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Last update 08 May 2025

PEAR1

Last update 08 May 2025

Basic Info

Synonyms

FLJ00193, hPEAR1, JEDI

+ [5]

Introduction

Required for SVEP1-mediated platelet activation, via its interaction with SVEP1 and subsequent activation of AKT/mTOR signaling (PubMed:36792666). May be involved in the early stages of hematopoiesis (By similarity).

Drugs associated with PEAR1

Recombinant humanized anti-PEAR1 monoclonal antibody(Shanghai Xunyao)

Target

PEAR1

Mechanism

PEAR1 inhibitors

Active Org.

Shanghai Xunyao Biotechnology Co., Ltd.

Originator Org.

Shanghai Xunyao Biotechnology Co., Ltd.

Active Indication

Idiopathic Pulmonary Fibrosis

Inactive Indication-

Drug Highest PhasePhase 1

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

WO2023001304

Patent Mining

Target

PEAR1

Mechanism-

Active Org.

Shanghai Xunyao Biotechnology Co., Ltd.

Originator Org.

Shanghai Xunyao Biotechnology Co., Ltd.

Active Indication

Infectious Diseases [+2]

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with PEAR1

CTR20234287

/ RecruitingPhase 1

单中心、随机、双盲、单次给药、剂量递增、安慰剂对照设计，评价SV001雾化吸入溶液在中国健康成年受试者中的安全性、耐受性、药代动力学特征和免疫原性的I期临床试验

[Translation] A single-center, randomized, double-blind, single-dose, dose-escalation, placebo-controlled Phase I clinical trial to evaluate the safety, tolerability, pharmacokinetic characteristics and immunogenicity of SV001 nebulized inhalation solution in healthy Chinese adult subjects

评估SV001雾化吸入溶液单次给药在中国健康成年受试者中的安全性和耐受性。

[Translation]

To evaluate the safety and tolerability of a single dose of SV001 nebulized inhalation solution in healthy Chinese adult subjects.

Start Date08 Jan 2024

Sponsor / Collaborator

Shanghai Xunyao Biotechnology Co., Ltd.

ChiCTR2300072620

/ RecruitingPhase 3

A randomized, double-blind, placebo-controlled clinical study for 52 weeks to evaluate the effect of recombinant anti human GLP-1 receptor humanized monoclonal antibody injection on blood glucose fluctuation and bone metabolism in patients with type 2 diabetes

Start Date01 Jul 2023

Sponsor / Collaborator

NanJing First Pharmaceutical Co., Ltd.

100 Clinical Results associated with PEAR1

100 Translational Medicine associated with PEAR1

0 Patents (Medical) associated with PEAR1

116

Literatures (Medical) associated with PEAR1

31 Dec 2025·Hematology

Potential role of hemopexin in venous thromboembolism (VTE) mediated through effects on apoptosis-related proteins

Article

Author: Yu, Xiao-hui ; Tang, Peng ; Liu, Hua-gang ; Zhuang, Jun-li ; Zhou, Jiang-qiao ; Li, Jie ; Deng, Hong-ping ; Zhang, Zhong-jun

OBJECTIVEThe limited understanding of venous thromboembolism (VTE) has hindered the development of novel treatment approaches. This study aimed to identify critical factors underlying VTE.METHODSThe isobaric tags for relative and absolute quantitation (iTRAQ) method was applied to identify differentially expressed proteins in plasma samples from patients with VTE and healthy volunteers. Gene overexpression and knockdown techniques were used for cultured human umbilical vein endothelial cells (HUVECs) and VTE mouse models. Thrombosis and apoptosis related to the identified proteins were verified using qRT-PCR, western blot, and flow cytometry analyses.RESULTSiTRAQ analysis revealed significant upregulation of keratin 1, pro-platelet basic protein, and hemopexin (HPX) in the plasma of VTE patients. HPX was highly expressed in both plasma and GSE19151 and GSE48000 datasets. qRT-PCR and western blot results for HPX overexpressing HUVECs and VTE mouse models revealed that HPX positively regulated the expression of platelet endothelium aggregation receptor 1 and von Willebrand factor, but negatively regulated the expression of serpin family D member 1 and alpha-2-macroglobulin. Flow cytometry revealed that HPX exhibited pro-apoptotic activity in HPX overexpressing HUVECs. Furthermore, HPX elevated cleaved caspase-3 expression and inhibited B-cell lymphoma-2 expression in HUVECs and VTE mouse models.CONCLUSIONHPX exhibits possible prothrombotic activity by regulating thrombosis - apoptosis-related proteins.

