Adoptive cellular gene therapy using T cells engineered with a chimeric antigen receptor (e.g., anti-CD19) to target and eliminate malignant B cells in DLBCL.
Autologous T cells are genetically engineered to express a chimeric antigen receptor (e.g., anti-CD19) that binds antigen on malignant B cells independent of MHC, activating the T cells to proliferate, release cytokines, and kill target cells via perforin/granzyme-mediated cytotoxicity, resulting in elimination of the tumor.
YES
DIRECT
CAR-T cells bind CD19 on target cells, form an immune synapse, and kill via perforin/granzyme-mediated cytotoxicity (and Fas–FasL apoptosis).
A nectin‑4–targeted antibody–drug conjugate that binds nectin‑4 on tumor cells, is internalized, and releases a cytotoxic payload to induce tumor cell death.
CRB-701 is a nectin-4–targeted IgG1 antibody-drug conjugate linked via a cleavable linker to monomethyl auristatin E (MMAE). After binding nectin-4 on tumor cells, it is internalized and releases MMAE, which inhibits tubulin polymerization, causing G2/M cell-cycle arrest and apoptosis; the antibody component may also mediate ADCC and CDC against nectin-4–expressing cells.
NO
INDIRECT
CRB-701 binds nectin-4, is internalized, and releases MMAE, which inhibits beta-tubulin polymerization to cause G2/M arrest and apoptosis (with possible ADCC/CDC) in nectin-4–positive cells; tubulin itself is not the targeting antigen.
Allogeneic, off-the-shelf anti-CD70 UCAR-T cell therapy (genetically engineered CAR T cells) that targets CD70 on tumor cells to trigger T-cell activation, cytotoxic killing, and cytokine release.
Allogeneic, off-the-shelf CAR T cells engineered with an anti-CD70 chimeric antigen receptor bind CD70 on tumor cells and activate CAR signaling, leading to T-cell activation, cytokine release, and cytotoxic lysis of CD70-expressing tumor cells.
YES
DIRECT
Anti-CD70 CAR T cells bind CD70 on target cells, activate CAR signaling, and kill them via T-cell effector mechanisms (perforin/granzyme and death receptor pathways), with cytokine release.
Autologous patient T cells retrovirally transduced to co-express three CARs targeting CD19, CD20, and CD22, each with 4-1BB costimulation and CD3ζ signaling, to enhance activation, proliferation, persistence, and cytotoxicity against B-lineage leukemia.
Autologous T cells are retrovirally engineered to co-express three CARs specific for CD19, CD20, and CD22, each with 4-1BB costimulation and a CD3zeta signaling domain. Upon binding these B-lineage antigens on leukemic cells, CAR signaling activates the T cells, driving proliferation, persistence, and cytotoxicity (perforin/granzyme release and cytokine-mediated killing). Targeting three antigens aims to prevent antigen escape.
YES
DIRECT
Anti-CD19 CAR T cells recognize CD19 on target cells, become activated, and kill them via contact-dependent perforin/granzyme cytolysis (with additional apoptosis via cytokine/FasL pathways).
Autologous patient T cells retrovirally transduced to co-express three CARs targeting CD19, CD20, and CD22, each with 4-1BB costimulation and CD3ζ signaling, to enhance activation, proliferation, persistence, and cytotoxicity against B-lineage leukemia.
Autologous T cells are retrovirally engineered to co-express three CARs specific for CD19, CD20, and CD22, each with 4-1BB costimulation and a CD3zeta signaling domain. Upon binding these B-lineage antigens on leukemic cells, CAR signaling activates the T cells, driving proliferation, persistence, and cytotoxicity (perforin/granzyme release and cytokine-mediated killing). Targeting three antigens aims to prevent antigen escape.
YES
DIRECT
CAR T cells bind CD20 via the CAR, become activated, form an immunologic synapse, and kill target cells via perforin/granzyme cytolysis and death-receptor pathways (with supportive cytokine-mediated effects).