Humanized IgG1 bi-epitope anti-HER2 monoclonal antibody that binds HER2 extracellular domains 2 and 4 to block signaling, promote receptor internalization, and trigger ADCC.
Humanized IgG1 bi-epitope anti-HER2 monoclonal antibody that binds two non-overlapping HER2 extracellular domains (ECD2 and ECD4), blocking HER2 signaling, inducing receptor clustering and internalization/downregulation, and activating Fc-mediated effector functions (ADCC and ADCP) to eliminate HER2-overexpressing tumor cells.
Zanidatamab binds HER2 ECD4 (and ECD2) on target cells and recruits immune effectors via its IgG1 Fc to trigger ADCC and ADCP, leading to killing of HER2-expressing cells; receptor clustering/internalization also occurs.
Autologous CMV-specific T cells genetically engineered to express an anti-CD19 chimeric antigen receptor, enabling targeted cytotoxicity against CD19-positive malignant B cells; endogenous CMV-specific TCRs allow antigen-driven recall responses to support in vivo expansion and persistence after transplant.
Autologous CMV-specific T cells engineered to express an anti-CD19 chimeric antigen receptor that redirects T-cell cytotoxicity to CD19-positive malignant B cells; native CMV-specific TCRs enable antigen-driven recall responses to enhance in vivo expansion and persistence, which can be boosted by CMV vaccination post-transplant.
Anti-CD19 CAR-expressing T cells recognize CD19 on target cells and directly kill them via cytotoxic T-cell mechanisms (perforin/granzyme release and Fas/FasL-mediated apoptosis).
A CD20×CD3 bispecific monoclonal antibody T‑cell engager that binds bivalently to CD20 on B cells and monovalently to CD3 on T cells to form an immune synapse, activate TCR/CD3 signaling, and drive T‑cell–mediated cytotoxicity against CD20+ lymphoma.
CD20×CD3 bispecific antibody that binds bivalently to CD20 on B cells and monovalently to CD3 on T cells, forming an immune synapse that activates TCR/CD3 signaling and drives T‑cell–mediated cytotoxicity against CD20‑positive lymphoma cells.
The CD20×CD3 bispecific antibody bridges CD20+ cells to T cells, activating CD3/TCR signaling and inducing perforin/granzyme-mediated killing of the CD20-expressing cells.
Allogeneic T cells from a new donor engineered to express an anti-CD7 chimeric antigen receptor; CAR engagement drives cytotoxic killing of CD7+ malignant T cells through TCR-like signaling, perforin/granzyme release, and cytokine secretion. Expected on-target depletion of normal CD7+ T cells and some NK cells, leading to T-cell aplasia.
Allogeneic donor-derived T cells are engineered to express an anti-CD7 chimeric antigen receptor. Upon binding CD7 on malignant T cells, the CAR triggers TCR-like signaling that activates cytotoxic effector functions, including perforin/granzyme-mediated killing and cytokine secretion. On-target effects also deplete normal CD7+ T cells and some NK cells, leading to T-cell aplasia.
Anti-CD7 CAR T cells bind CD7 and are activated to kill CD7+ cells via perforin/granzyme-mediated cytolysis (and related T-cell effector pathways).
A type II anti‑CD20 monoclonal antibody used as priming to deplete circulating B cells and reduce cytokine release syndrome risk prior to glofitamab administration.
Obinutuzumab is a glycoengineered, humanized type II anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells and depletes them by enhanced FcγRIIIa-mediated antibody-dependent cellular cytotoxicity and phagocytosis, and by inducing direct, caspase-independent cell death; it has reduced reliance on complement-dependent cytotoxicity.
Binds CD20 on B cells and triggers FcγRIIIa-mediated ADCC by NK cells and phagocytosis by macrophages; also induces direct, caspase‑independent cell death (with reduced reliance on complement).