Anti-HER2 monoclonal antibody that blocks HER2 signaling and induces antibody-dependent cellular cytotoxicity (ADCC).
Humanized monoclonal antibody against HER2 that binds the receptor’s extracellular domain, inhibits HER2-driven signaling/heterodimerization, and engages Fcγ receptors to trigger antibody-dependent cellular cytotoxicity (ADCC) against HER2-overexpressing tumor cells.
Trastuzumab binds HER2 on target cells and its Fc engages Fcγ receptor–bearing effector cells (e.g., NK cells), inducing antibody-dependent cellular cytotoxicity (ADCC); complement activation may also contribute.
Autologous whole-tumor cell vaccine designed to prime and expand neoantigen-specific T-cell responses in newly diagnosed GBM.
Autologous T cells are primed in vivo by a personalized whole-tumor cell vaccine to generate neoantigen-reactive clones, then collected by leukapheresis, activated and expanded ex vivo, and reinfused to recognize patient-specific neoantigens on GBM cells and kill them via TCR-mediated cytotoxic activity; low-dose IL-2 supports T-cell survival and proliferation.
Adoptively transferred neoantigen-specific T cells recognize the patient-specific peptide–MHC II via their TCR and directly kill target cells through perforin/granzyme release and Fas–FasL-mediated apoptosis.
Patient-derived T lymphocytes activated and expanded ex vivo and reinfused to mediate anti-tumor cytotoxicity via TCR recognition of tumor neoantigens.
Autologous patient T lymphocytes are activated and expanded ex vivo to enrich neoantigen-specific TCR clones. Upon reinfusion, they recognize patient-specific tumor neoantigens presented on HLA and kill tumor cells via TCR-mediated cytotoxicity (perforin/granzyme and cytokine release). No genetic engineering is involved.
Neoantigen-specific TCRs on the reinfused autologous T cells recognize the peptide–HLA class I complex and directly kill target cells via cytotoxic T cell mechanisms (perforin/granzyme-mediated apoptosis, plus Fas–FasL).
Patient-derived T lymphocytes activated and expanded ex vivo and reinfused to mediate anti-tumor cytotoxicity via TCR recognition of tumor neoantigens.
Autologous patient T lymphocytes are activated and expanded ex vivo to enrich neoantigen-specific TCR clones. Upon reinfusion, they recognize patient-specific tumor neoantigens presented on HLA and kill tumor cells via TCR-mediated cytotoxicity (perforin/granzyme and cytokine release). No genetic engineering is involved.
Infused neoantigen-specific T cells recognize the tumor neoantigen peptide–HLA class II complex via their TCR and directly kill the presenting cells through perforin/granzyme release and Fas–FasL/cytokine-mediated apoptosis.
First-in-human antibody-drug conjugate: an anti-HER3 (ERBB3) monoclonal antibody linked to a topoisomerase I–inhibiting exatecan-derivative payload. Binds HER3 on tumor cells, is internalized, releases the cytotoxic payload to inhibit topo I, causing DNA damage; may also dampen HER3 signaling.
Anti-HER3 (ERBB3) monoclonal antibody linked to a topoisomerase I–inhibiting exatecan-derivative payload; binds HER3 on tumor cells, is internalized, and releases the payload to inhibit topoisomerase I, causing DNA damage, cell-cycle arrest, and apoptosis; may also reduce HER3 signaling.
ADC binds HER3 on tumor cells, is internalized, and releases a topoisomerase I–inhibitor payload that causes DNA damage, cell‑cycle arrest, and apoptosis.