Autologous T lymphocytes genetically modified to express dual chimeric antigen receptors targeting CD19 and CD20; binding activates CAR signaling to mediate expansion and cytotoxic elimination of B-cell malignancies while aiming to reduce antigen-loss escape.
Autologous T cells are genetically engineered to express dual chimeric antigen receptors recognizing CD19 and CD20 on B cells. Antigen binding triggers CAR signaling (CD3ζ with costimulatory domains), driving T‑cell activation, expansion, cytokine release, and perforin/granzyme‑mediated cytotoxic killing of malignant B cells. Dual targeting aims to reduce antigen‑loss escape; on‑target effects include B‑cell aplasia.
CAR-T cells recognize CD19 via the CAR, become activated, and kill CD19+ cells through perforin/granzyme-mediated cytolysis (and Fas–FasL apoptosis).
Autologous T lymphocytes genetically modified to express dual chimeric antigen receptors targeting CD19 and CD20; binding activates CAR signaling to mediate expansion and cytotoxic elimination of B-cell malignancies while aiming to reduce antigen-loss escape.
Autologous T cells are genetically engineered to express dual chimeric antigen receptors recognizing CD19 and CD20 on B cells. Antigen binding triggers CAR signaling (CD3ζ with costimulatory domains), driving T‑cell activation, expansion, cytokine release, and perforin/granzyme‑mediated cytotoxic killing of malignant B cells. Dual targeting aims to reduce antigen‑loss escape; on‑target effects include B‑cell aplasia.
CAR-T cells bind CD20 on target cells, triggering T-cell activation and perforin/granzyme-mediated cytolysis (plus death-receptor pathways).
Human IgG1 monoclonal antibody (VAY736) administered subcutaneously (300 mg) that targets the BAFF receptor (BAFF-R/TNFRSF13C). It blocks BAFF/BLyS binding to BAFF-R and depletes BAFF-R–positive B cells via Fc-mediated ADCC, reducing BAFF-driven survival/maturation signals and lowering autoreactive B-cell activity and autoantibody production.
Fully human IgG1 monoclonal antibody targeting the BAFF receptor (BAFF-R/TNFRSF13C). It blocks BAFF/BLyS binding and downstream BAFF-R signaling and depletes BAFF-R–positive B cells via Fc-mediated ADCC, reducing BAFF-driven B-cell survival/maturation and autoantibody production.
Ianalumab is an anti–BAFF-R IgG1 that opsonizes BAFF-R+ B cells and recruits FcγR-expressing effector cells to mediate ADCC (and possibly complement-mediated lysis), depleting the target cells.
Anti-CD38 IgG1 monoclonal antibody that targets CD38 on malignant plasma cells, mediating ADCC/CDC, inducing apoptosis, and modulating CD38 ectoenzyme activity.
Human IgG1 monoclonal antibody against CD38 on malignant plasma cells; binding triggers Fc-mediated ADCC and complement-dependent cytotoxicity, directly induces apoptosis, and inhibits/modulates CD38 ectoenzyme activity, leading to depletion of CD38-positive tumor cells.
Isatuximab binds CD38 on target cells and triggers Fc-mediated ADCC and complement-dependent cytotoxicity; it can also directly induce apoptosis, killing CD38+ cells.
Disitamab vedotin (RC48) is an anti-HER2 antibody–drug conjugate composed of a humanized monoclonal antibody linked to the cytotoxic payload monomethyl auristatin E (MMAE), a microtubule inhibitor. After binding HER2 on tumor cells, the ADC is internalized and releases MMAE to disrupt microtubules, causing G2/M arrest and apoptosis; the antibody may also mediate ADCC and inhibit HER2 signaling.
Anti-HER2 antibody-drug conjugate that binds HER2 on tumor cells, is internalized, and releases the microtubule inhibitor MMAE to inhibit tubulin polymerization, causing G2/M cell-cycle arrest and apoptosis; the antibody may also mediate ADCC and inhibit HER2 signaling.
The ADC binds HER2, is internalized, and releases MMAE, which inhibits tubulin polymerization causing G2/M arrest and apoptosis; the antibody Fc can also mediate ADCC against HER2+ cells.