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.
T-cell redirection to CD20+ cells via CD3 engagement forms an immune synapse, leading to perforin/granzyme-mediated killing of the target B cells.
A bispecific T‑cell engager (BiTE) antibody that binds CD19 on B‑lymphoblasts and CD3 on T cells to redirect and activate cytotoxic T cells against CD19+ leukemia.
A BiTE antibody that binds CD19 on B cells and CD3 on T cells, juxtaposing and activating T cells to form an immune synapse and induce perforin/granzyme-mediated lysis of CD19-positive leukemia cells.
Blinatumomab links CD3 on T cells to CD19 on target cells, activating T cells to form an immune synapse and kill CD19+ cells via perforin/granzyme-mediated cytolysis/apoptosis.
An anti–PD-L1 antibody–drug conjugate administered IV every 3 weeks. The monoclonal antibody blocks the PD-1/PD-L1 immune checkpoint to restore T-cell antitumor activity and, after PD-L1–mediated internalization, releases a DNA topoisomerase I inhibitor payload that induces DNA damage, replication stress, and apoptosis in PD-L1–expressing cells.
HLX43 is an anti-PD-L1 IgG1 antibody–drug conjugate that both blocks the PD-1/PD-L1 immune checkpoint to restore T-cell antitumor activity and, after PD-L1–mediated internalization and linker cleavage, releases a camptothecin-based topoisomerase I inhibitor payload that causes DNA damage, replication stress, and apoptosis in PD-L1–expressing cells (with potential bystander killing).
ADC binds PD-L1 on target cells, is internalized, and releases a camptothecin-based topoisomerase I inhibitor that causes DNA damage and apoptosis (with potential bystander killing).
An antibody–drug conjugate comprising a humanized anti-HER2 monoclonal antibody linked via a cleavable linker to deruxtecan, a topoisomerase I inhibitor. It binds HER2 (including HER2-low), is internalized, and releases deruxtecan in lysosomes to inhibit topoisomerase I, causing DNA damage and apoptosis; the membrane-permeable payload enables a bystander effect and the Fc region may mediate ADCC.
Humanized anti‑HER2 monoclonal antibody linked via a cleavable linker to deruxtecan (topoisomerase I inhibitor). Binds HER2 (including HER2‑low), is internalized, and releases deruxtecan in lysosomes to inhibit Topo I, causing DNA damage, cell‑cycle arrest, and apoptosis; membrane‑permeable payload enables a bystander effect, and the Fc region can mediate ADCC.
The anti-HER2 antibody–drug conjugate binds HER2, is internalized, and releases the topoisomerase I inhibitor deruxtecan in lysosomes, causing DNA damage, cell-cycle arrest, and apoptosis; Fc-mediated ADCC and a bystander effect can also contribute.
Autologous CD19-directed CAR T-cell therapy; engineered T cells target CD19+ B cells (naive, memory, plasmablasts) to deplete autoreactive B-cell compartments and reduce autoantibody production.
Autologous T cells are engineered to express a chimeric antigen receptor targeting CD19, enabling recognition and cytotoxic elimination of CD19+ B cells (naive, memory, plasmablasts). This depletes autoreactive B-cell compartments, reduces autoantibody production, and dampens B cell–driven immune inflammation.
CD19-directed CAR T cells bind CD19 on target cells, triggering T-cell activation and cytotoxic killing via perforin/granzyme release and death-receptor pathways, inducing apoptosis of CD19+ cells.