A bispecific T-cell–engaging antibody (PF-06863135) targeting BCMA on myeloma cells and CD3 on T cells to redirect T-cell cytotoxicity against BCMA-positive cells.
Elranatamab is a bispecific antibody that binds BCMA on malignant plasma cells and CD3 on T cells, cross-linking them to form an immune synapse and activate cytotoxic T-cell killing of BCMA-positive myeloma cells.
NO
INDIRECT
Elranatamab binds CD3ε on T cells to recruit/activate them; these T cells then kill BCMA-positive myeloma cells via immune synapse–mediated perforin/granzyme cytotoxicity.
Autologous T cells genetically engineered to express chimeric antigen receptors that recognize CLL1 (CLEC12A) and CD38 on AML cells, enabling antigen-dependent T-cell activation and cytotoxic killing independent of the native TCR; designed to broaden AML coverage and reduce antigen escape.
Autologous T cells are genetically engineered to express chimeric antigen receptors that recognize CLL1 (CLEC12A) and CD38 on AML cells. Antigen binding triggers CAR signaling (CD3ζ with costimulatory domains) independent of the native TCR, leading to T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of AML blasts and leukemic stem/progenitor cells. Dual targeting is intended to broaden AML coverage and reduce antigen escape.
YES
DIRECT
CAR-T cells recognize CLL1 on target cells, triggering CAR signaling and T‑cell effector functions that lyse the cells via perforin/granzyme-mediated cytotoxicity (and Fas/FasL pathways).
Autologous T cells genetically engineered to express chimeric antigen receptors that recognize CLL1 (CLEC12A) and CD38 on AML cells, enabling antigen-dependent T-cell activation and cytotoxic killing independent of the native TCR; designed to broaden AML coverage and reduce antigen escape.
Autologous T cells are genetically engineered to express chimeric antigen receptors that recognize CLL1 (CLEC12A) and CD38 on AML cells. Antigen binding triggers CAR signaling (CD3ζ with costimulatory domains) independent of the native TCR, leading to T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of AML blasts and leukemic stem/progenitor cells. Dual targeting is intended to broaden AML coverage and reduce antigen escape.
YES
DIRECT
CAR-T cells bind CD38 via the CAR, triggering T-cell activation and perforin/granzyme-mediated killing (and death receptor pathways) of CD38+ cells.
Autologous genetically engineered TCR-T cell product; patient T cells are transduced with a TCR recognizing the KRAS G12V neoepitope presented by HLA-A*11:01 to mediate MHC class I–restricted cytotoxic killing of KRAS G12V–mutant tumor cells.
Autologous T cells are genetically engineered to express a T-cell receptor specific for the KRAS G12V neoepitope presented by HLA-A*11:01. Upon peptide-HLA recognition, TCR signaling activates cytotoxic effector functions, leading to MHC class I-restricted killing of KRAS G12V–mutant tumor cells.
YES
DIRECT
Engineered TCR-T cells recognize the KRAS G12V peptide presented by HLA-A*11:01 and directly kill target cells via TCR-triggered cytotoxic effector functions (perforin/granzyme and Fas–FasL), MHC class I–restricted.