Anti-CD38 IgG1 monoclonal antibody that targets CD38 on myeloma plasma cells, mediating CDC, ADCC, ADCP, direct apoptosis, and depletion of CD38+ immunosuppressive cells.
Human IgG1κ anti-CD38 monoclonal antibody that binds CD38 on myeloma cells and induces tumor cell death via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, antibody-dependent cellular phagocytosis, and direct apoptosis; also depletes CD38+ immunosuppressive cells (e.g., Tregs, Bregs, MDSCs), enhancing anti-tumor immunity.
Daratumumab binds CD38 on target cells and induces complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity (via NK cells), antibody-dependent cellular phagocytosis (via macrophages), and can trigger direct apoptosis.
CMAB008; a chimeric IgG1 monoclonal antibody biologic targeting TNF-α. It binds soluble and transmembrane TNF-α to neutralize its activity, blocks TNFR1/TNFR2 signaling, downregulates NF-κB–mediated inflammatory cascades (e.g., IL-1, IL-6, adhesion molecules), reduces leukocyte trafficking, and may induce apoptosis of activated immune cells via ADCC/CDC.
Chimeric IgG1 monoclonal antibody that binds soluble and transmembrane TNF-α, neutralizing its activity and blocking TNFR1/TNFR2 signaling. This suppresses NF-κB–driven inflammatory pathways (e.g., IL-1, IL-6, adhesion molecules), reduces leukocyte trafficking, and can induce apoptosis of activated immune cells via ADCC/CDC.
Binding to transmembrane TNF enables IgG1 Fc–mediated ADCC and complement-dependent cytotoxicity against TNF-expressing cells, and can induce apoptosis via reverse signaling through membrane TNF.
Autologous gene-modified T lymphocytes engineered to express a chimeric antigen receptor targeting B-cell antigens, intended to deplete pathogenic B cells and plasma-lineage cells, reduce autoantibody production, and dampen B–T cell interactions.
Autologous T cells are genetically engineered ex vivo to express a chimeric antigen receptor that recognizes B‑cell antigens. After infusion, these CAR‑T cells bind and kill B cells and plasma‑lineage cells, depleting pathogenic B cells, reducing autoantibody production, and disrupting B–T cell interactions/antigen presentation to dampen downstream inflammatory responses and enable immune reconstitution.
CAR-T cells recognize the B-cell surface antigen via the CAR and directly kill the bound B cell through T-cell effector functions (perforin/granzyme cytolysis and death receptor–mediated apoptosis).
Allogeneic, off-the-shelf CAR T-cell therapy targeting CD19; engineered donor T cells mediate cytotoxic killing of CD19-positive B cells via perforin/granzyme and cytokine release pathways.
Allogeneic donor-derived T cells engineered with a CD19-specific chimeric antigen receptor recognize CD19 on B-lineage cells and, upon engagement, activate T-cell effector functions to kill CD19-positive cells via perforin/granzyme-mediated cytolysis and cytokine release, leading to depletion of malignant B cells.
CAR T cells bind CD19 and kill target cells via T-cell effector functions, primarily perforin/granzyme-mediated cytolysis (± Fas/FasL apoptosis).
Autologous T lymphocytes genetically engineered to express a tumor antigen–specific chimeric antigen receptor, used to treat hematologic malignancies and associated with immune effector cell–associated neurotoxicity syndrome (ICANS).
Autologous T cells are genetically engineered to express a chimeric antigen receptor that recognizes a tumor antigen (e.g., CD19). CAR engagement activates CD3ζ and costimulatory domains (such as CD28 or 4‑1BB), leading to T‑cell expansion, cytokine release, and perforin/granzyme‑mediated cytotoxic killing of antigen‑expressing malignant cells; this immune activation can cause toxicities including ICANS.
CAR T cells recognize CD19 on target cells; CAR signaling triggers T-cell degranulation with perforin/granzyme and death receptor pathways, inducing apoptosis of CD19-expressing cells.