Immune checkpoint inhibitor; a human IgG1 monoclonal antibody against PD-L1 that blocks PD-L1 interaction with PD-1 and CD80 (B7.1), restoring T-cell activation and antitumor immunity. Its IgG1 Fc can engage FcγRIIIa on NK cells to promote ADCC.
A human IgG1 monoclonal antibody targeting PD-L1 that blocks its interaction with PD-1 and CD80, preventing PD-1–mediated inhibitory signaling and restoring T‑cell activation; its IgG1 Fc can engage FcγRIIIa on NK cells to mediate ADCC against PD‑L1–expressing cells.
Avelumab binds PD-L1 on target cells and its IgG1 Fc engages CD16 (FcγRIIIa) on NK cells, triggering antibody-dependent cellular cytotoxicity (ADCC) that kills PD-L1–expressing cells.
Autologous adoptive T-cell therapy consisting of patient-derived T cells expanded ex vivo to recognize HPV-16 E6/E7 peptides presented by HLA-A*0201 on tumor cells, inducing TCR-mediated cytotoxic killing; administered IV at 5×10^9 or 1.5×10^10 cells per infusion for up to 4 cycles.
Autologous T cells selected and expanded ex vivo for specificity to HPV-16 E6/E7. After infusion, their native TCRs recognize E6/E7 peptides presented by HLA-A*0201 on tumor cells, leading to MHC class I-restricted cytotoxic killing and cytokine-mediated anti-tumor activity.
Adoptively transferred T cells recognize HPV-16 E6 peptide–HLA-A*0201 complexes via their native TCRs and induce CTL killing of target cells through perforin/granzyme-mediated apoptosis (and Fas–FasL).
Autologous adoptive T-cell therapy consisting of patient-derived T cells expanded ex vivo to recognize HPV-16 E6/E7 peptides presented by HLA-A*0201 on tumor cells, inducing TCR-mediated cytotoxic killing; administered IV at 5×10^9 or 1.5×10^10 cells per infusion for up to 4 cycles.
Autologous T cells selected and expanded ex vivo for specificity to HPV-16 E6/E7. After infusion, their native TCRs recognize E6/E7 peptides presented by HLA-A*0201 on tumor cells, leading to MHC class I-restricted cytotoxic killing and cytokine-mediated anti-tumor activity.
Adoptively transferred T cells recognize HPV-16 E7 peptide–HLA-A*0201 complexes via their TCRs and directly kill the presenting tumor cells through MHC I–restricted CTL mechanisms (perforin/granzyme-mediated apoptosis, with possible Fas/FasL and cytokine effects).
Anti-EGFR monoclonal antibody that blocks ligand binding and downstream EGFR signaling (RAS–MAPK, PI3K–AKT) and may induce antibody-dependent cellular cytotoxicity (ADCC).
Anti-EGFR monoclonal antibody that blocks ligand binding to EGFR, shutting down downstream RAS–MAPK and PI3K–AKT signaling to inhibit tumor cell proliferation and survival; Fc domain may engage immune effector cells to mediate ADCC against EGFR-expressing cells.
Binds EGFR on target cells and engages Fcγ receptors on immune effectors to induce ADCC (± CDC), leading to lysis of EGFR-expressing cells; signaling blockade mainly inhibits proliferation.
Anti-PD-L1 monoclonal antibody (immune checkpoint inhibitor) that blocks PD-L1 to restore T-cell antitumor activity.
Human IgG1 anti-PD-L1 monoclonal antibody that blocks PD-L1 binding to PD-1, reversing T-cell inhibition to restore antitumor activity; its Fc region can also mediate ADCC against PD-L1-expressing tumor cells.
Avelumab binds PD-L1 on target cells and recruits FcγR-bearing effector cells (e.g., NK cells) to mediate ADCC; it also blocks PD-1/PD-L1 to restore CTL killing (indirect).