Rabbit polyclonal anti-thymocyte globulin that depletes T cells to prevent rejection and GVHD.
Rabbit polyclonal anti-thymocyte IgG that binds multiple T-cell surface antigens and depletes T cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, producing immunosuppression to prevent rejection and GVHD.
YES
DIRECT
Thymoglobulin binds CD3ε on T cells and induces complement-dependent lysis and Fc-mediated ADCC; crosslinking can also trigger apoptosis, depleting CD3+ cells.
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 CD30 on target cells, triggering MHC‑independent T‑cell activation and cytolysis via perforin/granzyme (and Fas/FasL) pathways.
Autologous T cells engineered to express a chimeric antigen receptor targeting B7-H3 (CD276) and incorporating an inducible caspase-9 (iC9) safety switch; administered intraperitoneally to mediate T-cell cytotoxicity against B7-H3–positive ovarian cancer.
Autologous T cells are gene-modified to express a chimeric antigen receptor that binds B7-H3 (CD276) on tumor cells, triggering T-cell activation and cytotoxic killing via perforin/granzyme and cytokine release. The product includes an inducible caspase-9 (iC9) safety switch that can be activated (e.g., by rimiducid) to ablate the CAR-T cells in case of severe toxicity; administered intraperitoneally for B7-H3–positive ovarian cancer.
YES
DIRECT
CAR-T cells bind B7-H3 on target cells, form an immunologic synapse, and kill via perforin/granzyme-mediated apoptosis (and cytokine-dependent cytotoxicity).
Autologous T cells engineered to express a chimeric antigen receptor targeting B7-H3 (CD276) and incorporating an inducible caspase-9 (iC9) safety switch; administered intraperitoneally to mediate T-cell cytotoxicity against B7-H3–positive ovarian cancer.
Autologous T cells are gene-modified to express a chimeric antigen receptor that binds B7-H3 (CD276) on tumor cells, triggering T-cell activation and cytotoxic killing via perforin/granzyme and cytokine release. The product includes an inducible caspase-9 (iC9) safety switch that can be activated (e.g., by rimiducid) to ablate the CAR-T cells in case of severe toxicity; administered intraperitoneally for B7-H3–positive ovarian cancer.
NO
INDIRECT
iC9 is a suicide switch within the engineered CAR-T cells; when activated by a small-molecule dimerizer (e.g., rimiducid), it dimerizes caspase-9 and triggers apoptosis of the CAR-T cells themselves. The CAR-T does not recognize iC9 on target cells.
An autologous, gene-edited CAR T-cell therapy targeting BCMA on myeloma cells. The CAR construct is integrated non-virally at the PD-1 locus to modulate/abrogate PD-1 signaling, aiming to reduce T-cell exhaustion and enhance antitumor activity. Ex vivo–expanded CAR T cells bind BCMA, activate cytotoxic responses, and kill BCMA+ malignant plasma cells while countering PD-1/PD-L1–mediated immunosuppression.
Autologous gene-edited CAR T cells engineered with a BCMA-specific chimeric antigen receptor recognize and bind BCMA on myeloma cells, triggering cytotoxic killing of BCMA-positive malignant plasma cells. The CAR construct is integrated at the PD-1 locus to disrupt/modulate PD-1 signaling, reducing T-cell exhaustion and countering PD-1/PD-L1-mediated immunosuppression, thereby enhancing persistence and antitumor activity.
YES
DIRECT
BCMA-specific CAR T cells bind BCMA on target cells, form an immune synapse, and kill via perforin/granzyme release and death-receptor (e.g., Fas/FasL) signaling, leading to apoptosis/lysis of BCMA+ cells.