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Last update 08 May 2025

FCER1A

Last update 08 May 2025

Basic Info

Synonyms

Fc epsilon receptor Ia, Fc fragment of IgE receptor Ia, Fc fragment of IgE, high affinity I, receptor for; alpha polypeptide

+ [8]

Introduction

High-affinity receptor for immunoglobulin epsilon/IgE. Mediates IgE effector functions in myeloid cells. Upon IgE binding and antigen/allergen cross-linking initiates signaling pathways that lead to myeloid cell activation and differentiation. On mast cells, basophils and eosinophils stimulates the secretion of vasoactive amines, lipid mediators and cytokines that contribute to inflammatory response, tissue remodeling and cytotoxicity against microbes. Triggers the immediate hypersensitivity response to allergens as a host defense mechanism against helminth parasites, pathogenic bacteria and venom toxicity. When dysregulated, it can elicit harmful life-threatening allergic and anaphylactic reactions.

Drugs associated with FCER1A

Benzylpenicilloyl Polylysine

Target

FCER1A

Mechanism

FCER1A agonists

Active Org.

AllerQuest LLC

Originator Org.

AllerQuest LLC

Active Indication

Hypersensitivity

Inactive Indication-

Drug Highest PhaseApproved

First Approval Ctry. / Loc.

United States

First Approval Date25 Jul 1974

Lesigercept

Target

FCER1A

Mechanism

FCER1A antagonists

Active Org.

Yuhan Corp.

Originator Org.

GI Innovation, Inc.

Active Indication

Chronic Urticaria [+1]

Inactive Indication-

Drug Highest PhasePhase 1

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Anti-Her2-FCεRI antibody fusion proteins (Tianchen Biomedical)

Target

FCER1A x HER2

Mechanism

FCER1A antagonists [+1]

Active Org.

Tianchen Biomedical (Suzhou) Co., Ltd.

Originator Org.

Tianchen Biomedical (Suzhou) Co., Ltd.

Active Indication

Neoplasms

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with FCER1A

NCT06406114

/ Not yet recruitingPhase 2IIT

Optimizing the Diagnostic Approach to Cephalosporin Allergy Testing

Cephalosporin antibiotics are commonly used but can result in allergic reactions and anaphylaxis. There is no clear diagnostic approach for cephalosporin-allergic patients, and guidance for the use of other antibiotics in allergic patients is based on side chain chemical similarity and limited skin testing evidence. This project includes a clinical trial and mechanistic studies to optimize the approach to cephalosporin allergy and advance future diagnostics.

Start Date15 Apr 2025

Sponsor / Collaborator

The General Hospital Corp.

[+1]

NCT05960708

/ CompletedPhase 1

A Randomized, Double-Blind, Placebo/Active Controlled, Single Dose, Phase 1 Study to Evaluate the Safety, Tolerability, Pharmacokinetics and Pharmacodynamics Following Subcutaneous Injections of YH35324 in Patients with Various Allergic Diseases

This study aims to evaluate the safety, tolerability, pharmacokinetics (PK), and pharmacodynamics (PD) following a single subcutaneous injection of YH35324 in subjects with various allergic diseases.

Start Date23 Aug 2023

Sponsor / Collaborator

Yuhan Corp.

NCT05564221

/ CompletedPhase 1

A Randomized, Double-Blind, Placebo/Active Controlled, Multiple Ascending Dose, Phase 1b Study to Evaluate the Safety, Tolerability, Pharmacokinetics and Pharmacodynamics Following Subcutaneous Injections of YH35324 in Atopic Healthy Subjects or Subjects With Allergic Diseases

This study aims to evaluate the safety, tolerability, pharmacokinetic (PK) and pharmacodynamic (PD) profiles following multiple subcutaneous injections of YH35324 in healthy subjects or subjects with allergic diseases, who have atopy.

Start Date01 Nov 2022

Sponsor / Collaborator

Yuhan Corp.

100 Clinical Results associated with FCER1A

100 Translational Medicine associated with FCER1A

0 Patents (Medical) associated with FCER1A

723

Literatures (Medical) associated with FCER1A

31 Dec 2025·Human Vaccines & Immunotherapeutics

Drug survival of omalizumab in atopic asthma: Impact of clinical and genetic variables

Article

Author: Pineda-Lancheros, Laura E ; Morales-García, Concepción ; Caballero-Vázquez, Alberto ; Jiménez-Morales, Alberto ; Sánchez-Martínez, José A ; González-Gutiérrez, María V ; Jiménez-Gálvez, Gonzalo ; Rojo-Tolosa, Susana

