Autologous, gene-engineered TCR-T cell therapy expressing an HLA-A*02:01–restricted TCR specific for the TP53 R175H mutant peptide to mediate antigen-specific tumor cell killing.
Autologous T cells are gene-engineered to express an HLA-A*02:01–restricted T-cell receptor that recognizes the TP53 R175H mutant peptide presented on tumor MHC class I. After infusion, these TCR-T cells bind the peptide–MHC complex, become activated, and kill antigen-positive tumor cells via cytotoxic effector functions (perforin/granzymes and cytokines).
Engineered TCR-T cells recognize the HLA-A*02:01–TP53 R175H peptide complex, become activated, and kill the antigen-positive cells via perforin/granzyme-mediated cytolysis (and related CTL effector mechanisms).
HER2-directed antibody-drug conjugate (T-DXd; DS-8201a, ENHERTU) consisting of the humanized IgG1 monoclonal antibody trastuzumab linked via a cleavable tetrapeptide linker to DXd, a membrane-permeable exatecan derivative and topoisomerase I inhibitor; administered IV 5.4 mg/kg every 3 weeks. Binds HER2, is internalized, and releases DXd in lysosomes to inhibit topoisomerase I, causing DNA damage and apoptosis with a bystander effect; also inhibits HER2 signaling and mediates ADCC.
Humanized anti-HER2 IgG1 (trastuzumab) linked via a cleavable tetrapeptide to DXd, a membrane-permeable exatecan derivative and topoisomerase I inhibitor. After binding HER2 and internalization, the linker is cleaved in lysosomes to release DXd, which inhibits Top1, leading to DNA damage, replication arrest, and apoptosis with a bystander effect; the antibody also inhibits HER2 signaling and mediates ADCC.
HER2-binding ADC is internalized; lysosomal cleavage releases the topoisomerase I inhibitor DXd, causing DNA damage and apoptosis; Fc also mediates ADCC and there is a bystander killing effect.
Bispecific T-cell engager (BiTE) that links CD3 on T cells to CD19 on B-ALL cells to drive T-cell cytotoxicity.
Bispecific T-cell engager (BiTE) antibody that simultaneously binds CD3 on T cells and CD19 on B cells, bringing them into proximity to trigger TCR/CD3 signaling and T-cell–mediated cytotoxicity (perforin/granzyme) against CD19-positive B-lymphoblasts.
Blinatumomab links CD19 on target B cells to CD3 on T cells, activating T cells to form a cytolytic synapse and kill CD19+ cells via perforin/granzyme-mediated apoptosis.
Anti-CD22 antibody–drug conjugate delivering calicheamicin to CD22-positive blasts.
Humanized anti-CD22 monoclonal antibody linked to calicheamicin; binds CD22 on B-cell blasts, is internalized, and releases calicheamicin, which binds the DNA minor groove to induce double-strand breaks and apoptosis.
ADC binds CD22, is internalized, and releases calicheamicin that binds DNA minor groove, causing double-strand breaks and apoptosis in the target cell.
Chimeric anti-CD20 monoclonal antibody used to deplete CD20+ B cells (including memory B cells) to reduce new anti-HLA antibody formation before transplant.
Chimeric anti-CD20 monoclonal IgG1 that binds CD20 on pre‑B and mature B lymphocytes, triggering complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity and inducing apoptosis, thereby depleting CD20+ B cells (including memory B cells) to reduce new anti-HLA antibody formation.
Rituximab binds CD20 on B cells, triggering complement-dependent cytotoxicity and Fcγ receptor–mediated ADCC, and can induce apoptosis, leading to depletion of CD20+ cells.