Anti-PD-L1 monoclonal antibody (immune checkpoint inhibitor) that blocks PD-L1 to restore T-cell antitumor activity.
Human IgG1 anti-PD-L1 monoclonal antibody that blocks PD-L1 binding to PD-1, reversing T-cell inhibition to restore antitumor activity; its Fc region can also mediate ADCC against PD-L1-expressing tumor cells.
YES
DIRECT
Avelumab binds PD-L1 on target cells and recruits FcγR-bearing effector cells (e.g., NK cells) to mediate ADCC; it also blocks PD-1/PD-L1 to restore CTL killing (indirect).
Autologous gene-modified T cells expressing a chimeric antigen receptor targeting CD19, CD20, and BCMA; infused after lymphodepletion to treat relapsed/refractory B-cell NHL.
Autologous T cells are genetically engineered to express chimeric antigen receptors that bind CD19, CD20, and BCMA on malignant B-lineage cells. Antigen engagement activates CAR signaling (CD3ζ with co‑stimulatory domains), driving T‑cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of target cells. Multi-antigen targeting reduces antigen escape, and prior lymphodepletion supports in vivo expansion and persistence.
YES
DIRECT
CAR T cells recognize CD19 on target cells, triggering T-cell activation and perforin/granzyme-mediated lysis (and death receptor signaling), killing CD19+ cells.
Autologous GPC3-targeted chimeric antigen receptor T-cell therapy; patient T cells engineered with an anti-GPC3 scFv, costimulatory domains (4-1BB/CD28), and CD3zeta, plus immune microenvironment-activating elements; delivered via hepatic arterial infusion for HCC.
Autologous T cells are engineered to express a chimeric antigen receptor with an anti-GPC3 scFv, 4-1BB/CD28 costimulatory domains, and CD3ζ, enabling MHC-independent recognition and killing of GPC3-positive hepatocellular carcinoma cells via cytotoxic granule release and cytokine secretion. Added immune microenvironment–activating elements are intended to enhance CAR-T activation, expansion, and recruitment/activation of bystander immune cells to overcome the suppressive HCC tumor microenvironment; delivery via hepatic arterial infusion increases exposure to liver tumors.
YES
DIRECT
CAR-T cells bind GPC3 via the CAR and directly kill target cells through perforin/granzyme-mediated apoptosis (and Fas/FasL).
Autologous gene-modified T cells expressing a chimeric antigen receptor targeting CD19, CD20, and BCMA; infused after lymphodepletion to treat relapsed/refractory B-cell NHL.
Autologous T cells are genetically engineered to express chimeric antigen receptors that bind CD19, CD20, and BCMA on malignant B-lineage cells. Antigen engagement activates CAR signaling (CD3ζ with co‑stimulatory domains), driving T‑cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of target cells. Multi-antigen targeting reduces antigen escape, and prior lymphodepletion supports in vivo expansion and persistence.
YES
DIRECT
CAR T cells bind CD20 on target cells, triggering activation and degranulation with perforin/granzymes (and Fas–FasL), inducing apoptosis of CD20+ cells.
Autologous gene-modified T cells expressing a chimeric antigen receptor targeting CD19, CD20, and BCMA; infused after lymphodepletion to treat relapsed/refractory B-cell NHL.
Autologous T cells are genetically engineered to express chimeric antigen receptors that bind CD19, CD20, and BCMA on malignant B-lineage cells. Antigen engagement activates CAR signaling (CD3ζ with co‑stimulatory domains), driving T‑cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of target cells. Multi-antigen targeting reduces antigen escape, and prior lymphodepletion supports in vivo expansion and persistence.
YES
DIRECT
CAR T cells bind BCMA on target cells, triggering CAR signaling and direct cytolysis via perforin/granzyme (and death-receptor) pathways.