Autologous T cells genetically engineered to express a HER2 (ERBB2)-specific chimeric antigen receptor, enabling recognition and killing of HER2-expressing tumor cells via T-cell activation and cytokine release.
Autologous T cells engineered to express a HER2-specific chimeric antigen receptor bind HER2 on tumor cells, triggering T‑cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of HER2-expressing cells.
HER2-specific CAR-T cells bind HER2 on target cells, activate, form an immune synapse, and kill via perforin/granzyme-mediated cytolysis (and Fas–FasL), with accompanying cytokine release.
Human IgG1κ monoclonal antibody targeting CD38; mediates Fc-dependent ADCC and ADCP, complement-dependent cytotoxicity (CDC), and apoptosis, and depletes CD38+ immunosuppressive cells to remodel the tumor microenvironment.
Human IgG1κ monoclonal antibody targeting CD38 that induces tumor-cell killing via Fc-dependent ADCC and ADCP, complement-dependent cytotoxicity, and apoptosis, while depleting CD38+ immunosuppressive cells to remodel the tumor microenvironment.
Anti-CD38 IgG1 binds CD38 on target cells and induces Fc-dependent ADCC by NK cells, ADCP by macrophages, complement-dependent cytotoxicity (CDC), and can trigger apoptosis upon crosslinking.
Chimeric IgG1 monoclonal antibody against EGFR that blocks ligand binding and downstream signaling (e.g., RAS/RAF/MEK/ERK, PI3K/AKT), inhibits proliferation, and mediates ADCC.
Chimeric IgG1 monoclonal antibody against EGFR that binds the extracellular domain to block ligand binding and receptor activation/dimerization, suppressing downstream RAS/RAF/MEK/ERK and PI3K/AKT signaling to inhibit tumor cell proliferation; additionally mediates Fc-dependent ADCC against EGFR-expressing cells.
Cetuximab coats EGFR-expressing cells and engages Fcγ receptors on NK cells to trigger antibody-dependent cellular cytotoxicity (ADCC), with possible complement-dependent cytotoxicity (CDC); signaling blockade is mainly cytostatic.
Anti-HER2 monoclonal antibody that blocks HER2 dimerization.
Humanized anti-HER2 IgG1 monoclonal antibody that binds the HER2 extracellular dimerization domain (subdomain II), blocking HER2 heterodimerization (especially with HER3), thereby preventing downstream signaling (PI3K/AKT, MAPK) and inhibiting tumor cell proliferation; can also mediate ADCC.
Pertuzumab binds HER2 on target cells and its Fc engages FcγR-expressing immune cells (e.g., NK cells), triggering antibody-dependent cellular cytotoxicity (ADCC) to kill the cells; HER2 signaling blockade can also promote apoptosis.
Autologous, gene-modified chimeric antigen receptor (CAR) T cells produced with a non-viral vector, engineered to target mesothelin and MUC1 on tumor cells and to auto-secrete multifunctional antibodies to enhance antitumor immunity within the tumor microenvironment; evaluated in a dose-escalation regimen (5×10^5, 1×10^6, 5×10^6 cells/kg).
Autologous T cells engineered with a non-viral vector to express chimeric antigen receptors recognizing mesothelin and MUC1 on tumor cells, triggering CAR-mediated T-cell activation and cytolytic killing via CD3ζ and costimulatory signaling; additionally engineered to secrete multifunctional antibodies within the tumor microenvironment to enhance antitumor immunity (e.g., overcoming immunosuppression/checkpoints) and amplify T-cell activity.
CAR T cells recognize mesothelin via their CAR, activating CD3ζ/costimulatory signaling and killing mesothelin-expressing cells through perforin/granzyme release and death-receptor pathways.