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Last update 08 May 2025

P2Y6 receptor

Last update 08 May 2025

Basic Info

Synonyms

P2RY6, P2Y purinoceptor 6, P2Y6

+ [2]

Introduction

Receptor for extracellular UDP > UTP > ATP. The activity of this receptor is mediated by G proteins which activate a phosphatidylinositol-calcium second messenger system.

Drugs associated with P2Y6 receptor

GC-021109

Target

P2Y6 receptor

Mechanism

P2Y6 receptor agonists

Active Org.

Gliacure, Inc. [+1]

Originator Org.

Tufts University

Active Indication

Alzheimer Disease [+1]

Inactive Indication-

Drug Highest PhasePhase 1

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

TG-46

Target

P2Y6 receptor

Mechanism

P2Y6 receptor agonists

Active Org.

Glaucopharm Ltd.

Originator Org.

Glaucopharm Ltd.

Active Indication

Glaucoma

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

P2Y6 receptor agonists(Bar-Ilan University)

Target

P2Y6 receptor

Mechanism

P2Y6 receptor agonists

Active Org.-

Originator Org.

Bar-Ilan University

Active Indication-

Inactive Indication-

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with P2Y6 receptor

NCT02386306

/ CompletedPhase 1

A Randomized, Double-Blind, Placebo-Controlled; Phase 1b, Safety, Tolerability, and Pharmacokinetic Study of Multiple Ascending Doses of GC021109 in Subjects With Mild to Moderate Alzheimer's Disease

This is a Phase 1b, multi-center, randomized, double-blind, placebo-controlled study designed to evaluate the safety, tolerability, and pharmacokinetics of GC021109 in subjects with mild to moderate Alzheimer's Disease (as determined by 2011 National Institute on Aging- Alzheimer's Association [NIA-AA] criteria and Mini Mental State Examination [MMSE]). The Investigator, study site staff, (with exception of a designated pharmacist/pharmacy technician) and all study subjects will be blinded to randomized study medication assignment until database lock. Treatment assignments may be unblinded for select pre-authorized individuals involved in the safety and PK data reviews in order to accurately determine how to proceed with dose escalation.

Start Date01 Feb 2015

Sponsor / Collaborator

Gliacure, Inc.

NCT02254369

/ CompletedPhase 1

A Randomized, Phase 1, Double-Blind, Placebo-Controlled, First-in-Human, Safety, Tolerability, and Pharmacokinetic Study of Single Ascending Doses of GC021109 in Healthy Subjects

The primary objective of the study is to assess the safety and tolerability of single oral doses of GC021109 when administered to healthy adult subjects.

Start Date01 Sep 2014

Sponsor / Collaborator

Gliacure, Inc.

100 Clinical Results associated with P2Y6 receptor

100 Translational Medicine associated with P2Y6 receptor

0 Patents (Medical) associated with P2Y6 receptor

329

Literatures (Medical) associated with P2Y6 receptor

01 Jul 2025·European Journal of Pharmacology

P2Y6 receptor: A promising therapeutic target for atherosclerosis

Review

Author: Zhang, Tingyu ; Lai, Liting ; Qiu, Dan ; Li, Lixia ; Wang, Shuzhi ; Ding, Yang ; Yu, Meiling ; Wang, Zongbao

Atherosclerosis is induced by lipid accumulation, inflammation, and endothelial dysfunction, and is the leading cause of death from cardiovascular disease worldwide. The P2Y₆ receptor can be activated by the extracellular release of UDP. The evidence from the last decade has highlighted its critical therapeutic effect in atherosclerosis, yet with unclear mechanisms. This review introduced the P2Y₆ receptor in atherosclerosis, and its mechanisms of atherosclerosis-promoting in macrophages, endothelial cells, and vascular smooth muscle cells. Finally, we discussed the development and potential of P2Y₆ receptor antagonists in treating atherosclerosis.

01 Feb 2025·Purinergic Signalling

Purinergic signaling in liver disease: calcium signaling and induction of inflammation

Review

Author: Ulrich, Henning ; Thomas, Andrew P ; Glaser, Talita

Purinergic signaling regulates many metabolic functions and is implicated in liver physiology and pathophysiology. Liver functionality is modulated by ionotropic P2X and metabotropic P2Y receptors, specifically P2Y1, P2Y2, and P2Y6 subtypes, which physiologically exert their influence through calcium signaling, a key second messenger controlling glucose and fat metabolism in hepatocytes. Purinergic receptors, acting through calcium signaling, play an important role in a range of liver diseases. Ionotropic P2X receptors, such as the P2X7 subtype, and certain metabotropic P2Y receptors can induce aberrant intracellular calcium transients that impact normal hepatocyte function and initiate the activation of other liver cell types, including Kupffer and stellate cells. These P2Y- and P2X-dependent intracellular calcium increases are particularly relevant in hepatic disease states, where stellate and Kupffer cells respond with innate immune reactions to challenges, such as excess fat accumulation, chronic alcohol abuse, or infections, and can eventually lead to liver fibrosis. This review explores the consequences of excessive extracellular ATP accumulation, triggering calcium influx through P2X4 and P2X7 receptors, inflammasome activation, and programmed cell death. In addition, P2Y2 receptors contribute to hepatic steatosis and insulin resistance, while inhibiting the expression of P2Y6 receptors can alleviate alcoholic liver steatosis. Adenosine receptors may also contribute to fibrosis through extracellular matrix production by fibroblasts. Thus, pharmacological modulation of P1 and P2 receptors and downstream calcium signaling may open novel therapeutic avenues.

01 Jan 2025·Cancer Science

P2RY6 deletion promotes UVB‐induced skin carcinogenesis by activating the PI3K/AKT signal pathway

Article

Author: Shi, Yuling ; Yang, Zile ; Gao, Xiaoxuan ; Dang, Yongyan ; Zang, Kai ; Liu, Tanglin ; Ye, Xiyun ; Xu, Peng

AbstractOur previous research has demonstrated that P2RY6 functions as an oncogene in DMBA/TPA‐induced two‐stage chemical skin carcinogenesis in mice. However, considering that human skin cancer is predominantly attributed to UV radiation from sunlight, additional investigations are needed to elucidate the role of P2RY6 in UVB‐induced skin carcinogenesis. Surprisingly, we found that P2ry6‐deficient mice exhibited marked promotion to UVB‐induced skin papilloma formation compared with wild‐type mice, suggesting its tumor‐suppressive role in UVB‐induced skin cancer. Additionally, a P2ry6 gene knockout promoted skin hyperplasia induced by short‐term UVB irradiation, while UDP, the ligand of P2RY6, could inhibit the short‐term UVB‐induced increase of epiderma thickness in mouse skin. Furthermore, UVB irradiation could significantly upregulate P2RY6 expression in human and mouse skin cells. These results indicated that P2RY6 may play a crucial protective role in resisting the UVB‐induced formation of skin tumors. At the molecular level, the loss of the P2RY6 gene inhibits the ubiquitination modification and expression of XPC after UVB irradiation in skin keratinocytes, resulting in the accumulation of CPDs (cyclobutane pyrimidine dimers). We have also demonstrated that P2RY6 deletion activates the PI3K/AKT signaling pathway both in vitro and in vivo. The CPD accumulation and acute inflammatory response enhanced by the loss of the P2RY6 gene can be reversed by an AKT inhibitor. These findings suggest that P2RY6 may act as a tumor suppressor in UVB‐induced skin cancer by regulating the PI3K/AKT signaling pathway.

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P2Y6 receptor

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