It is estimated that 40-50% of severe asthma has an atopic basis, representing a clinical challenge and a significant economic burden for healthcare systems. The most effective treatment has emerged with the use of biologic therapies such as omalizumab; however, the rate of therapy switching due to loss of efficacy is high, which has a negative impact on the healthcare system. The aim was to evaluate the influence of genetic polymorphisms as predictors of omalizumab survival. We conducted a retrospective observational cohort study of 110 patients with uncontrolled severe allergic asthma treated with omalizumab in a tertiary hospital. We analyzed FCER1A (rs2251746, rs2427837), FCER1B (rs1441586, rs573790, rs1054485, rs569108), C3 (rs2230199), FCGR2A (rs1801274), FCGR2B (rs3219018, rs1050501), FCGR3A (rs10127939, rs396991), IL1RL1 (rs1420101, rs17026974, rs1921622) and GATA2 (rs4857855) by real-time PCR using Taqman probes. Drug survival was defined as the time from initiation to discontinuation of omalizumab. Cox regression analysis adjusted for the presence of respiratory disease, GERD, SAHS and years with asthma showed that the SNPs FCER1B rs573790 - CT (p < .001; HR = 3.38; CI95% = 1.66-6.87), FCGR3A rs10127939-AC (p = .018; HR = 3.85; CI95% = 1.25-11.81) and FCGR3A rs396991-CC (p = .020; HR = 2.23; CI95% = 1.14-4.38) were the independent variables associated with worse survival in patients diagnosed with asthma. A trend toward statistical significance was also found between and FCGR3A rs10127939-CC (p = .080; HR = 0.13; CI95% = 0.01-1.28) and longer drug survival. The results of this study demonstrate the potential influence of the polymorphisms studied on omalizumab survival and the clinical benefit that could be achieved by defining predictive biomarkers of drug survival.

01 Apr 2025·Allergology International

Elevated MS4A2 and IgE interaction in nasal polyps contributing to poor postoperative prognosis in patients with eosinophilic chronic rhinosinusitis

Article

Author: Hatano, Akihiro ; Okada, Naoko ; Yoshikawa, Mamoru ; Inoue, Natsuki ; Yamaguchi, Sota ; Inoue, Hiroko ; Nakano, Mika

BACKGROUNDChronic rhinosinusitis (CRS) is a persistent inflammatory disease of various endotypes, including eosinophilic CRS (eCRS), which is characterized by marked eosinophilic infiltration and high refractory rates despite treatment. Recent findings suggest the interaction between local IgE and mast cells in nasal polyps (NPs) is key to eCRS pathogenesis; however, the details remain unclear. This study investigated the involvement of MS4A2, a component of the IgE receptor, in the pathogenesis of refractory eCRS.METHODSNP tissue samples were collected from 47 patients with eCRS who underwent sinus surgery and classified into refractory and nonrefractory groups based on postoperative outcomes. Quantitative PCR was used to analyze the mRNA expression of IgE receptor components (MS4A2, FCER1A, and FCER1G) and cell-specific markers (CLC, TPSAB1, and GPR56) in NP tissues. Immunofluorescence staining was used to confirm MS4A2 expression and colocalization with tryptase, ProMBP1, and IgE. ROC analysis was conducted to assess MS4A2 mRNA levels as a predictor of refractory eCRS.RESULTSMS4A2 mRNA expression was significantly elevated in the refractory group, whereas FCER1A and FCER1G mRNA expression levels showed no significant differences. Immunofluorescence revealed an increased number of MS4A2-positive cells, particularly those colocalized with tryptase-positive mast cells, in the refractory group. Cells coexpressing MS4A2 and IgE were more prevalent in this group. ROC analysis indicated that MS4A2 mRNA expression can predict prognosis with high specificity.CONCLUSIONSOur findings suggest the significance of the interaction between MS4A2-expressing mast cells and local IgE in the pathogenesis of refractory eCRS, highlighting MS4A2 as a potential therapeutic target.

04 Mar 2025·Journal of Asthma

Assessing prospective molecular biomarkers and functional pathways in severe asthma based on a machine learning method and bioinformatics analyses

Article

Author: Tang, Bin-Qing ; Zhang, Wei ; Zhang, Ya-Da ; Chen, Yi-Ren

BACKGROUNDSevere asthma, which differs significantly from typical asthma, involves specific molecular biomarkers that enhance our understanding and diagnostic capabilities. The objective of this study is to assess the biological processes underlying severe asthma and to detect key molecular biomarkers.METHODSWe used Weighted Gene Co-Expression Network Analysis (WGCNA) to detect hub genes in the GSE143303 dataset and indicated their functions and regulatory mechanisms using Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis and Gene Ontology (GO) annotations. In the GSE147878 dataset, we used Gene Set Enrichment Analysis (GSEA) to determine the regulatory directions of gene sets. We detected differentially expressed genes in the GSE143303 and GSE64913 datasets, constructed a Least Absolute Shrinkage and Selection Operator (LASSO) regression model, and validated the model using the GSE147878 dataset and real-time quantitative PCR (RT-qPCR) to confirm the molecular biomarkers.RESULTSUsing WGCNA, we discovered modules that were strongly correlated with clinical features, specifically the purple module (r = 0.53) and the midnight blue module (r = -0.65). The hub genes within these modules were enriched in pathways related to mitochondrial function and oxidative phosphorylation. GSEA in the GSE147878 dataset revealed significant enrichment of upregulated gene sets associated with oxidative phosphorylation and downregulated gene sets related to asthma. We discovered 12 commonly regulated genes in the GSE143303 and GSE64913 datasets and developed a LASSO regression model. The model corresponding to lambda.min selected nine genes, including TFCP2L1, KRT6A, FCER1A, and CCL5, which demonstrated predictive value. These genes were significantly upregulated or under expressed in severe asthma, as validated by RT-qPCR.CONCLUSIONMitochondrial abnormalities affecting oxidative phosphorylation play a critical role in severe asthma. Key molecular biomarkers like TFCP2L1, KRT6A, FCER1A, and CCL5, are essential for detecting severe asthma. This research significantly enhances the understanding and diagnosis of severe asthma.

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FCER1A

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