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.
ATG contains antibodies that can bind HLA-DR; bound cells are killed via complement-dependent lysis, Fc-mediated ADCC, and apoptosis.
Autologous CD19-directed CAR T-cell therapy. Patient T cells are engineered ex vivo to express a chimeric antigen receptor targeting CD19 and are administered as a single intravenous infusion (0.2–2 million cells/kg) after lymphodepleting chemotherapy to promote expansion. The CAR engages CD19 on B-lineage cells to trigger T-cell activation, proliferation, and cytotoxic killing of malignant CD19+ cells, with expected on-target B-cell aplasia.
Autologous T cells are engineered ex vivo to express a chimeric antigen receptor that binds CD19 on B‑lineage cells. Upon engagement, CAR signaling (CD3ζ with costimulatory domains) activates the T cells, driving proliferation and cytotoxic killing of CD19+ malignant cells, resulting in tumor cell lysis and on‑target B‑cell aplasia; lymphodepleting chemotherapy is used to enhance CAR T‑cell expansion and persistence.
CD19-directed CAR T cells bind CD19 on target cells, activate, and directly kill CD19+ cells via T-cell cytotoxic mechanisms (perforin/granzyme release and Fas–FasL–mediated apoptosis).
An IgG1 monoclonal antibody targeting Claudin 18.2 (CLDN18.2) on gastric/GEJ tumor cells, mediating immune effector functions including Fcγ receptor–driven antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and potential antibody-dependent cellular phagocytosis (ADCP).
A tumor-targeting IgG1 monoclonal antibody that binds Claudin 18.2 on gastric/GEJ cancer cells and induces immune-mediated killing via Fcγ receptor–dependent ADCC, complement-dependent cytotoxicity (CDC), and antibody-dependent cellular phagocytosis (ADCP).
The antibody binds Claudin 18.2 on tumor cells and recruits immune effectors to kill via FcγR-mediated ADCC, complement-dependent cytotoxicity (CDC/MAC), and antibody-dependent cellular phagocytosis (ADCP).
Autologous gene-modified T cells engineered to express a dual-target chimeric antigen receptor recognizing TIM-3 and CD123, designed to induce T-cell mediated cytotoxicity against TIM-3+ CD123+ leukemia stem cells and CD123+ AML blasts while sparing normal hematopoietic cells.
Autologous T cells are gene-modified to express a dual-target chimeric antigen receptor that recognizes TIM-3 and CD123. Antigen engagement on TIM-3+ CD123+ leukemia stem cells and CD123+ AML blasts activates CAR signaling (CD3zeta/co-stimulation), driving T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing. Dual recognition is intended to enhance specificity and reduce on-target/off-tumor toxicity to normal hematopoietic cells, which have minimal TIM-3 expression.
Dual-target CAR-T cells recognize TIM-3 together with CD123 on the same cell, activating CAR signaling and inducing perforin/granzyme-mediated cytolysis (with cytokine-driven apoptosis).
Autologous gene-modified T cells engineered to express a dual-target chimeric antigen receptor recognizing TIM-3 and CD123, designed to induce T-cell mediated cytotoxicity against TIM-3+ CD123+ leukemia stem cells and CD123+ AML blasts while sparing normal hematopoietic cells.
Autologous T cells are gene-modified to express a dual-target chimeric antigen receptor that recognizes TIM-3 and CD123. Antigen engagement on TIM-3+ CD123+ leukemia stem cells and CD123+ AML blasts activates CAR signaling (CD3zeta/co-stimulation), driving T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing. Dual recognition is intended to enhance specificity and reduce on-target/off-tumor toxicity to normal hematopoietic cells, which have minimal TIM-3 expression.
CAR-T cells recognize CD123 (often with TIM-3) via the dual CAR, triggering T-cell activation and perforin/granzyme-mediated lysis of CD123+ target cells.