A subcutaneous GPRC5D×CD3 bispecific T‑cell–engaging monoclonal antibody that redirects T cells to kill malignant plasma cells in multiple myeloma.
Humanized CD3×GPRC5D bispecific antibody that binds CD3 on T cells and GPRC5D on malignant plasma cells, crosslinking them to form an immune synapse, activate TCR/CD3 signaling and cytokine release, and drive cytotoxic T‑cell–mediated killing of GPRC5D‑expressing myeloma cells (with limited expression on normal tissues).
Talquetamab links CD3 on T cells to GPRC5D on target cells, forming an immune synapse and activating T-cell cytotoxicity (perforin/granzyme, Fas–FasL) to kill GPRC5D-expressing cells.
An autologous BCMA‑directed CAR T‑cell therapy (ide‑cel) in which patient T cells are genetically modified to express an anti‑BCMA chimeric antigen receptor to induce cytotoxicity against myeloma cells.
Autologous T cells are genetically engineered to express a BCMA‑specific chimeric antigen receptor. Upon binding BCMA on malignant plasma cells, CAR signaling activates T‑cell proliferation, cytokine release, and perforin/granzyme‑mediated cytotoxicity, leading to selective killing of BCMA‑expressing myeloma cells.
BCMA-directed CAR T cells bind BCMA on target cells and directly kill them via T-cell effector mechanisms (perforin/granzyme release and apoptosis).
Autologous, lentivirally transduced CAR T-cell therapy for glioblastoma. The CAR (CARv3) targets EGFRvIII on tumor cells and the engineered T cells secrete TEAM-E, an EGFR×CD3 bispecific T-cell–engaging antibody that recruits and activates endogenous T cells against EGFR/EGFR-amplified tumor cells. Administered intraventricularly via an Ommaya reservoir.
Autologous lentivirally transduced CAR T cells that recognize EGFRvIII on glioblastoma cells to mediate targeted T-cell cytotoxicity; the engineered cells also secrete TEAM-E, an EGFR×CD3 bispecific T-cell–engaging antibody that recruits and activates endogenous T cells against EGFR/EGFR-amplified tumor cells, broadening tumor targeting and reducing antigen escape.
CARv3 T cells bind EGFRvIII on tumor cells, form an immunologic synapse, and kill via T‑cell cytotoxic mechanisms (perforin/granzyme and apoptosis pathways).
Autologous, lentivirally transduced CAR T-cell therapy for glioblastoma. The CAR (CARv3) targets EGFRvIII on tumor cells and the engineered T cells secrete TEAM-E, an EGFR×CD3 bispecific T-cell–engaging antibody that recruits and activates endogenous T cells against EGFR/EGFR-amplified tumor cells. Administered intraventricularly via an Ommaya reservoir.
Autologous lentivirally transduced CAR T cells that recognize EGFRvIII on glioblastoma cells to mediate targeted T-cell cytotoxicity; the engineered cells also secrete TEAM-E, an EGFR×CD3 bispecific T-cell–engaging antibody that recruits and activates endogenous T cells against EGFR/EGFR-amplified tumor cells, broadening tumor targeting and reducing antigen escape.
The engineered T cells secrete an EGFR×CD3 bispecific (TEAM-E) that binds EGFR on tumor cells and CD3 on T cells, recruiting and activating T cells to kill EGFR+ cells via perforin/granzyme (and Fas/FasL) cytotoxicity.
Autologous T cells engineered with a chimeric antigen receptor targeting Cadherin 17 (CDH17); infused IV after lymphodepletion to induce targeted cytotoxicity against CDH17-positive gastrointestinal tumors.
Autologous T cells are engineered ex vivo to express a chimeric antigen receptor that recognizes Cadherin 17 (CDH17). Upon binding CDH17 on tumor cells, the CAR triggers T‑cell activation, cytokine release, proliferation, and perforin/granzyme-mediated cytotoxicity independent of the native TCR, leading to targeted killing of CDH17-positive gastrointestinal tumors; lymphodepletion is used to enhance expansion and persistence.
CAR-T cells bind CDH17 on target cells and induce T‑cell–mediated cytotoxicity via perforin/granzyme release (and Fas–FasL apoptosis), leading to direct lysis of CDH17-positive cells.