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).
NO
INDIRECT
Zolbetuximab binds Claudin 18.2 on tumor cells and triggers ADCC, CDC (via C1q binding to Fc), and ADCP to kill CLDN18.2+ cells. C1q is part of complement activation but is not the antigen targeted; cells expressing C1q are not directly killed.
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).
NO
INDIRECT
Zolbetuximab binds CLDN18.2 on tumor cells; its Fc engages Fc gamma receptor IIa (CD32A) on immune effector cells to trigger ADCC/ADCP and complement-mediated killing of CLDN18.2+ cells. FcγRIIa-expressing cells are not targeted or killed.
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.
YES
DIRECT
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.
YES
DIRECT
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.
Bispecific IgG monoclonal antibody that binds CD20 on B cells and CD3 on T cells, redirecting and activating T cells to kill CD20+ malignant B cells.
Humanized bispecific IgG that binds CD20 on B cells and CD3 on T cells, physically linking T cells to CD20+ malignant B cells to trigger T‑cell activation, immune synapse formation, and cytotoxic killing of the target B cells.
YES
DIRECT
Mosunetuzumab bridges CD20 on B cells to CD3 on T cells, forming an immune synapse and activating T cells to kill the CD20+ cells via perforin/granzyme-mediated cytotoxicity (and related apoptotic pathways).