A subcutaneous, full-length humanized bispecific IgG1 antibody (T-cell–redirecting biologic) that binds CD20 on B cells and CD3 on T cells, bringing T cells into contact with malignant B cells to trigger TCR/CD3 activation, immune synapse formation, cytokine release, and perforin/granzyme-mediated cytotoxicity; depletes CD20+ B cells. Step-up dosing: 5 mg C1D1; 45 mg C1D8 and C1D15; then 45 mg on Day 1 of Cycles 2–8 (21-day cycles).
Humanized bispecific IgG1 antibody that binds CD20 on B cells and CD3 on T cells to physically redirect and activate T cells against CD20+ malignant B cells, inducing immune synapse formation, cytokine release, and perforin/granzyme-mediated cytotoxicity leading to B-cell depletion.
NO
INDIRECT
CD3 is on T cells and is engaged to activate them; the activated T cells kill CD20+ B cells via perforin/granzyme cytotoxicity, not the CD3+ cells.
Allogeneic anti-CD20 CAR-engineered gamma-delta (γδ) T-cell therapy that targets and depletes CD20-positive B cells to reduce autoantibody production and B cell–driven inflammation in autoimmune diseases.
Allogeneic gamma-delta T cells engineered with an anti-CD20 chimeric antigen receptor bind CD20 on B cells independent of MHC, become activated, and kill CD20+ B cells via cytotoxic effector mechanisms, depleting pathogenic B cells and reducing autoantibody-driven inflammation.
YES
DIRECT
Anti-CD20 CAR γδ T cells bind CD20 on B cells, become activated, and directly kill the CD20+ cells via cytotoxic effector mechanisms (perforin/granzyme-mediated lysis and apoptosis; Fas/FasL), independent of MHC.
Autologous TCR-engineered T cell therapy targeting an HPV18-derived peptide presented by HLA-DRB1*0901; infused T cells recognize HPV18+ tumor cells and mediate cytotoxicity via TCR signaling, cytokine release, and perforin/granzyme pathways.
Autologous T cells are engineered to express a T-cell receptor that recognizes an HPV18-derived peptide presented by HLA-DRB1*0901 on tumor cells. Antigen recognition activates TCR signaling, leading to cytokine release and cytotoxic killing via perforin/granzyme pathways, selectively eliminating HPV18-positive tumor cells.
YES
DIRECT
Engineered TCR T cells recognize the HPV18-derived peptide presented by HLA-DRB1*0901 on tumor cells, triggering TCR signaling and killing via perforin/granzyme-mediated cytolysis (with cytokine-driven apoptosis).
Autologous TCR-engineered T cell therapy targeting an HPV18-derived peptide presented by HLA-DRB1*0901; infused T cells recognize HPV18+ tumor cells and mediate cytotoxicity via TCR signaling, cytokine release, and perforin/granzyme pathways.
Autologous T cells are engineered to express a T-cell receptor that recognizes an HPV18-derived peptide presented by HLA-DRB1*0901 on tumor cells. Antigen recognition activates TCR signaling, leading to cytokine release and cytotoxic killing via perforin/granzyme pathways, selectively eliminating HPV18-positive tumor cells.
NO
DIRECT
Engineered T cells kill cells that present the HPV18-derived peptide in complex with HLA‑DRB1*09:01 via TCR activation and perforin/granzyme-mediated lysis; HLA‑DRB1*09:01 expression alone is not sufficient.
Chimeric IgG1 anti‑EGFR monoclonal antibody that inhibits EGFR signaling (RAS/RAF/MEK/ERK, PI3K/AKT), impairs DNA repair and cell‑cycle progression, and induces ADCC via NK cells; increases radiosensitivity.
Chimeric IgG1 monoclonal antibody against EGFR that binds the extracellular domain to block ligand binding, receptor activation and dimerization, thereby inhibiting downstream RAS/RAF/MEK/ERK and PI3K/AKT signaling; reduces proliferation, cell-cycle progression and DNA repair, induces NK cell–mediated ADCC via its Fc region, and increases radiosensitivity.
YES
DIRECT
Cetuximab binds EGFR on target cells and its IgG1 Fc engages Fcγ receptors on NK cells to trigger antibody-dependent cellular cytotoxicity (ADCC), killing EGFR+ cells (with possible complement-mediated cytotoxicity). Signaling blockade is primarily cytostatic.