Last update 01 Nov 2024

P2Y1

Last update 01 Nov 2024

Basic Info

Synonyms

ADP receptor, P2RY1, P2Y purinoceptor 1

+ [6]

Introduction

Receptor for extracellular adenine nucleotides such as ADP (PubMed:9442040, PubMed:9038354, PubMed:25822790). In platelets, binding to ADP leads to mobilization of intracellular calcium ions via activation of phospholipase C, a change in platelet shape, and ultimately platelet aggregation (PubMed:9442040).

Drugs associated with P2Y1

P2Y1 Antagonist(Bristol Myers Squibb)

Target

P2Y1

Mechanism

P2Y1 antagonists

Active Org.

Bristol Myers Squibb Co.

Originator Org.

Bristol Myers Squibb Co.

Active Indication

Thrombosis

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

MRS 2603

Target

P2Y1 x P2Y13 receptor

Mechanism

P2Y1 antagonists [+1]

Active Org.

Gwangju Institute of Science & Technology

Originator Org.

Gwangju Institute of Science & Technology

Active Indication-

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

BMS-884775

Target

P2Y1

Mechanism

P2Y1 antagonists

Active Org.

Bristol Myers Squibb Co.

Originator Org.

Bristol Myers Squibb Co.

Active Indication

Thrombosis

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with P2Y1

100 Translational Medicine associated with P2Y1

0 Patents (Medical) associated with P2Y1

1,179

Literatures (Medical) associated with P2Y1

01 Feb 2025·Neural Regeneration Research

P2Y1 receptor in Alzheimer’s disease

Article

Author: Luo, Shan ; Wang, Yifei ; Hisatsune, Tatsuhiro

Alzheimer’s disease is the most frequent form of dementia characterized by the deposition of amyloid-beta plaques and neurofibrillary tangles consisting of hyperphosphorylated tau. Targeting amyloid-beta plaques has been a primary direction for developing Alzheimer’s disease treatments in the last decades. However, existing drugs targeting amyloid-beta plaques have not fully yielded the expected results in the clinic, necessitating the exploration of alternative therapeutic strategies. Increasing evidence unravels that astrocyte morphology and function alter in the brain of Alzheimer’s disease patients, with dysregulated astrocytic purinergic receptors, particularly the P2Y1 receptor, all of which constitute the pathophysiology of Alzheimer’s disease. These receptors are not only crucial for maintaining normal astrocyte function but are also highly implicated in neuroinflammation in Alzheimer’s disease. This review delves into recent insights into the association between P2Y1 receptor and Alzheimer’s disease to underscore the potential neuroprotective role of P2Y1 receptor in Alzheimer’s disease by mitigating neuroinflammation, thus offering promising avenues for developing drugs for Alzheimer’s disease and potentially contributing to the development of more effective treatments.

01 Nov 2024·Journal of Neurochemistry

Astrocytic purinergic signalling contributes to the development and maintenance of neuropathic pain via modulation of glutamate release

Article

Author: Liu, Suting ; Ji, Qing ; Tang, Jun ; Zhu, Chao ; Cui, Liying ; Li, Yunzi ; Jin, Li ; Cheng, Hao

AbstractAlthough activation of astrocytes is critical in developing neuropathic pain (NP) following nerve injury, the underlying mechanisms of NP and therapeutic management for NP are still vague. Importantly, the decreases in the levels of astrocytic glutamate transporter‐1 (GLT‐1) in the spinal dorsal horn result in enhanced excitatory transmission and cause persistent pain. P2Y1 purinergic receptor (P2Y1R) has been shown to enhance many inflammatory processes. The up‐regulated expression of astrocytic P2Y1R is crucial to participate in pain transduction under conditions of nerve injury and peripheral inflammation considering that P2Y1R is potentially involved in glutamate release and synaptic transmission. This study indicates that the expression of P2Y1R in the spinal cord was increased accompanied by the activation of A1 phenotype astrocytes in the rat model of spinal nerve ligation (SNL). Astrocyte‐specific knockdown of P2Y1R alleviated SNL‐induced nociceptive responses and mitigated A1 reactive astrocytes, which subsequently increased GLT‐1 expression. Conversely, in naïve rats, P2Y1R over‐expression induced a canonical NP‐like phenotype and spontaneous hypernociceptive responses and increased the concentration of glutamate in the spinal dorsal horn. Besides, our in vitro data showed that the proinflammatory cytokine tumour necrosis factor‐alpha contributes to A1/A2 astrocyte reactivity and Ca2+‐dependent release of glutamate. Conclusively, our results provide novel insights that as a significant regulator of astrocytic A1/A2 polarization and neuroinflammation, P2Y1R may represent a potential target for the treatment of SNL‐induced NP.

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01 Sep 2024·The American Surgeon™

The Impact of ADP Inhibition on Traumatic Brain Injury Outcomes

Article

Author: Briggs, Steven ; Howe, Chase ; Cao, Li ; Mathies, Amanda ; Sang, Tyler ; Nielsen, Dana

Platelet inhibition correlates with severity of traumatic brain injury and may be associated with mortality. Adenosine diphosphate participates in platelet aggregation via the activation of the ADP receptors, P2Y1 and P2Y12. Prior work suggests this ADP pathway is significant in managing patients with head injuries. This study aimed to measure the influence of ADP inhibition on outcomes after a traumatic brain injury (TBI), as measured by thromboelastography with platelet mapping (TEG-PM). Outcomes were defined as (a) hospital length of stay; (b) ICU length of stay, (c) mortality, and (d) progression of hemorrhage on CT. The resulting cohort was split into quartiles to compare the effect of increasingly inhibited ADP values on the identified outcomes. Comparisons of 2 groups of patients were also conducted, one defined by ADP inhibition less than or equal to 60% and the other group by ADP inhibition of greater than 60%. 98 patients were included in final analysis, with 72.4% having ADP inhibition less than 60%. These patients were significantly older and had lower global injury severity scores (ISSs), although their head-specific ISS was equivalent. Compared to the group with ADP inhibition over 60%, there was no significant difference in mortality, hospital or ICU length of stay, or progression of lesion on CT. Patients with ADP less than 60% inhibited had smaller ISS and higher GCS, indicating they were less injured than those with greater ADP inhibition, consistent with prior literature. The equivalent ICU and hospital length of stay and mortality suggests that ADP inhibition plays a smaller role in outcomes. Additional study with a larger sample size and guideline-based assessments is necessary to further define the impact of ADP inhibition and to determine the role of platelet transfusion in this population.

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P2Y1

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