Ask about this productRelated genes to: IL13RA2 Blocking Peptide
- Gene:
- IL13RA2 NIH gene
- Name:
- interleukin 13 receptor subunit alpha 2
- Previous symbol:
- -
- Synonyms:
- IL-13R, IL13BP, CD213a2, CT19
- Chromosome:
- Xq23
- Locus Type:
- gene with protein product
- Date approved:
- 1998-03-26
- Date modifiied:
- 2015-12-11
Related products to: IL13RA2 Blocking Peptide
Related articles to: IL13RA2 Blocking Peptide
- Atopic dermatitis (AD) is a prevalent chronic inflammatory skin disease. Dupilumab is a new targeted drug used to treat moderate to severe AD. However, some patients with AD exhibit poor response to dupilumab treatment. - Source: PubMed
Publication date: 2026/05/01
Wei Qiu-JuLu Jia-RongXiang Wan-YanLiang Hai-QiZhang Si-QiHuang Si-YuPeng Jun-WenZhou Ze-FengLi Qiu-JuZheng Wen-Jun - Bispecific T cell engagers (BTEs) induce MHC-independent cytotoxicity by bridging T cells to tumor cells via binding a T cell-activating receptor and a tumor-associated antigen. BTEs have proven effective in hematologic malignancies and some solid tumors, yet their potential in glioblastoma (GBM) is largely unexplored. We developed a fully humanized BTE (hBTE) targeting interleukin-13 receptor alpha 2 (IL13RA2), a tumor-associated antigen widely expressed in GBM and associated with poor prognosis. In vitro, hBTE activated T cells and induced antigen-dependent cytokine release and cytotoxicity against IL13RA2-positive GBM cells. In vivo, hBTE showed robust target-specific activity and markedly prolonged survival in primary and recurrent GBM xenograft models, without detectable off-target local or systemic toxicity. Beyond GBM, hBTE also exhibited antitumor activity in IL13RA2-expressing solid tumors, demonstrating selective tumor accumulation and therapeutic efficacy in models of breast cancer brain metastases and extracranial lung cancer. This work highlights the therapeutic potential of BTEs in IL13RA2-expressing tumors and establishes a strong preclinical rationale for advancing hBTE therapy toward clinical translation in GBM and other tumors. - Source: PubMed
Publication date: 2026/04/30
Duffy Joseph TMartin-Regalado AngelaHaupt Benedikt EPogue Jacob RThakur AditiCota Manuel FierroZannikou MarkellaMisener SolKrymskaya Vera PMcCortney KathleenMiska JasonHorbinski CraigSimberg DmitriLesniak Maciej SJames Charles DStupp RogerBalyasnikova Irina V - Progressive IL-13 signaling is closely associated with liver fibrosis. Among fibrotic diseases, liver fibrosis induced by in advanced schistosomiasis is the primary driver of portal hypertension, which is the leading cause of mortality in affected patients. RNA sequencing analysis of human hepatic stellate cells revealed that was markedly upregulated in activated hepatic stellate cells and enriched in the cytokine-receptor interaction pathways, suggesting a potential role for IL-13RA2 in hepatic stellate cell activation and fibrosis progression. Based on these findings, we aimed to investigate whether IL-13RA2 also contributes to liver fibrosis during infection. In this study, we established a murine model of infection. Compared with IL-13RA1, IL-13RA2 expression was significantly increased at week 9 post-infection in mice. IL-13RA2 was enriched within fibrotic regions and increased in parallel with collagen accumulation and stellate cell activation. The phosphorylation levels of MEK and ERK changed in parallel with IL-13RA2 abundance. Furthermore, overexpression of IL-13RA2 markedly accelerated hepatic fibrogenesis, while knockdown of IL-13RA2 attenuated liver fibrosis induced by schistosomiasis the MEK/ERK pathway. Hence, IL-13RA2 may represent an effective and promising therapeutic target for the attenuation of liver fibrosis. - Source: PubMed
