Autologous tumor-infiltrating lymphocyte (TIL) cellular therapy manufactured from a patient’s tumor, expanded ex vivo, and reinfused to mediate antitumor activity through native TCR recognition, cytotoxic mechanisms, and cytokine secretion.
Autologous TILs expanded ex vivo and reinfused; they recognize patient-specific tumor antigens via native TCR–MHC interactions and mediate antitumor effects through cytotoxic killing (perforin/granzymes) and cytokine secretion within the tumor microenvironment.
TILs recognize the tumor-associated peptide–HLA class I complex via native TCRs and directly kill target cells through cytotoxic T-cell mechanisms (perforin/granzymes, and Fas–FasL apoptosis).
An anti-HER2 antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and releases the cytotoxic payload MMAE to inhibit microtubule polymerization, causing mitotic arrest and apoptosis; may also mediate ADCC.
Anti-HER2 antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and releases the cytotoxic payload MMAE to inhibit microtubule polymerization, leading to mitotic arrest and apoptosis; may also mediate Fc-dependent ADCC.
The anti-HER2 ADC binds HER2, is internalized, and releases MMAE, which inhibits microtubule polymerization causing mitotic arrest and apoptosis; Fc engagement may also induce ADCC.
Humanized IgG1 monoclonal antibody targeting HER2/ERBB2 that inhibits receptor signaling and dimerization, induces receptor internalization/degradation, and mediates Fc-dependent antibody‑dependent cellular cytotoxicity (ADCC) against HER2-overexpressing tumor cells.
Trastuzumab binds HER2 and engages Fcγ receptors on immune effectors to trigger antibody‑dependent cellular cytotoxicity (ADCC), killing HER2+ cells; it also inhibits HER2 signaling, which can promote apoptosis.
Autologous bispecific CAR-T cell therapy engineered to target BCMA and CS1 (SLAMF7) on myeloma cells; CAR engagement activates T cells (CD3ζ with co-stimulatory signaling) leading to cytokine release and tumor cell killing.
Autologous bispecific CAR-T cells engineered (e.g., via lentiviral transduction) to recognize BCMA and CS1/SLAMF7 on myeloma cells. Antigen binding activates CD3zeta and co-stimulatory signaling domains, driving T-cell activation, expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing of BCMA/CS1-positive tumor cells, with dual targeting intended to reduce antigen escape.
BCMA engagement by bispecific CAR-T cells activates CD3ζ/co-stimulatory signaling, leading to perforin/granzyme-mediated cytolysis (and Fas/FasL) of BCMA-positive cells.
Autologous bispecific CAR-T cell therapy engineered to target BCMA and CS1 (SLAMF7) on myeloma cells; CAR engagement activates T cells (CD3ζ with co-stimulatory signaling) leading to cytokine release and tumor cell killing.
Autologous bispecific CAR-T cells engineered (e.g., via lentiviral transduction) to recognize BCMA and CS1/SLAMF7 on myeloma cells. Antigen binding activates CD3zeta and co-stimulatory signaling domains, driving T-cell activation, expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing of BCMA/CS1-positive tumor cells, with dual targeting intended to reduce antigen escape.
CAR-T cells bind CS1 (SLAMF7) on target cells, activating CD3zeta/co-stimulatory signaling and inducing T-cell cytotoxicity via perforin/granzyme-mediated apoptosis (and Fas-FasL).