Off-the-shelf allogeneic CAR NK cell therapy targeting GPC3 for advanced hepatocellular carcinoma; armed with calibrated-release IL-15 to support NK-cell survival, proliferation, and persistence.
Off-the-shelf allogeneic NK cells engineered with a CAR targeting glypican-3 (GPC3) recognize GPC3-expressing tumor cells and trigger NK-mediated cytotoxicity (perforin/granzyme and cytokine release). The product includes calibrated-release IL-15 to enhance NK-cell survival, proliferation, and persistence in vivo.
NO
INDIRECT
SN301A CAR NK cells kill GPC3-positive tumor cells via CAR-triggered perforin/granzyme release. CD132 (common gamma chain) is engaged by IL-15 to support NK-cell survival and is not a cytotoxic target.
Rabbit polyclonal antilymphocyte globulin used for in vivo T-cell depletion to reduce graft-versus-host disease risk.
Rabbit polyclonal IgG against multiple human T‑cell surface antigens (e.g., CD2, CD3, CD4, CD8, HLA) that depletes T lymphocytes via complement-dependent cytotoxicity, Fc-mediated ADCC/phagocytosis, and apoptosis, producing in vivo T‑cell immunosuppression to reduce GVHD risk.
YES
DIRECT
rATG contains antibodies that bind CD28 on T cells and deplete them via complement-dependent lysis and Fc-mediated ADCC/phagocytosis, with additional apoptosis induction.
Autologous anti-CD19 CAR T-cell therapy; patient T cells are engineered to express a CD19-directed chimeric antigen receptor, activating T-cell cytotoxicity to eliminate CD19+ malignant and normal B cells (often causing B-cell aplasia).
Autologous T cells are engineered ex vivo to express a CD19-directed chimeric antigen receptor; upon binding CD19 on malignant and normal B cells, CAR signaling activates T-cell cytotoxicity and cytokine release, resulting in targeted lysis and depletion of CD19+ cells (often causing B-cell aplasia).
YES
DIRECT
Anti-CD19 CAR T cells bind CD19 on target B cells; CAR signaling triggers a cytolytic synapse and release of perforin/granzymes (and Fas–FasL), inducing apoptosis/lysis of CD19+ cells.
Afucosylated humanized IgG1κ monoclonal antibody (brand name Fasenra) that binds IL‑5 receptor alpha (IL‑5Rα) on eosinophils and basophils, blocks IL‑5 signaling, and induces antibody‑dependent cell‑mediated cytotoxicity (ADCC), leading to near-complete eosinophil depletion and reduction of type‑2 eosinophilic inflammation in severe eosinophilic asthma.
Afucosylated humanized IgG1κ monoclonal antibody that binds IL‑5 receptor alpha (IL‑5Rα) on eosinophils and basophils, blocks IL‑5 signaling, and induces potent NK cell–mediated ADCC, leading to near-complete eosinophil depletion and reduction of type‑2 eosinophilic inflammation.
YES
DIRECT
Benralizumab binds IL-5Ralpha on eosinophils/basophils and engages Fc gamma RIIIa on NK cells to trigger potent ADCC, directly killing IL-5Ralpha+ cells (with additional IL-5 signaling blockade).
An antibody-drug conjugate targeting mesothelin (MSLN). The monoclonal antibody binds MSLN on tumor cells, is internalized, and releases a cytotoxic payload intracellularly to induce tumor cell death, with potential bystander effect.
Monoclonal antibody targets mesothelin (MSLN) on tumor cells, is internalized, and releases an attached cytotoxic payload inside the cell to induce tumor cell death, with potential bystander killing of adjacent cells.
YES
DIRECT
ADC binds mesothelin on target cells, is internalized, and releases a cytotoxic payload inside the cell, causing cell death (with potential bystander killing).