EphA3 antibody
- Known as:
- EphA3 (anti-)
- Catalog number:
- orb100577
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- EphA3 antibody
Related genes to: EphA3 antibody
- Gene:
- EPHA3 NIH gene
- Name:
- EPH receptor A3
- Previous symbol:
- ETK, ETK1, TYRO4
- Synonyms:
- HEK, HEK4
- Chromosome:
- 3p11.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-06-23
- Date modifiied:
- 2016-10-05
Related products to: EphA3 antibody
Related articles to: EphA3 antibody
- Adoptive cellular therapies may expand treatment options for pediatric brain tumors by focusing activity on tumor antigens and limiting off-tumor effects. We systematically reviewed preclinical and clinical evidence for CAR T cells, TCR-engineered T cells, and NK or γδ T-cell platforms directed against HER2, B7-H3 (CD276), EGFR806-reactive EGFR, GD2, IL13Rα2, and EphA2 or EphA3, with attention to delivery route, safety, persistence, and combination strategies. Following PRISMA, we searched PubMed, Embase, and Scopus from inception through September 17, 2025, restricted to English. The search yielded 324 records; 103 duplicates were removed; 221 titles and abstracts were screened; 180 full texts were reviewed; and 34 studies were extracted by two independent reviewers. We captured design, tumor and molecular features, product engineering, route and schedule, lymphodepletion, toxicities including cytokine release syndrome, immune effector cell associated neurotoxicity, and tumor inflammation associated neurotoxicity, radiographic or clinical response, survival, and correlatives such as persistence or trafficking in blood, cerebrospinal fluid, or tumor tissue, cytokines, and antigen dynamics. In vivo studies showed reproducible antitumor activity for HER2 in medulloblastoma, GD2 in diffuse midline glioma, and multi-antigen constructs incorporating IL13Rα2 and EphA2 in medulloblastoma and ependymoma, with significant survival advantages compared with controls. γδ T cells targeting the EphA axis selectively killed medulloblastoma with neural sparing; GD2 CAR NK-92 inhibited diffuse intrinsic pontine glioma growth. In early clinical programs, route shaped safety and pharmacodynamics. For GD2, low-dose intravenous induction followed by repeated intraventricular dosing produced objective radiographic regressions and manageable tumor inflammation associated neurotoxicity, while dose-limiting cytokine release syndrome was confined to higher intravenous doses. Intraventricular B7-H3 CAR T cells, given without lymphodepletion, enabled multi-cycle dosing with mainly grade 1 to 2 events and cerebrospinal fluid localized persistence. Weekly intracranial EGFR806 CAR T cells were feasible and well tolerated, with stable disease as the best response in a small cohort. Across trials, persistence and immune activation were most evident in cerebrospinal fluid, supporting cerebrospinal fluid centered pharmacodynamic monitoring. Mechanism-based combinations, including IGF-axis inhibition in diffuse midline glioma and epigenetic priming of GD2 with an integrated safety switch in medulloblastoma, enhanced activity. The evidence supports pediatric-centric antigen selection and a CNS-first, locoregional dosing approach to increase on-tumor exposure and reduce systemic toxicity. Priorities include multi-antigen strategies to prevent escape, incorporation of safety switches, earlier deployment when tumor burden is low, and prospective cerebrospinal fluid pharmacodynamics in multisite phase II studies. - Source: PubMed
Publication date: 2026/08/07
Carrion Yaxel LevinBhasin JayantAnne SraavyaSawhney ArmanHa Caryn JSharaf IbraheemSantana JacobTitkov KevinJean MarvensThibault DrewPando AlejandroNovakovic NemanjaParikh Nehal SVojnic MoranaSherman Jonathan H - In this study, we evaluated the in silico and in vitro anticancer activity of the antimicrobial peptide epinecidin-1 (Epi-1) and its lysine-substituted variants (Variant-1 (Var-1) & Variant-2 (Var-2)). Computational docking demonstrated energetically favourable and structurally consistent interactions between the peptides and cancer-associated receptors (MerTK (PDB ID: 7OLX), EphA3 (PDB ID: 2QO9), TGF-β receptor I/ ALK5 (PDB ID: 3TZM), TrkA / NTRK1 (PDB ID: 4AOJ), and progesterone receptor (PDB ID: 1A28)), with distinct binding orientations and interaction profiles observed across the variants. Molecular dynamics simulation further substantiated these findings by confirming the stability of the selected receptor-ligand complex, with consistent root mean square deviation (RMSD), root mean square fluctuation (RMSF), radius of gyration (Rg), solvent-accessible surface area (SASA), and intermolecular hydrogen-bond interactions profiles indicating