Glycoengineered type II anti‑CD20 monoclonal antibody used for B‑cell depletion/bridging and to mitigate cytokine release syndrome.
Glycoengineered humanized anti‑CD20 IgG1 that binds CD20 on B cells and, via enhanced FcγRIIIa engagement from afucosylated Fc glycans, drives potent antibody‑dependent cellular cytotoxicity and phagocytosis, while its type II binding induces direct, caspase‑independent cell death, resulting in efficient B‑cell depletion.
Anti-CD20 mAb binds CD20 on B cells; its afucosylated Fc engages Fc-gamma RIIIa to drive strong ADCC by NK cells and ADCP by macrophages, and type II binding triggers direct, caspase-independent cell death (with minimal complement involvement).
Patient‑derived T cells engineered to express a CD19‑directed chimeric antigen receptor; adoptive cellular therapy administered after lymphodepletion.
Autologous T cells are engineered ex vivo to express a chimeric antigen receptor that binds CD19 on B cells. Upon CD19 engagement, the CAR’s activation (CD3ζ) and co‑stimulatory domains (e.g., CD28 or 4‑1BB) trigger T‑cell activation, proliferation, cytokine release, and cytotoxic killing (perforin/granzyme) of CD19+ malignant and normal B cells after lymphodepleting chemotherapy enhances expansion.
CAR on infused T cells binds CD19 on target cells, triggering CD3ζ/co‑stimulatory signaling that activates the T cells to kill CD19+ cells via perforin/granzyme and death‑receptor–mediated apoptosis.
An antibody–drug conjugate immunotherapy consisting of a humanized anti-CD22 IgG4 monoclonal antibody linked to the cytotoxic agent calicheamicin; it binds CD22 on B-lineage blasts, is internalized, and releases calicheamicin to induce DNA double-strand breaks leading to apoptosis.
Humanized anti-CD22 monoclonal antibody targets CD22 on B-lineage cells, is internalized, and releases the cytotoxic payload calicheamicin, which binds the DNA minor groove to induce double-strand breaks and apoptosis.
Antibody-drug conjugate binds CD22, is internalized, and releases calicheamicin, which induces DNA double-strand breaks leading to apoptosis.
Autologous CD19-targeted Nex-T CAR T-cell therapy; engineered T cells recognize CD19 and deplete pathogenic B-cell subsets to reduce autoantibodies and reset immune tolerance.
Autologous T cells engineered to express a CD19-specific chimeric antigen receptor; after infusion they recognize and kill CD19-positive B-cell subsets (naive/memory B cells and plasmablasts), depleting pathogenic B cells to reduce autoantibody production and help reset immune tolerance.
CD19-directed CAR T cells bind CD19 on B cells, form an immune synapse, and kill target cells via perforin/granzyme-mediated apoptosis (and Fas–FasL pathways).
Subcutaneous anti-CD20 monoclonal antibody that depletes CD20+ B cells via complement-dependent cytotoxicity and ADCC.
Fully human anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells and depletes CD20+ B lymphocytes via complement-dependent cytotoxicity (CDC) and antibody-dependent cellular cytotoxicity (ADCC), thereby reducing pathogenic B-cell activity.
Ofatumumab binds CD20 on B cells and induces complement-dependent cytotoxicity and Fc-mediated effector killing (ADCC/ADCP), leading to lysis of CD20+ cells.