Intravenous T-cell–engaging bispecific antibody (CD20×CD3; 2:1 format) that redirects patient T cells via CD3 to kill CD20-positive malignant B cells.
Glofitamab is an intravenous CD20×CD3 bispecific antibody (2:1 format, two CD20 arms and one CD3 arm) that simultaneously binds CD20 on B cells and CD3 on T cells, cross-linking them to form an immune synapse. This redirects and activates patient T cells to kill CD20-positive malignant B cells via perforin/granzyme-mediated cytotoxicity and apoptosis, independent of MHC presentation.
The CD20×CD3 bispecific links T cells to CD20+ cells, forming an immune synapse and activating T cells to release perforin and granzymes, causing lysis/apoptosis of the CD20-expressing cells (MHC-independent).
Intravenous type II, glycoengineered anti-CD20 monoclonal antibody used as lead-in/debulking to reduce CRS risk; depletes B cells via enhanced ADCC/ADCP and direct cell death.
Type II, glycoengineered anti‑CD20 IgG1 that binds CD20 on B cells; afucosylated Fc increases FcγRIIIa affinity to enhance ADCC and ADCP, and the type II binding/elbow‑hinge modifications promote strong, largely caspase‑independent direct cell death, resulting in potent B‑cell depletion.
Obinutuzumab binds CD20 on B cells and eliminates them via enhanced Fc-gamma RIIIa–mediated ADCC and ADCP by effector cells, plus type II antibody–induced, largely caspase-independent direct cell death (with minimal complement involvement).
Rabbit polyclonal anti-thymocyte globulin (polyclonal IgG) given as a single IV dose (1 mg/kg) 48–72 hours after emergence from aplasia to reinforce GVHD prophylaxis after haploidentical allo-HSCT. Binds multiple T‑cell surface antigens (e.g., CD2, CD3, CD4, CD8, HLA‑DR) leading to T‑cell depletion via complement-dependent cytotoxicity and apoptosis, with Fc-mediated clearance and immunomodulatory effects; also impacts B cells, NK cells, and dendritic cells.
Rabbit polyclonal IgG that binds multiple T‑cell surface antigens (e.g., CD2, CD3, CD4, CD8, HLA‑DR), causing T‑cell depletion via complement‑dependent cytotoxicity and apoptosis, with Fc‑mediated clearance (ADCC/ADCP) and immunomodulatory effects; also impacts B cells, NK cells, and dendritic cells to reduce alloreactivity and GVHD risk.
Thymoglobulin antibodies bind CD2 on T cells, triggering complement-dependent lysis and Fc-mediated ADCC/ADCP, and inducing apoptosis, thereby depleting CD2+ cells.
Rabbit polyclonal anti-thymocyte globulin (polyclonal IgG) given as a single IV dose (1 mg/kg) 48–72 hours after emergence from aplasia to reinforce GVHD prophylaxis after haploidentical allo-HSCT. Binds multiple T‑cell surface antigens (e.g., CD2, CD3, CD4, CD8, HLA‑DR) leading to T‑cell depletion via complement-dependent cytotoxicity and apoptosis, with Fc-mediated clearance and immunomodulatory effects; also impacts B cells, NK cells, and dendritic cells.
Rabbit polyclonal IgG that binds multiple T‑cell surface antigens (e.g., CD2, CD3, CD4, CD8, HLA‑DR), causing T‑cell depletion via complement‑dependent cytotoxicity and apoptosis, with Fc‑mediated clearance (ADCC/ADCP) and immunomodulatory effects; also impacts B cells, NK cells, and dendritic cells to reduce alloreactivity and GVHD risk.
Rabbit polyclonal IgG binds the CD3 complex (including CD3D) on T cells, leading to complement-dependent lysis and Fc-mediated ADCC/ADCP, with additional apoptosis induced upon receptor cross-linking, resulting in T-cell depletion.
Rabbit polyclonal anti-thymocyte globulin (polyclonal IgG) given as a single IV dose (1 mg/kg) 48–72 hours after emergence from aplasia to reinforce GVHD prophylaxis after haploidentical allo-HSCT. Binds multiple T‑cell surface antigens (e.g., CD2, CD3, CD4, CD8, HLA‑DR) leading to T‑cell depletion via complement-dependent cytotoxicity and apoptosis, with Fc-mediated clearance and immunomodulatory effects; also impacts B cells, NK cells, and dendritic cells.
Rabbit polyclonal IgG that binds multiple T‑cell surface antigens (e.g., CD2, CD3, CD4, CD8, HLA‑DR), causing T‑cell depletion via complement‑dependent cytotoxicity and apoptosis, with Fc‑mediated clearance (ADCC/ADCP) and immunomodulatory effects; also impacts B cells, NK cells, and dendritic cells to reduce alloreactivity and GVHD risk.
Rabbit polyclonal IgG binds CD3E on T cells, fixing complement (CDC) and engaging Fc receptors to induce ADCC/ADCP, with apoptosis, leading to T‑cell depletion.