sustained interaction integrity under dynamic conditions. The in vitro antiproliferative activity of Epi-1 and its variants was assessed by MTT assays against A549, HeLa, HepG2, IMR-32 and MCF-7 cell lines. Both variants exhibited a two- to four-fold increase in cytotoxic activity compared with native Epi-1. We also evaluated the combinational activity of each peptide with doxorubicin, where peptide-doxorubicin treatments resulted in effective cancer cell killing at reduced drug concentrations relative to individual treatments, the Var-2 + doxorubicin combination reduced cancer cell survival to below 10% at a combined concentration of 1 µg/mL (0.5 µg/mL peptide + 0.5 µg/mL doxorubicin), compared with ~ 30% survival in doxorubicin alone. This has been added alongside the existing two- to four-fold cytotoxicity enhancement of the variants over wild-type Epi-1, to better convey the impact of the synergistic response. While inducing selective lysis in cancer cells, the peptides exhibited minimal cytotoxicity toward non-cancerous HEK 293 cells, indicating improved therapeutic selectivity. DCFH-DA staining confirmed intracellular reactive oxygen species generation, and Acridine Orange/Ethidium Bromide (AO/EtBr) staining demonstrated apoptosis as the predominant mode of cell death across the cancer cell lines, although Var-1 induced necrotic death in HepG2 cells. - Source: PubMed
Publication date: 2026/07/22
Jeyarajan SivakumarRanjith SukumarAnbarasu AtchyasriKandasamy IndiraChidambaram PrahalathanKumarasamy Anbarasu - The metabolic reprogramming of tumor microenvironment is a critical driver of colorectal cancer (CRC) pathogenesis. In this context, dysregulated lactate metabolism plays a pivotal role in immunosuppression and therapeutic resistance. Integrating single-cell transcriptomics, spatial transcriptomics, and bulk sequencing datasets, this research delineated the lactate metabolic landscape across colorectal cancer (CRC) tumor ecosystems. Single-cell profiling revealed significant metabolic activity in both the epithelial and myeloid compartments. Consequently, a lactate metabolism score (LMscore) was developed, which is based on four core genes (COX15, SLC25A13, COX10, MPC1). An elevated LMscore has been demonstrated to reprogram epithelial developmental trajectories and reconfigure intercellular communication networks, notably through EFNA1-EPHA3-mediated crosstalk with fibroblasts and endothelial cells. Spatial transcriptomics corroborated intimate spatial colocalization and metabolic pathway co-enrichment between lactate-active epithelia and fibroblasts. Clinically, high LMscore independently predicts a decreased overall survival across multiple cohorts and defines a "cold" tumor immune phenotype. This phenotype is characterized by an accumulation of immunosuppressive cells including M2 macrophages and cancer-associated fibroblasts (CAFs) and a reduction in effector T-cell infiltration. This ultimately results in a refractory response to immune checkpoint blockade. Mechanistically, COX15 emerges as a central regulator of lactate metabolic dysregulation, coinciding with fibroblast-derived TGF-β secretion and immunosuppressive niche formation. Functional validation confirms that COX15 targeting suppresses tumor proliferation. This work establishes LMscore as a clinically robust biomarker for prognostication and immunotherapy response prediction, thereby providing a mechanistic foundation for metabolic reprogramming-targeted combinatorial therapies in CRC. - Source: PubMed
Publication date: 2026/06/19
Lan HaishengLi YangLi HuaGuo JunyuWang CunchuanTang Qianli - To undertake a Phase 1 and Biodistribution study of the EphA3 antibody ifabotuzumab, and its zirconium labelled derivative 89Zr-ifabotuzumab, in glioblastoma patients. - Source: PubMed
Publication date: 2026/06/10
Gan Hui KCher LawrenceInglis Po-LingLwin ZarnieGunjur AshrayBalasubramanian AdiSchmidt AndrewWichmann Christian WGuo NancyLee Sze TingThomas PaulScott Fiona EShard ChloeFluck KateCoombs NicolePalmer JodieVail Mary EAllen StaceyPatil AshwiniPal BhupinderO'Keefe Graeme JGong Sylvia JNinatti GaiaDay Bryan WGomez Guillermo AJanes Peter WScott Andrew M - Degenerative temporomandibular joint diseases (TMJ-DJD) are increasingly affecting elderly populations, with aging being a significant risk factor driving the TMJ degenerative changes. This study aims to explore the shared characteristics between aging and TMJ degenerative diseases at the tissue level, and to identify aging-related signature genes in TMJ degenerations using bioinformatics approaches. - Source: PubMed
Publication date: 2026/06/09
Wang XinyiXia ZiyangZhou YanzhangWang MindaJiang TingYang Jingwen