Publication date: 2026/04/25
Xiong RuiyanDu JiangyuanYang YuchenZhu YuxiaoNi YangyueChen LinHou MinXu ZhipengChen LuJi Minjun - Glioblastoma (GBM) is characterized by pronounced tumor heterogeneity and a complex immune microenvironment, contributing to poor patient survival outcomes. In this study, we comprehensively dissected the tumor microenvironment (TME) and uncovered potential molecular mechanisms by integrating single-cell, bulk, and spatial transcriptomic data. Hallmarks of malignancy and cell cycle regulatory pathways were consistently enriched across these modalities, promoting tumor cell proliferation and progression. Using machine learning algorithm, we identified seven hallmark-related prognostic signatures (HMsig), namely AEBP1, ASF1A, PRPS1, DCC, OPHN1, IL13RA2, and HDAC5-whose predictive importance was validated through SHAP analysis. Ligand-receptor (LR) interaction analysis further revealed that interactions involving OPHN1 were associated with poorer prognosis. Along the pseudotime trajectory of T-cell differentiation, immune checkpoint genes (ICGs) LAG3, PDCD1, and HAVCR2 were substantially upregulated. Notably, synergistic transcriptional regulation between tumor-related HMsig genes and ICGs in T cells was identified as a key factor influencing patient survival. Spatial transcriptomic analysis demonstrated the existence of synergistic gene interactions, deciphering the immunomodulatory functions of GBM biomarkers within the TME. - Source: PubMed
Publication date: 2026/03/25
Li TengyueMi WanqiYan HuaruiMa YiningJiang HanYang XiaoxuZhang YunpengHu Congxue - Breast cancer (BCa) remains a leading cause of cancer-related deaths in women worldwide. Triple-negative BCa (TNBC) is highly metastatic with treatment limited by off-target toxicity. Cannabidiol (CBD) has anti-cancer and anti-inflammatory activity in BCa. This study addresses the poor oral bioavailability of CBD by utilizing exosomes (Exo) as a drug delivery system. CBD was loaded onto non-functionalized exosomes and folic acid-functionalized exosomes (FA-Exo), achieving an average CBD drug load of ∼20%. The FA-ExoCBD averaged 136 ± 2.9 nm in size. TNBC cell lines MDA-MB-231 and taxol-resistant MDA-MB-231TR were sensitive to growth inhibition by CBD than estrogen receptor positive (ER+) MCF-7 and its taxol-resistant derivative MCF-7TR. Exosomal formulations (ExoCBD and FA-ExoCBD) demonstrated time-dependent CBD release under physiologically relevant simulated gastric and intestinal conditions and withstand acidic conditions, retained canonical exosomal markers (CD81 and Alix) as well as physical parameters of exosomes including size, PDI and zeta potential. CBD downregulated key anti-apoptotic and anti-inflammatory markers. Oral FA-ExoCBD showed enhanced tumor targeting, tumor retention and inhibition of orthotopic MDA-MB-231-tumor growth in NOD Scid mice than ExoCBD or free CBD. RNA-Seq analysis of tumor tissues revealed that both CBD and FA-ExoCBD treatments modulated over 1000 genes, with FA-ExoCBD significantly downregulating IL13RA2 (associated with lung metastasis) and tumor biomarkers TRPM2 and SAMHD1, while upregulating tumor suppressors PRDM1, PCDHGB2, and ICAM1. These findings highlight the potential of FA-ExoCBD to enhance CBD's anticancer efficacy through targeted gene modulation. Overall, FA-ExoCBD improves CBD's therapeutic profile by enhancing efficacy, tumor selectivity, improved bioavailability and anticancer efficacy. - Source: PubMed
Publication date: 2026/03/09
Moholkar Disha NageshKandimalla RaghuramJeyabalan JeyaprakashSinghal RichaMayer KatarinaKlinge Carolyn MGupta Ramesh CAqil Farrukh