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.
YES
DIRECT
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.
NO
INDIRECT
Infliximab neutralizes soluble TNF-α and blocks TNFR1/2 signaling, reducing inflammation; it does not bind a cell-surface target on TNF-secreting cells, so no direct ADCC/CDC-mediated killing. (Direct cytotoxicity occurs only when binding transmembrane TNF.)
Autologous cellular immunotherapy in which patient-derived dendritic cells are pulsed with tumor-specific neoantigen peptides to present via HLA class I/II and prime/expand neoantigen-specific CD8+ cytotoxic and CD4+ helper T cells.
Autologous dendritic cells are loaded ex vivo with patient-specific tumor neoantigen peptides and, upon reinfusion, present these antigens via HLA class I and II to prime and expand neoantigen-specific CD8+ cytotoxic and CD4+ helper T cells, driving tumor-specific immune responses and killing of neoantigen-expressing cancer cells.
YES
INDIRECT
DC vaccine primes/expands neoantigen-specific CD8+ T cells, which recognize HLA-I–presented neoantigen on tumor cells and kill them via TCR-mediated cytolysis (perforin/granzyme and Fas–FasL pathways).
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.
YES
DIRECT
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.
YES
DIRECT
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).