04 Apr 2025·Cardiovascular & Hematological Disorders-Drug Targets

The Impact of Single Nucleotide Polymorphisms and Other Mechanisms on Aspirin Resistance

Article

Author: Kurguzov, Aleksei Vitalievich ; Sergeevichev, David Sergeevich ; Nuzhdina, Natalia Sergeevna

Abstract:Atherosclerosis and ischemic events play a pivotal role in the pathogenesis of several cardiovascular diseases (CVD). The primary aim of preventing recurrent thrombosis in patients who underwent cardiovascular surgery is the antiplatelet agent administration. Nevertheless, despite the aspirin therapy or double (aspirin plus clopidogrel) therapy, the effectiveness of antithrombotic treatment remains controversial. In recent years, we have learned that some percentage of patients still demonstrate no clinical response to aspirin treatment and may experience a vascular complication. This article provides an overview of recent scientific studies that have focused on experimental detection and genotyping of single nucleotide polymorphisms (SNPs) in patients, involving the main therapeutic target genes: cyclooxygenase COX-1 and COX-2, guanylate cyclase GUCY1A3, the glycoprotein complex GPIIb-IIIa, and the platelet receptor protein PEAR1." The aspirin resistance (AR) ranges considerably from 0 % to 66% in patients with ischemic heart disease (IHD) and relatively healthy people (control group). SNP distribution analysis has been proposed to explain the inadequate high platelet reactivity (HPR) among patients with IHD under aspirin treatment. Various SNPs have been proposed to explain the development of CVD and the persistent HPR under aspirin treatment widely used in the prevention of recurrent cardiovascular thrombotic events. Meanwhile, the efficacy of aspirin therapy in secondary thrombosis prevention in patients with IHD is not strongly associated with known SNP. The inconsistent results of different AR clinical trials are likely due to the design of the experiments and methodological and quantitative issues; therefore, careful interpretation of the SNP genotyping results is necessary.

01 Apr 2025·World Neurosurgery

Genetically Proxied Antiplatelet Drug Target Perturbation and Risk of Aneurysmal Subarachnoid Hemorrhage: A Mendelian Randomization Analysis

Article

Author: Yang, Cheng-Bin ; Yang, Xu ; Fan, Yu-Xiang ; Ma, Yong-Jie ; Zhang, Hong-Qi ; Song, Zi-Hao

BACKGROUNDThe impact of antiplatelet drugs (APDs) on the rupture risk of unruptured intracranial aneurysms (uIAs) remains controversial. This study aimed to evaluate the causal effects of APDs on aneurysmal subarachnoid hemorrhage (aSAH) and uIA.METHODSA two-sample Mendelian randomization (TSMR) analysis examined associations between genetically proxied platelet reactivity and aSAH. The therapeutic inhibition of platelet aggregation by 5 widely used APDs was proxied by expression quantitative trait loci from eqtlGen consortium and Genotype-Tissue Expression project v8 consortium and protein quantitative trait loci from deCODE database. Causal effects were estimated with summary-data-based MR, TSMR, colocalization analysis, and sensitivity analysis. Mediation MR analysis explored potential pathways.RESULTSThe platelet reactivity was inversely associated with the risk of aSAH, exhibiting no discernible heterogeneity or pleiotropic effects (odds ratio, 0.883; 95% confidential interval, 0.833-0.936; P = 2.67E-05). No causal effects on the aSAH and uIA were observed for the majority of APD target genes by summary-data-based MR, TSMR, and colocalization analysis. However, elevated genetic expression of platelet endothelial aggregation receptor 1 was associated with increased platelet reactivity with an odds ratio of 1.46 (β1=0.375, se=0.072; P = 1.99E-07), and this elevation showed significant inverse association with aSAH risks (β2=-0.125, se=0.030; P = 2.67E-05).CONCLUSIONSThe platelet reactivity was inversely associated with aSAH risk. However, APDs were not identified as either risk or protective agents for aSAH or uIA. Targeting platelet endothelial aggregation receptor 1 might reduce platelet reactivity and increase aSAH risk, highlighting the need for further research.

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PEAR1

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