Autologous gene-modified T-cell therapy expressing a bispecific CAR targeting BCMA (TNFRSF17) and GPRC5D; engagement triggers CD3ζ/costimulatory signaling, T-cell activation, and cytotoxic killing of malignant plasma cells, with dual targeting intended to reduce BCMA antigen escape.
Autologous T cells engineered to express a bispecific chimeric antigen receptor that recognizes BCMA (TNFRSF17) and GPRC5D on malignant plasma cells. Antigen binding triggers CAR CD3z and costimulatory signaling to activate and expand the T cells, leading to cytokine release and perforin/granzyme-mediated cytotoxic killing. Dual targeting is intended to reduce BCMA antigen escape and improve tumor clearance.
CAR recognition of BCMA activates engineered T cells to kill BCMA+ cells via perforin/granzyme-mediated cytolysis (and death-receptor pathways).
Autologous gene-modified T-cell therapy expressing a bispecific CAR targeting BCMA (TNFRSF17) and GPRC5D; engagement triggers CD3ζ/costimulatory signaling, T-cell activation, and cytotoxic killing of malignant plasma cells, with dual targeting intended to reduce BCMA antigen escape.
Autologous T cells engineered to express a bispecific chimeric antigen receptor that recognizes BCMA (TNFRSF17) and GPRC5D on malignant plasma cells. Antigen binding triggers CAR CD3z and costimulatory signaling to activate and expand the T cells, leading to cytokine release and perforin/granzyme-mediated cytotoxic killing. Dual targeting is intended to reduce BCMA antigen escape and improve tumor clearance.
CAR recognition of GPRC5D activates the engineered T cells via CD3ζ/costimulatory signaling, triggering perforin/granzyme (and Fas–FasL)–mediated killing of GPRC5D-expressing cells.
Autologous chimeric antigen receptor T-cell (CAR-T) therapy targeting guanylyl cyclase C (GCC). Patient T cells are engineered to express a GCC-specific CAR and, after intravenous infusion, recognize GCC-positive tumor cells and mediate cytotoxic killing and cytokine release.
Autologous T cells are genetically engineered to express a guanylyl cyclase C (GCC)-specific chimeric antigen receptor. After intravenous infusion, the CAR T cells recognize GCC on tumor cells, become activated, and induce tumor cell lysis through perforin/granzyme-mediated cytotoxicity and cytokine release.
GCC-specific CAR T cells bind GCC on target cells, activate, and kill via perforin/granzyme-mediated cytotoxicity with accompanying cytokine release.
Adoptive γδ T‑cell therapy using Vγ9Vδ2 T cells expanded from healthy donors and administered intraventricularly/intracavitary via an Ommaya reservoir. These innate‑like cytotoxic lymphocytes recognize tumor phosphoantigens via BTN3A1/BTN2A1 independent of MHC, triggering perforin/granzyme‑mediated killing and cytokine release; they can also respond via NKG2D and mediate ADCC.
Allogeneic Vγ9Vδ2 T cells recognize tumor-derived phosphoantigens generated by dysregulated mevalonate metabolism via BTN3A1/BTN2A1 in an MHC-independent manner, triggering perforin/granzyme-mediated cytotoxicity and cytokine release. They also respond to stress ligands through NKG2D and can mediate ADCC.
MICB engages NKG2D on Vγ9Vδ2 T cells, activating them to release perforin/granzymes and kill the target cell.
IV humanized IgG1 monoclonal antibody targeting SLAMF7 (CS1); activates NK cells and mediates Fcγ-dependent ADCC against SLAMF7-positive myeloma cells.
Humanized IgG1 monoclonal antibody targeting SLAMF7 (CS1) that activates NK cells and mediates Fcγ receptor–dependent antibody‑dependent cellular cytotoxicity (ADCC) against SLAMF7‑positive myeloma cells.
Elotuzumab binds SLAMF7 on myeloma cells and its Fc engages Fcγ receptors on NK cells to trigger antibody-dependent cellular cytotoxicity (ADCC); it also activates NK cells via SLAMF7, enhancing lysis of SLAMF7+ target cells.