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 CD22 via the engineered CAR, become activated, and kill target cells primarily through perforin/granzyme-mediated lysis, with contribution from Fas/FasL apoptosis and cytokine-mediated effects.
Autologous, gene-modified CD19-directed CAR T-cell therapy with metabolic armoring designed to enhance T-cell metabolic fitness, expansion, persistence, and function in the tumor microenvironment; mediates CD19-specific cytotoxicity against B-cell lymphomas.
Autologous T cells engineered to express a CD19-directed chimeric antigen receptor. Binding to CD19 on B-cell lymphomas activates the T cells to proliferate, release cytokines, and kill target cells via perforin/granzyme. Metabolic armoring enhances T-cell metabolic fitness, expansion, and persistence in the tumor microenvironment to improve anti-tumor activity.
YES
DIRECT
CD19-directed CAR T cells bind CD19 on target B cells, become activated, and kill them via perforin/granzyme-mediated cytolysis (and apoptosis).
A human IgG1 monoclonal antibody targeting OX40 (CD134) on activated T cells; blocks OX40–OX40L costimulatory signaling and can deplete OX40+ T cells via ADCC, reducing T‑cell survival and pathogenic type 2 inflammation.
Human IgG1 monoclonal antibody that binds OX40 (CD134) on activated T cells, blocks OX40-OX40L costimulatory signaling to suppress T-cell survival/activation and type 2 cytokine responses, and can deplete OX40+ T cells via ADCC.
YES
DIRECT
IgG1 Fc engages effector cells to mediate ADCC (and related Fc-effector functions), depleting OX40+ T cells bound by the antibody.
A CD20×CD3 bispecific antibody that binds CD20 on B cells and CD3 on T cells to trigger targeted T‑cell–mediated cytotoxicity.
Humanized CD20×CD3 bispecific antibody that binds CD20 on B cells and CD3 on T cells, crosslinking them to activate T cells and induce targeted cytotoxic killing of CD20-positive B-cell malignancies via immune synapse formation and perforin/granzyme release.
YES
DIRECT
Bispecific antibody crosslinks CD3 on T cells with CD20 on target B cells, forming an immune synapse that triggers T‑cell–mediated killing via perforin/granzyme release.
A CD20×CD3 bispecific antibody that binds CD20 on B cells and CD3 on T cells to trigger targeted T‑cell–mediated cytotoxicity.
Humanized CD20×CD3 bispecific antibody that binds CD20 on B cells and CD3 on T cells, crosslinking them to activate T cells and induce targeted cytotoxic killing of CD20-positive B-cell malignancies via immune synapse formation and perforin/granzyme release.
NO
INDIRECT
Mosunetuzumab binds CD3ε on T cells to activate and redirect them to kill CD20+ B cells via immune synapse formation and perforin/granzyme release; CD3ε-expressing cells are engaged as effectors, not killed.