IL13 _ ALRH Antibody
- Known as:
- IL13 _ ALRH Antibody
- Catalog number:
- 10369-MM02
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Smart Serology
- Gene target:
- IL13 _ ALRH Antibody
Related genes to: IL13 _ ALRH Antibody
- Gene:
- IL13 NIH gene
- Name:
- interleukin 13
- Previous symbol:
- -
- Synonyms:
- P600, IL-13, ALRH, BHR1, MGC116786, MGC116788, MGC116789
- Chromosome:
- 5q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-04-07
- Date modifiied:
- 2016-10-05
- 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: IL13 _ ALRH Antibody
Related articles to: IL13 _ ALRH Antibody
- The failure of therapy in muscle invasive bladder cancer (MIBC) is primarily attributed to tumor heterogeneity and therapy resistance. We propose a novel approach targeting interleukin-13 receptor subunit alpha 2 (IL-13Rα2), which is expressed on bladder cancer (BC) cells but absent in normal urothelial cells. We investigated the therapeutic effects of WPD101a immunotoxin (IL-13-DT390) on IL-13Rα2-expressing BC cells in relation to BC cell phenotype and functional characteristics in vitro using both 2-dimensional (2D) and 3-dimensional (3D) models. Cell phenotype and IL-13Rα2 expression were assessed using flow cytometry, immunofluorescence, and Western blot analysis. The biological effects of WPD101a were evaluated by measuring cell viability and proliferation using the MTT, sulforhodamine B (SRB), CellTiter-Glo and Live/Dead assays. Apoptosis was assessed using Annexin V/propidium iodide (PI) staining, and quantitative reverse transcription polymerase chain reaction (qRT-PCR) analysis of genes expression. We found that the reference BC cell lines TCC-SUP, JMSU-1 and UM-UC-3 express IL-13Rα2 at various level in contrast to RT-4, HCV-29 and 5637 cells. Cells expressing IL-13Rα2 were sensitive to WPD101a at lower concentrations in the 2D model (0.1 ng/mL) compared to the 3D model (1.0 ng/mL). IL-13Rα2-negative cells remain resistant to the immunotoxin. WPD101a induces apoptosis in BC cells expressing IL-13Rα2 as confirmed by the presence of apoptotic cells, increase the proportion of cells in the subG1 phase, and by the effector , , and initiator , genes expression. This study confirmed receptor-dependent cytotoxic effects of WPD101a and the ability and specificity to inhibit growth and apoptosis induction in MIBC cells expressing IL-13Rα2. - Source: PubMed
Publication date: 2026/06/19
Klimczak AleksandraKrawczenko AgnieszkaStamnitz SandraBielawska-Pohl AleksandraPiotrowska PaulinaGrzelenska HannaWypychowska AleksandraKisielewicz AlicjaMielecki MarcinBorowski RadoslawOlejniczak MariuszPajak-Tarnacka Beata - Glioblastoma (GBM) is the most aggressive primary malignant brain tumor, and while chimeric antigen receptor-T (CAR-T) cell therapy has shown promise, its efficacy remains limited by antigen heterogeneity and immune escape. Here, we investigated the expression of B7 homolog 3 (B7-H3), epidermal growth factor receptor (EGFR), and interleukin-13 receptor alpha 2 (IL-13RA2) in GBM tissues and cell lines. Although all three antigens were highly expressed, sustained exposure to B7-H3 CAR-T cells led to significant B7-H3 downregulation but concurrent EGFR upregulation, revealing a potential immune escape mechanism. To address this heterogeneity, we engineered T cells to express an anti-B7-H3 CAR and secrete an EGFR-targeting bispecific T-cell engager (EGFR-BsTe). These B7-H3-CAR-T-EGFR-BsTe cells exerted dual functionality: direct B7-H3-dependent cytotoxicity and recruitment of unmodified T cells via secreted EGFR-BsTe to eliminate EGFR-expressing tumor cells. Notably, EGFR-BsTe secretion promoted CAR-T cell proliferation and effector differentiation. In orthotopic GBM xenograft models, including mixed tumors with heterogeneous antigen expression, B7-H3-CAR-T-EGFR-BsTe cells demonstrated superior antitumor activity and prolonged survival compared to conventional B7-H3 CAR-T cells. Quantitative analysis revealed that EGFR-BsTe secretion abrogated EGFR upregulation and enhanced B7-H3 downregulation in a target-dependent manner; however, efficacy was diminished when the CAR-Target (B7-H3) was absent on a substantial fraction of tumor cells. Our findings suggest that arming B7-H3 CAR-T cells with EGFR-targeting bispecific engagers represents a promising strategy to overcome antigen heterogeneity and improve therapeutic outcomes for GBM patients. - Source: PubMed
Publication date: 2026/06/16
Zhang ZongliangYang NianZeng HuiChen YongdongLu HuaqingXu LongWang ZengWang GuoqingZhou LiangxueTong Aiping - Diffuse intrinsic pontine glioma (DIPG) is a rare pediatric brain tumor with a critical unmet need due to the lack of approved, curative interventions available. The interweaving of malignant cells with normal tissue makes surgical extraction essentially impossible, and radiation provides only transient benefit. The recent ONC201 FDA approval, however, suggests DIPG therapy is tractable. Having identified overexpression of IL13Rα2 in DIPG tumor tissue versus normal brain tissue, we investigated binding of commercially available IL13Rα2 monoclonal antibodies. The top candidate antibody was used to generate a chimeric antibody, to which we conjugated deruxtecan to create a preclinical therapeutic candidate. - Source: PubMed
Publication date: 2026/05/19
Lian XiaoleiAllanson Victoria JRasmussen Samuel VChauhan ShefaliTan Guak-KimMorrow PaigeHanson KyleLian Emily BingHaight Anthony RHoshino TyujiLiu XianzhiBerlow Noah EKeller CharlesLian Yajun - 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