Chimeric IgG1 monoclonal antibody targeting soluble and transmembrane TNF-α; blocks TNFR1/2-mediated signaling to reduce NF-κB–driven inflammation (cytokines/chemokines, adhesion molecules, leukocyte trafficking) and can induce apoptosis of activated TNF-expressing immune cells.
Chimeric IgG1 monoclonal antibody that binds soluble and transmembrane TNF-alpha, neutralizing TNF and preventing TNFR1/2 signaling. This suppresses NF-kB–driven inflammatory pathways (proinflammatory cytokines/chemokines, adhesion molecules, leukocyte trafficking) and can induce apoptosis of activated TNF-expressing immune cells via Fc-mediated effects/reverse signaling.
NO
INDIRECT
Infliximab neutralizes soluble TNF-α and blocks TNFR signaling; it does not directly engage or kill cells via the soluble target. Any direct cytotoxicity occurs only when binding transmembrane TNF (reverse signaling/ADCC), not the soluble form.
Chimeric IgG1 monoclonal antibody targeting soluble and transmembrane TNF-α; blocks TNFR1/2-mediated signaling to reduce NF-κB–driven inflammation (cytokines/chemokines, adhesion molecules, leukocyte trafficking) and can induce apoptosis of activated TNF-expressing immune cells.
Chimeric IgG1 monoclonal antibody that binds soluble and transmembrane TNF-alpha, neutralizing TNF and preventing TNFR1/2 signaling. This suppresses NF-kB–driven inflammatory pathways (proinflammatory cytokines/chemokines, adhesion molecules, leukocyte trafficking) and can induce apoptosis of activated TNF-expressing immune cells via Fc-mediated effects/reverse signaling.
YES
DIRECT
Infliximab binds transmembrane TNF-α; antibody cross-linking induces reverse signaling–mediated apoptosis of TNF-expressing immune cells and its IgG1 Fc triggers ADCC and complement-dependent cytotoxicity against tmTNF+ cells.
Autologous T cells engineered to express a chimeric antigen receptor targeting CD19 to induce MHC-independent T-cell activation, proliferation, cytokine release, and cytotoxic killing of CD19-positive malignant B cells.
Autologous T cells engineered to express an anti-CD19 chimeric antigen receptor bind CD19 on B cells, triggering MHC-independent activation via CD3z and costimulatory domains, leading to T-cell expansion, cytokine release, and cytotoxic killing of CD19-positive malignant B cells.
YES
DIRECT
Anti-CD19 CAR T cells bind CD19 and, upon CAR signaling, directly kill CD19+ cells via perforin/granzyme cytolysis and Fas–FasL–mediated apoptosis, with associated cytokine release.
Autologous T cells engineered to express a chimeric antigen receptor targeting CD30 for MHC-independent activation and killing of CD30-positive Hodgkin and T-cell lymphomas.
Autologous T cells are engineered to express a chimeric antigen receptor specific for CD30, enabling MHC-independent recognition of CD30-positive tumor cells. Upon binding CD30, CAR signaling activates the T cells, inducing proliferation, cytokine release, and cytotoxic killing via perforin/granzyme-mediated lysis of CD30-expressing Hodgkin and T-cell lymphoma cells.
YES
DIRECT
Anti-CD30 CAR T cells bind CD30 on target cells, triggering T-cell activation and direct killing via perforin/granzyme-mediated cytolysis (and Fas/FasL apoptosis).
Autologous CAR T-cell product designed to recognize both CD20 and CD30 antigens to mediate MHC-independent cytotoxicity against CD20-positive or CD20/CD30 double-positive lymphomas, including post–CD19 CAR T relapse.
Autologous T cells engineered with a bispecific chimeric antigen receptor that binds CD20 and CD30 on malignant cells, triggering MHC-independent T-cell activation, cytokine release, and cytotoxic killing of CD20+ or CD20/CD30+ lymphomas, helping prevent antigen escape after CD19-directed therapy.
YES
DIRECT
CAR T cells bind CD20 via the CAR, triggering MHC-independent activation and perforin/granzyme-mediated cytolysis (and Fas/FasL apoptosis) of CD20+ cells.