Chimeric IgG1 monoclonal antibody targeting TNF-α; binds soluble and membrane TNF-α to block TNFR1/2 signaling, dampening NF-κB/MAPK pathways, reducing pro-inflammatory cytokines and leukocyte trafficking, and potentially inducing apoptosis of activated T cells/macrophages to promote mucosal healing.
Chimeric IgG1 monoclonal antibody against TNF-α; binds soluble and transmembrane TNF-α to prevent TNFR1/2 signaling, suppressing NF-κB/MAPK–mediated inflammation, lowering pro‑inflammatory cytokines and leukocyte trafficking, and can induce apoptosis of activated immune cells to promote mucosal healing.
Infliximab binds transmembrane TNF on activated immune cells; its IgG1 Fc recruits effector functions (ADCC/CDC) and triggers reverse signaling through tmTNF, inducing apoptosis of TNF-expressing cells.
Anti-CD20 monoclonal antibody that depletes B cells via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and direct apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and mediates B-cell depletion via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and direct apoptosis.
Rituximab binds CD20 on B cells and induces killing via Fc-mediated ADCC by NK cells/macrophages, complement-dependent cytotoxicity, and can trigger direct apoptosis.
Also known as Inati‑cel or CNCT19, this is an autologous, gene‑modified CD19‑directed CAR T‑cell therapy. It is administered as a single IV infusion of 0.2–0.6×10^8 CAR‑T cells (with an optional second infusion at 5–6 months). Patient T cells are engineered to express an anti‑CD19 CAR with CD3ζ/costimulatory signaling, leading to T‑cell activation, proliferation, cytokine release, and cytotoxic killing of CD19+ B‑ALL blasts and normal B cells, aiming to clear minimal residual disease and induce durable B‑cell aplasia.
Autologous T cells are genetically modified to express a CD19-directed chimeric antigen receptor with CD3zeta and costimulatory signaling domains. Engagement of CD19 on B-ALL blasts and normal B cells activates the CAR T cells, leading to proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing, aiming to eradicate minimal residual disease and induce durable B-cell aplasia.
CD19-directed CAR T cells bind CD19 on target cells, become activated via CD3ζ/costimulatory signaling, and kill through immune-synapse–mediated perforin/granzyme cytolysis (and related death receptor pathways).
Chimeric anti-CD20 monoclonal antibody that depletes B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B lymphocytes and depletes CD20-positive cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis.
Anti-CD20 antibody binds CD20 on B cells and triggers killing via Fc-mediated ADCC (NK cells/macrophages) and complement-dependent cytotoxicity; CD20 crosslinking can also induce apoptosis.
Autologous PSMA-specific chimeric antigen receptor T cells; patient T cells engineered to express a CAR that recognizes prostate-specific membrane antigen (PSMA), leading to T-cell activation and cytotoxic killing of PSMA-positive prostate cancer cells. Administered as a single infusion, with or without prior lymphodepletion.
Autologous T cells are genetically engineered to express a PSMA-specific chimeric antigen receptor. Upon binding PSMA on prostate cancer cells, the CAR triggers T-cell activation, proliferation, cytokine release, and targeted cytotoxic killing of PSMA-positive tumor cells; lymphodepletion may be used to enhance CAR-T expansion and activity.
PSMA CAR-T cells bind PSMA on target cells and induce T-cell cytotoxicity, primarily via perforin/granzyme-mediated apoptosis (and Fas–FasL), leading to lysis of PSMA-positive cells.