates the safety, tolerability, pharmacokinetics, and pharmacodynamics of (PEG)-BHD1028 in healthy overweight/obese subjects with insulin resistance.

Start Date18 Apr 2022

Sponsor / Collaborator

EncuraGen Co., Ltd.

100 Clinical Results associated with ADIPOR2

100 Translational Medicine associated with ADIPOR2

0 Patents (Medical) associated with ADIPOR2

974

Literatures (Medical) associated with ADIPOR2

01 May 2025·International Immunopharmacology

Adiponectin receptor agonist adipoRon alleviates imiquimod-induced murine psoriasis

Article

Author: Chen, Cai-Ping ; Huang, Yuan-Yuan ; Ye, Hao-Nan ; Zhang, Lin ; Sun, Geng ; Wang, Xin-Yue ; Guo, Zhan-Ying ; Zhao, Hai-Qian ; Zhu, Hao

Psoriasis is a chronic inflammatory skin disease involving inflammation, immune responses and keratinocytes proliferation. It has been suggested that adiponectin/adiponectin receptor 1 (AdipoR1) signaling plays a role in regulating psoriatic skin inflammation. AdipoRon is a small molecule agonist of AdipoR1 and AdipoR2. The effect of adipoRon on psoriasis has not been elucidated. In this study, using a GEO database, we found that the expression of adiponectin was substantially decreased in skin lesions of psoriasis patients. This reduction was also validated in an imiquimod-induced psoriasis mouse model. Interestingly, we found that topical administration of adipoRon significantly ameliorated skin lesions induced by imiquimod. The critical pro-inflammatory cytokines (IL-6, IL-17A and IL-23) and the infiltration of macrophages, especially M1 macrophages were dramatically decreased while the infiltration of M2 macrophages were slightly increased in the skin lesions upon adipoRon treatment. Mechanistically, adipoRon inhibited macrophage inflammation and keratinocytes proliferation via activation of AMPK signaling pathway. Collectively, our study demonstrates that adipoRon displayed anti-inflammatory activity and anti-proliferation of keratinocytes, and attenuated psoriatic response. Activating AdipoR1 signaling pathway by adipoRon or others may represent a novel therapeutic approach to psoriasis.

01 Apr 2025·Annals of Surgical Oncology

Tumor-Infiltrating Lymphocytes as Mediators of the Obesity and Papillary Thyroid Carcinoma Lymph Node Metastasis Association: An Observational Retrospective Cohort Study

Article

Author: Dionigi, Gianlorenzo ; Zhang, Jiao ; Li, Changlin ; Sun, Hui

BACKGROUNDObesity increases the risk of papillary thyroid carcinoma (PTC) and lymph node metastasis (LNM), possibly via modulation of the tumor immunological microenvironment.MATERIALS AND METHODSThe STROCSS guideline was followed to conduct a retrospective cohort study. Binary logistic regression analysis with odds ratios (OR) was performed to assess the association between tumor-infiltrating lymphocytes (TILs), obesity, and LNM. Using The Cancer Genome Atlas (TCGA) data, we examined the relationship between immune cell subsets and obesity-regulating molecules in thyroid cancer tissues. The Cox regression risk model was used to analyze the prognosis of thyroid cancer.RESULTSAfter adjusting for confounding factors, our findings revealed that overweight and obesity were associated with a decrease in TIL infiltration (OR 0.876, p = 0.005 and OR 0.795, p = 0.001, respectively). Furthermore, these conditions were observed to be correlated with increased likelihood of LNM (OR 1.134, p = 0.005 and OR 1.307, p < 0.001, respectively). On the contrary, TIL infiltration was inversely associated with LNM (OR 0.868, p < 0.001). When controlling for TIL infiltration as the sole variable, the combination of obesity and TIL infiltration did not independently predict LNM (adjusted OR 1.442, p = 0.113). However, obesity alone was found to elevate the likelihood of LNM (adjusted OR 1.539, p = 0.02). Additionally, adiponectin (a crucial adipokine) was reduced in obesity and demonstrated a negative correlation with the abundance of infiltrated dendritic cells and regulatory T cells, as evidenced by TCGA data analysis. Furthermore, ADIPOR2 expression negatively correlated with LNM and positively associated with unfavorable prognosis in PTC, with a hazard ratio of 0.480 (p = 0.007).CONCLUSIONSTIL infiltration may affect obesity-associated PTC LNM. Obesity may affect LNM and result in poor prognosis through ADIPOR2 regulation of antitumor immune cells.

01 Mar 2025·Journal of Oral Biosciences

Expression and localization of adiponectin in myoepithelial cells in sublingual glands of normal and diabetic rats

Review

Author: Iseki, Shoichi ; Sakiyama, Koji ; Miyake, Genki ; Amano, Osamu ; Nagasaka, Arata ; Sakashita, Hideaki ; Bando, Yasuhiko

OBJECTIVESAdiponectin is a hormone produced by adipocytes with anti-atherosclerotic and anti-diabetic properties. We previously discovered that adiponectin is specifically localized in the myoepithelial cells of rat sublingual glands. This study aims to investigate the localization of adiponectin and its receptors, AdipoR1 and AdipoR2, in adult rats, postnatally developing rats, and diabetic model rats.METHODSWe examined the localization and expression of adiponectin and its receptors by immunohistochemistry and RT-PCR in the sublingual glands of adult rats and in two diabetic rat models: Streptozotocin (STZ)-treated rats for type 1 diabetes and GK rats for type 2 diabetes.RESULTSIn rat sublingual glands, adiponectin was localized in the cytoplasm of myoepithelial cells, while AdipoR1 and AdipoR2 were localized in the basolateral membrane of mucous acinar cells. In GK rats, there was a significant decrease in the immunoreactivity and mRNA levels of adiponectin, while both AdipoR1 and AdipoR2 expression levels were upregulated. In STZ-treated rats, both adiponectin and its receptors showed reduced expression.CONCLUSIONSAdiponectin acts as a paracrine factor in sublingual myoepithelial cells, influencing salivary secretion through upregulated receptors in acinar cells, particularly in type 2 diabetes. This process is associated with a reduction in myoepithelial adiponectin levels.

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ADIPOR2

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