Anti-CD20 monoclonal antibody mediating ADCC/CDC and direct B-cell apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive cells via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and direct induction of apoptosis.
YES
DIRECT
Rituximab binds CD20 on B cells, inducing killing via ADCC (through Fc gamma receptor–bearing effector cells), complement-mediated cytotoxicity (CDC), and direct apoptosis signaling.
Autologous T cells genetically engineered to express a HER2 (ERBB2)-specific chimeric antigen receptor; upon binding HER2 on tumor cells, they activate cytotoxic T-cell responses leading to tumor cell killing.
Autologous T cells are genetically engineered to express a HER2-specific chimeric antigen receptor. Upon binding HER2 (ERBB2) on tumor cells, the CAR transduces activation signals (CD3ζ with costimulatory domains), driving T-cell activation, expansion, cytokine release, and perforin/granzyme-mediated cytolytic killing of HER2-expressing cancer cells.
YES
DIRECT
HER2-specific CAR-T cells bind HER2 on target cells and, upon activation, kill them via perforin/granzyme-mediated cytolysis (and death receptor pathways).
Peptide-coated, conditionally replicating oncolytic adenovirus administered intratumorally (± subcutaneously) to induce tumor cell lysis and in situ vaccination by enhancing dendritic cell uptake and cross-priming of NY-ESO-1/MAGE-A3–specific CD8+ T cells.
PeptiCRAd-1 is a peptide-coated, conditionally replicating oncolytic adenovirus that selectively infects and replicates in tumor cells, causing oncolysis and release of danger signals and tumor antigens. The NY-ESO-1/MAGE-A3 peptide coating enhances dendritic cell uptake and cross-priming, driving NY-ESO-1/MAGE-A3–specific CD8+ T-cell responses. Administered intratumorally (± subcutaneously), it functions as an in situ vaccine to boost antitumor immunity.
YES
INDIRECT
Acts as an in situ vaccine that primes NY-ESO-1–specific CD8+ T cells; these CTLs recognize NY-ESO-1 peptide–MHC I on tumor cells and kill them via perforin/granzyme-mediated cytolysis.
Peptide-coated, conditionally replicating oncolytic adenovirus administered intratumorally (± subcutaneously) to induce tumor cell lysis and in situ vaccination by enhancing dendritic cell uptake and cross-priming of NY-ESO-1/MAGE-A3–specific CD8+ T cells.
PeptiCRAd-1 is a peptide-coated, conditionally replicating oncolytic adenovirus that selectively infects and replicates in tumor cells, causing oncolysis and release of danger signals and tumor antigens. The NY-ESO-1/MAGE-A3 peptide coating enhances dendritic cell uptake and cross-priming, driving NY-ESO-1/MAGE-A3–specific CD8+ T-cell responses. Administered intratumorally (± subcutaneously), it functions as an in situ vaccine to boost antitumor immunity.
YES
INDIRECT
Acts as an in situ vaccine: peptide coating drives DC cross-priming and expansion of MAGE-A3–specific CD8+ T cells that kill MAGE-A3+ tumor cells via cytotoxic T-lymphocyte mechanisms; viral oncolysis is not MAGE-A3-specific.
Autologous, genetically engineered CAR T-cell therapy that dual-targets CD19 and CD22 to deplete malignant B cells.
Autologous T cells are genetically engineered to express chimeric antigen receptors that recognize CD19 and CD22 on B cells. Upon antigen engagement, the CAR T cells activate, proliferate, release cytokines, and kill malignant B cells via cytotoxic mechanisms (perforin/granzyme), leading to depletion of CD19+/CD22+ tumor cells and on-target B-cell aplasia.
YES
DIRECT
CAR T cells bind CD19 on target cells and induce killing via immune synapse formation with perforin/granzyme-mediated apoptosis (and Fas/FasL pathways).