An anti-HER2 antibody–drug conjugate (RC48-ADC) consisting of a humanized anti‑HER2 monoclonal antibody linked via a cleavable linker to the microtubule inhibitor monomethyl auristatin E (MMAE); upon HER2 binding and internalization, MMAE is released to disrupt tubulin, causing G2/M arrest and apoptosis, with potential bystander effect.
Humanized anti-HER2 monoclonal antibody linked via a cleavable linker to monomethyl auristatin E (MMAE). After HER2 binding and internalization, the linker is cleaved to release MMAE, which binds tubulin and inhibits microtubule polymerization, causing G2/M cell-cycle arrest and apoptosis; the membrane-permeable payload can produce a bystander effect.
The anti-HER2 ADC binds HER2, is internalized, and releases MMAE via a cleavable linker; MMAE inhibits tubulin/microtubule polymerization, causing G2/M arrest and apoptosis (with potential bystander killing).
In vivo gene therapy delivered by viral vector to transduce patient immune cells to express an anti-CD19 CAR-like receptor, activating T-cell signaling to kill CD19+ B cells; administered IV or via splenic artery/lymph node.
Viral vector delivered in vivo transduces the patient's T cells to express an anti-CD19 CAR-like receptor. Upon binding CD19 on B cells, the engineered T cells activate CAR signaling, expand, and kill CD19-positive malignant B cells, resulting in on-target B-cell depletion.
Engineered anti-CD19 CAR T cells bind CD19 on B cells and induce cytolysis via perforin/granzyme and apoptosis signaling, depleting CD19+ cells.
Subcutaneous T-cell–engaging trispecific antibody that binds BCMA and GPRC5D on myeloma cells and CD3 on T cells, redirecting T-cell cytotoxicity.
Subcutaneous trispecific antibody that binds BCMA and GPRC5D on myeloma cells and CD3 on T cells, bridging them to activate CD3 signaling and redirect T-cell cytotoxicity for targeted lysis of malignant plasma cells.
The trispecific T-cell engager binds GPRC5D on myeloma cells and CD3 on T cells, forming an immunologic synapse that activates T-cell killing via perforin/granzyme-mediated cytolysis and apoptosis of GPRC5D-positive cells.
Patient-derived T cells genetically modified to express an HLA-A–restricted T-cell receptor recognizing mutant KRAS G12V/G12D neoantigens; administered as adoptive cellular therapy to mediate MHC-restricted cytotoxic tumor killing.
Autologous T cells are genetically engineered to express an HLA-A–restricted T-cell receptor specific for mutant KRAS G12V/G12D peptides. After infusion, these TCR-T cells recognize KRAS neoantigens presented on tumor MHC, become activated, and mediate MHC-restricted cytotoxic killing via perforin/granzyme release and cytokine secretion, leading to selective elimination of KRAS-mutant tumor cells.
Engineered TCR-T cells recognize the KRAS G12V neoantigen peptide presented on HLA-A on tumor cells and induce MHC-restricted killing via perforin/granzyme release (and Fas–FasL), causing apoptosis/lysis.
Patient-derived T cells genetically modified to express an HLA-A–restricted T-cell receptor recognizing mutant KRAS G12V/G12D neoantigens; administered as adoptive cellular therapy to mediate MHC-restricted cytotoxic tumor killing.
Autologous T cells are genetically engineered to express an HLA-A–restricted T-cell receptor specific for mutant KRAS G12V/G12D peptides. After infusion, these TCR-T cells recognize KRAS neoantigens presented on tumor MHC, become activated, and mediate MHC-restricted cytotoxic killing via perforin/granzyme release and cytokine secretion, leading to selective elimination of KRAS-mutant tumor cells.
TCR-engineered T cells recognize the HLA-presented KRAS G12D neoantigen on tumor cells and directly induce cytolysis via perforin/granzyme-mediated apoptosis (and related CTL effector pathways).