An anti-CD19 IgG1 antibody–drug conjugate that binds CD19 on B cells, is internalized, and releases a pyrrolobenzodiazepine (PBD) dimer cytotoxic payload that forms DNA interstrand crosslinks leading to apoptosis; Fc-mediated effector functions may contribute.
Anti-CD19 IgG1 antibody–drug conjugate that binds CD19 on B cells, is internalized, and releases a pyrrolobenzodiazepine (PBD) dimer payload via a cleavable linker; the PBD binds DNA minor grooves to form interstrand crosslinks, blocking DNA replication and inducing apoptosis; Fc-mediated effector functions may also contribute.
Anti-CD19 ADC binds CD19, is internalized, and releases a PBD dimer that crosslinks DNA, blocking replication and inducing apoptosis; Fc-mediated effector functions may also contribute.
An autologous, fully human anti-BCMA CAR T-cell therapy (CT103A) for relapsed/refractory multiple myeloma. Patient T cells are engineered to express a CAR targeting BCMA, leading to T-cell activation, expansion, cytokine release, and cytotoxic killing of BCMA-positive plasma cells.
Autologous T cells are engineered via lentiviral transduction to express a fully human anti-BCMA chimeric antigen receptor. Upon binding BCMA on malignant plasma cells, CAR signaling activates the T cells, inducing proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of BCMA-positive cells.
Anti-BCMA CAR T cells bind BCMA on target cells, become activated, and kill via perforin/granzyme-mediated cytotoxicity (leading to lysis/apoptosis).
Patient-derived tumor-resident T cells isolated, expanded, and activated ex vivo, then reinfused to mediate antigen-specific cytotoxicity via TCR recognition of tumor antigens.
Autologous tumor-resident T cells are isolated from the patient’s tumor, expanded and activated ex vivo, then reinfused to recognize tumor antigens via their native TCRs presented on MHC, mediating antigen-specific cytotoxicity through perforin/granzyme release and cytokine secretion; supportive IL-2 can enhance survival and expansion.
TILs recognize the neoantigen peptide–MHC I complex via their native TCR and directly lyse target cells through perforin/granzyme release (and Fas–FasL pathways).
Patient-derived tumor-resident T cells isolated, expanded, and activated ex vivo, then reinfused to mediate antigen-specific cytotoxicity via TCR recognition of tumor antigens.
Autologous tumor-resident T cells are isolated from the patient’s tumor, expanded and activated ex vivo, then reinfused to recognize tumor antigens via their native TCRs presented on MHC, mediating antigen-specific cytotoxicity through perforin/granzyme release and cytokine secretion; supportive IL-2 can enhance survival and expansion.
Reinfused TILs recognize tumor-associated peptide–HLA class I complexes via their native TCRs and directly kill target cells through perforin/granzyme-mediated apoptosis (and Fas–FasL), with cytokines supporting cytotoxicity.
Patient-derived tumor-resident T cells isolated, expanded, and activated ex vivo, then reinfused to mediate antigen-specific cytotoxicity via TCR recognition of tumor antigens.
Autologous tumor-resident T cells are isolated from the patient’s tumor, expanded and activated ex vivo, then reinfused to recognize tumor antigens via their native TCRs presented on MHC, mediating antigen-specific cytotoxicity through perforin/granzyme release and cytokine secretion; supportive IL-2 can enhance survival and expansion.
TILs recognize the neoantigen peptide–HLA class II complex via their native TCRs and directly kill target cells through perforin/granzyme-mediated cytolysis and Fas–FasL apoptosis, with supportive cytokine effects.