A bispecific T-cell engager (BiTE) antibody construct that binds CD19 on B-cell lymphoblasts and CD3 on T cells, redirecting cytotoxic T cells to lyse CD19-positive leukemia cells.
Blinatumomab is a bispecific antibody that simultaneously binds CD19 on B cells and CD3 on T cells, bringing T cells into close proximity with CD19+ leukemia cells to trigger TCR/CD3-mediated activation and perforin/granzyme-dependent cytotoxic killing of the target B cells.
Blinatumomab links CD19 on target cells to CD3 on T cells, activating T cells to kill CD19+ cells via perforin/granzyme-mediated cytotoxicity.
Gene-modified natural killer (NK) cells engineered to express an NKG2D-based chimeric antigen receptor (CAR) that recognizes NKG2D ligands (MICA, MICB, ULBP family) on tumor cells, activating NK cytotoxicity for treatment of relapsed/refractory multiple myeloma.
Gene‑modified NK cells expressing an NKG2D‑based CAR recognize stress‑induced NKG2D ligands (MICA, MICB, ULBP family) on tumor cells. CAR signaling activates NK cytotoxic functions, inducing degranulation (perforin/granzyme), cytokine‑mediated killing, and apoptosis of malignant cells, targeting relapsed/refractory multiple myeloma.
NKG2D-based CAR NK cells bind MICB on tumor cells, activating NK cytotoxicity and degranulation (perforin/granzyme) to induce apoptosis/lysis of the target cells.
Engineered autologous T cells expressing a chimeric antigen receptor targeting BCMA (TNFRSF17) on malignant plasma cells; administered twice around ASCT to mediate targeted cytotoxicity.
Autologous T cells engineered to express a chimeric antigen receptor targeting BCMA (TNFRSF17) on malignant plasma cells; antigen binding triggers CAR signaling (CD3ζ ± costimulatory domains), activating cytotoxicity, cytokine release, and proliferation to eliminate BCMA-positive cells.
BCMA-specific CAR-T cells bind BCMA on target cells, activate, and kill them via perforin/granzyme-mediated cytolysis and death-receptor pathways (e.g., Fas).
CAIX-targeted monoclonal antibody conjugated to the beta-emitter lutetium-177; delivers localized radiation to CAIX-expressing tumor cells (radioimmunotherapy).
CAIX-targeted monoclonal antibody linked to the beta-emitter lutetium-177; binds CAIX on tumor cells and delivers localized ionizing radiation, causing DNA damage (e.g., double-strand breaks) and tumor cell death, with potential bystander effects on adjacent cells.
The anti-CAIX antibody binds CAIX on tumor cells and delivers 177Lu beta radiation to the bound cell, inducing ionizing radiation–mediated DNA double-strand breaks and cell death (with some cross-fire/bystander effects).
Monoclonal antibody targeting OX40 (CD134) intended to block OX40–OX40L signaling and/or deplete OX40-positive activated T cells to reduce T-cell activation, survival, and type 2 inflammatory cytokines in atopic dermatitis.
Monoclonal antibody against OX40 (CD134) that blocks OX40–OX40L costimulatory signaling and can deplete OX40-positive activated T cells, thereby reducing T-cell activation, survival, and type 2 inflammatory cytokines in atopic dermatitis.
The anti-OX40 antibody binds OX40 on activated T cells and recruits Fc receptor–bearing effector cells to mediate ADCC (and possibly CDC), depleting OX40-positive cells.