Subcutaneous T-cell–engaging trispecific antibody that binds BCMA and GPRC5D on myeloma cells and CD3 on T cells, redirecting T-cell cytotoxicity.
Subcutaneous trispecific antibody that binds BCMA and GPRC5D on myeloma cells and CD3 on T cells, bridging them to activate CD3 signaling and redirect T-cell cytotoxicity for targeted lysis of malignant plasma cells.
The trispecific T-cell engager binds BCMA on tumor cells and CD3 on T cells, activating T cells to kill BCMA-positive cells via perforin/granzyme-mediated cytotoxicity.
Bispecific antibody (CD20xCD3 T-cell engager) that redirects CD3+ T cells to kill CD20+ malignant B cells.
Glofitamab is a bispecific antibody that binds CD20 on B cells and CD3 on T cells, bringing them into proximity to form an immune synapse. This redirects and activates CD3+ T cells to kill CD20+ malignant B cells via cytotoxic mechanisms.
The bispecific antibody links CD20 on B cells to CD3 on T cells, forming an immune synapse and activating T cells to kill CD20+ cells via perforin/granzyme-mediated apoptosis.
An autologous anti-CD19 CAR-T cell therapy generated by leukapheresis of patient T cells, CD3/CD28 activation, and lentiviral transduction to express a CD19-specific chimeric antigen receptor; administered after lymphodepleting chemotherapy to target CD19+ B-cell malignancies. Mechanism: CAR binding to CD19 triggers T-cell activation and cytotoxicity, leading to elimination of CD19-positive cells and on-target B-cell aplasia.
Autologous T cells are lentivirally transduced to express a CD19-specific chimeric antigen receptor; CAR engagement of CD19 on B cells triggers T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxicity, eliminating CD19-positive malignant cells and causing on-target B-cell aplasia.
Anti-CD19 CAR-T cells bind CD19 on target cells and induce cytotoxicity via immunologic synapse formation with perforin/granzyme release (and death-receptor signaling), killing CD19-positive cells.
Single intravenous infusion of haploidentical donor-derived CD3+ T cells (CD4+ and CD8+) enriched for cytomegalovirus- and adenovirus-specificity via antigen stimulation and IFN-γ capture; designed to restore antiviral immunity post-transplant by recognizing viral peptides and killing infected cells.
Allogeneic, haploidentical donor-derived virus-specific T cells (CD4+ and CD8+) enriched by antigen stimulation and IFN-γ capture are adoptively transferred to restore antiviral immunity. Their native TCRs recognize CMV and adenovirus peptides presented by HLA on infected cells, leading to activation, IFN-γ secretion, and cytotoxic killing via perforin/granzyme, thereby clearing infected cells without genetic engineering.
Adoptively transferred CMV-specific T cells recognize CMV peptide–HLA complexes via their native TCRs and induce apoptosis of infected cells through perforin/granzyme (and Fas–FasL) cytotoxic pathways.
Single intravenous infusion of haploidentical donor-derived CD3+ T cells (CD4+ and CD8+) enriched for cytomegalovirus- and adenovirus-specificity via antigen stimulation and IFN-γ capture; designed to restore antiviral immunity post-transplant by recognizing viral peptides and killing infected cells.
Allogeneic, haploidentical donor-derived virus-specific T cells (CD4+ and CD8+) enriched by antigen stimulation and IFN-γ capture are adoptively transferred to restore antiviral immunity. Their native TCRs recognize CMV and adenovirus peptides presented by HLA on infected cells, leading to activation, IFN-γ secretion, and cytotoxic killing via perforin/granzyme, thereby clearing infected cells without genetic engineering.
Virus-specific donor T cells recognize adenovirus peptide–HLA complexes via their native TCRs and kill the infected cells through perforin/granzyme-mediated cytolysis (and Fas–FasL apoptosis).