HER2 x IL-13Rα2 x EGFRvIII x EphA2

Last update 01 Nov 2024

Basic Info

Related Targets

HER2IL-13Rα2EGFRvIII[+1]

Drugs associated with HER2 x IL-13Rα2 x EGFRvIII x EphA2

GCK-03

Target

EGFRvIII x EphA2 x HER2 x IL-13Rα2

Mechanism

EGFRvIII antagonists [+3]

Active Org.

Shanghai Jingshan Biotechnology Co., Ltd.

Originator Org.

Shanghai Jingshan Biotechnology Co., Ltd.

Active Indication

Glioblastoma

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with HER2 x IL-13Rα2 x EGFRvIII x EphA2

100 Translational Medicine associated with HER2 x IL-13Rα2 x EGFRvIII x EphA2

0 Patents (Medical) associated with HER2 x IL-13Rα2 x EGFRvIII x EphA2

Literatures (Medical) associated with HER2 x IL-13Rα2 x EGFRvIII x EphA2

01 Mar 2013·Molecular TherapyQ1 · MEDICINE

T Cells Redirected to EphA2 for the Immunotherapy of Glioblastoma

Q1 · MEDICINE

Article

Author: Stephen Gottschalk ; Kevin Kh Chow ; Suzanne Zein-Eldin Powell ; Swati Naik ; Sunitha Kakarla ; Zhongzhen Yi ; Meng Fen Wu ; Robert G. Grossman ; Nabil Ahmed ; Donald R. Shaffer ; Yvonne Kew ; Vita S. Brawley ; Nino Rainusso ; Dean Lee ; Hao Liu

Outcomes for patients with glioblastoma (GBM) remain poor despite aggressive multimodal therapy. Immunotherapy with genetically modified T cells expressing chimeric antigen receptors (CARs) targeting interleukin (IL)-13Rα2, epidermal growth factor receptor variant III (EGFRvIII), or human epidermal growth factor receptor 2 (HER2) has shown promise for the treatment of gliomas in preclinical models and in a clinical study (IL-13Rα2). However, targeting IL-13Rα2 and EGFRvIII is associated with the development of antigen loss variants, and there are safety concerns with targeting HER2. Erythropoietin-producing hepatocellular carcinoma A2 (EphA2) has emerged as an attractive target for the immunotherapy of GBM as it is overexpressed in glioma and promotes its malignant phenotype. To generate EphA2-specific T cells, we constructed an EphA2-specific CAR with a CD28-ζ endodomain. EphA2-specific T cells recognized EphA2-positive glioma cells as judged by interferon-γ (IFN-γ) and IL-2 production and tumor cell killing. In addition, EphA2-specific T cells had potent activity against human glioma-initiating cells preventing neurosphere formation and destroying intact neurospheres in coculture assays. Adoptive transfer of EphA2-specific T cells resulted in the regression of glioma xenografts in severe combined immunodeficiency (SCID) mice and a significant survival advantage in comparison to untreated mice and mice treated with nontransduced T cells. Thus, EphA2-specific T-cell immunotherapy may be a promising approach for the treatment of EphA2-positive GBM.

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