Ex vivo engineered/expanded autologous T cells administered intravenously for antigen-directed adoptive cell therapy. These cells recognize a tumor-associated antigen on GI cancers (esophageal, gastric, pancreatic, colorectal) and mediate cytotoxic killing and cytokine-driven immune activation; in vivo expansion and persistence are assessed.
Autologous T cells engineered ex vivo to express a chimeric antigen receptor that recognizes a tumor‑associated antigen on gastrointestinal tumor cells. Upon antigen engagement, CAR signaling (CD3ζ with co‑stimulatory domains) activates the T cells to mediate targeted cytotoxic killing and cytokine release, with in vivo expansion and persistence supporting ongoing anti‑tumor activity.
YES
DIRECT
CAR T cells bind the tumor-associated antigen, form an immune synapse, and kill target cells via perforin/granzyme-mediated cytolysis and apoptosis (Fas–FasL), with cytokine release.
Type II, glycoengineered anti-CD20 monoclonal antibody that induces direct B-cell death and enhances antibody-dependent cellular cytotoxicity.
Type II, glycoengineered humanized anti-CD20 IgG1 that binds CD20 on B cells and, via enhanced FcγRIIIa engagement from afucosylated Fc glycans, drives potent antibody-dependent cellular cytotoxicity and phagocytosis, and induces direct, caspase-independent B‑cell death, leading to B‑cell depletion.
YES
DIRECT
Obinutuzumab binds CD20 on B cells, inducing direct caspase-independent cell death and engaging FcγRIIIa on effector cells to drive ADCC and phagocytosis (with some complement activity), depleting CD20+ cells.
Type II, glycoengineered anti-CD20 monoclonal antibody that induces direct B-cell death and enhances antibody-dependent cellular cytotoxicity.
Type II, glycoengineered humanized anti-CD20 IgG1 that binds CD20 on B cells and, via enhanced FcγRIIIa engagement from afucosylated Fc glycans, drives potent antibody-dependent cellular cytotoxicity and phagocytosis, and induces direct, caspase-independent B‑cell death, leading to B‑cell depletion.
NO
INDIRECT
Obinutuzumab binds CD20 on B cells; its afucosylated Fc engages FcγRIIIa (CD16a) on NK cells/macrophages to trigger ADCC/ADCP, killing CD20+ B cells (and also inducing direct B‑cell death). CD16a-expressing cells are effectors, not targets.
Chimeric anti-CD20 monoclonal antibody that depletes B cells via complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity.
Chimeric anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive cells via complement-dependent cytotoxicity and Fc-mediated antibody-dependent cellular cytotoxicity/phagocytosis, leading to apoptosis of targeted B cells.
YES
DIRECT
Rituximab binds CD20 on B cells and eliminates them via complement-dependent cytotoxicity and Fc-mediated ADCC/antibody-dependent phagocytosis; crosslinking can also trigger apoptosis.
Autologous CAR-T cells targeting CD22 on B-lineage cells; CAR activation induces T-cell effector functions to kill CD22-positive malignant B cells, potentially causing B-cell aplasia.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that binds CD22 on B-lineage cells. Antigen engagement activates CAR signaling (CD3zeta with co-stimulatory domains), leading to T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated killing of CD22-positive malignant B cells, with potential on-target B-cell aplasia.
YES
DIRECT
CD22-specific CAR-T cells bind CD22 on B cells; CAR signaling activates T-cell effector functions leading to perforin/granzyme-mediated lysis of CD22-positive cells.