Adoptive cell therapy consisting of a single IV infusion of ex vivo expanded autologous tumor-reactive T cells to augment anti-tumor immunity.
Autologous T cells are isolated and expanded ex vivo based on functional reactivity to tumor antigens. After infusion, these TCR-mediated tumor‑specific CD4+/CD8+ T cells recognize peptide–MHC complexes on tumor cells, release cytotoxic granules and inflammatory cytokines, and augment anti‑tumor immunity.
Adoptively transferred tumor‑reactive T cells recognize the neoantigen–HLA class II complex via their TCR and directly kill target cells through perforin/granzyme release and Fas–FasL–mediated apoptosis.
Adoptive cell therapy consisting of a single IV infusion of ex vivo expanded autologous tumor-reactive T cells to augment anti-tumor immunity.
Autologous T cells are isolated and expanded ex vivo based on functional reactivity to tumor antigens. After infusion, these TCR-mediated tumor‑specific CD4+/CD8+ T cells recognize peptide–MHC complexes on tumor cells, release cytotoxic granules and inflammatory cytokines, and augment anti‑tumor immunity.
Adoptively transferred tumor‑reactive T cells recognize the peptide–HLA class II complex via their TCR and directly lyse target cells through perforin/granzyme (and Fas–FasL) pathways, with supportive inflammatory cytokines.
An intravenous BCMA x CD3 bispecific T-cell–engaging antibody that binds BCMA (TNFRSF17) on multiple myeloma plasma cells and CD3 on T cells to form an immune synapse, activate TCR/CD3 signaling, and redirect T cells to lyse BCMA-positive tumor cells via perforin/granzyme release and cytokine-driven cytotoxicity.
Intravenous BCMA×CD3 bispecific antibody that binds BCMA on multiple myeloma cells and CD3 on T cells to form an immune synapse, activate TCR/CD3 signaling, and redirect T cells to kill BCMA-positive tumor cells via perforin/granzyme release and cytokine-mediated cytotoxicity.
The BCMA×CD3 bispecific bridges T cells to BCMA+ cells, activating TCR/CD3 and inducing perforin/granzyme-mediated cytolysis and cytokine-driven killing of the BCMA-expressing cells.
Humanized IgG1 monoclonal antibody targeting CD38 on myeloma cells, mediating ADCC, CDC, ADCP, and direct pro-apoptotic and immune-modulating effects.
Humanized IgG1 monoclonal antibody targeting CD38 on myeloma cells; mediates antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and antibody-dependent cellular phagocytosis (ADCP), and can induce direct pro-apoptotic and immune-modulating effects, leading to lysis of CD38-expressing tumor cells.
Isatuximab binds CD38 on target cells and recruits immune effectors via its Fc to mediate ADCC, CDC, and ADCP; it can also trigger direct pro‑apoptotic signaling, leading to lysis of CD38-expressing cells.