Humanized IgG1 anti-CTLA-4 monoclonal antibody immune checkpoint inhibitor that blocks CTLA-4 to restore CD28/B7 costimulation, enhance T-cell priming/expansion, and may deplete intratumoral Tregs via Fc-mediated cytotoxicity.
Humanized IgG1 anti-CTLA-4 monoclonal antibody that blocks CTLA-4 to relieve checkpoint inhibition, restoring CD28-B7 costimulation and enhancing T-cell priming and expansion; Fc-mediated effector function may deplete intratumoral regulatory T cells.
IgG1 anti-CTLA-4 binds CTLA-4 on (intratumoral) Tregs and engages FcγR-bearing effector cells to mediate ADCC/ADCP (±CDC), depleting CTLA-4–expressing cells.
PSMA-targeted radioligand therapy; a small-molecule PSMA ligand chelated to beta-emitter Lu-177 that binds PSMA, is internalized, and delivers beta radiation causing DNA double-strand breaks in tumor cells.
Small-molecule PSMA ligand chelated to lutetium‑177 binds PSMA on prostate cancer cells, is internalized, and emits β‑particles that cause DNA double‑strand breaks (with cross‑fire to nearby cells), leading to tumor cell death.
PSMA-binding Lu-177 radioligand is internalized and emits β-particles that cause DNA double-strand breaks, killing PSMA-positive cells (with beta crossfire to nearby cells).
Autologous TCR-engineered T-cell therapy targeting HPV18-derived peptide presented by HLA-DRB1*09:01; administered as a single infusion to mediate antigen-specific cytotoxicity.
Autologous T cells are engineered to express a T-cell receptor that recognizes an HPV18-derived peptide presented by HLA-DRB1*09:01 on tumor cells. Antigen engagement triggers TCR signaling, activation, proliferation, cytokine release, and cytotoxic killing (perforin/granzyme and death receptor pathways) of HPV18-positive tumor cells.
Engineered TCR-T cells recognize the HPV18-derived peptide presented by HLA-DRB1*09:01 and directly kill target cells via perforin/granzyme release and death receptor–mediated apoptosis.
Bispecific T-cell engager (BiTE) that links CD3 on T cells to CD19 on B cells, activating T-cell–mediated cytotoxicity.
A bispecific single-chain antibody (BiTE) that binds CD19 on B cells and CD3 on T cells, physically bringing T cells into contact with CD19+ cells to trigger TCR/CD3-mediated activation, cytolytic synapse formation, cytokine release, and perforin/granzyme-dependent killing of malignant B cells.
Blinatumomab bridges CD3+ T cells to CD19+ cells, activating T cells to form a cytolytic synapse and kill targets via perforin/granzyme-dependent apoptosis.
Autologous TCR-engineered T-cell therapy targeting HPV18-derived peptide presented by HLA-DRB1*09:01; administered as a single infusion to mediate antigen-specific cytotoxicity.
Autologous T cells are engineered to express a T-cell receptor that recognizes an HPV18-derived peptide presented by HLA-DRB1*09:01 on tumor cells. Antigen engagement triggers TCR signaling, activation, proliferation, cytokine release, and cytotoxic killing (perforin/granzyme and death receptor pathways) of HPV18-positive tumor cells.
TCR-engineered T cells recognize the HPV18-derived peptide presented by HLA-DRB1*09:01 on tumor cells and directly kill them via perforin/granzyme and death receptor pathways.