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.
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.
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.
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).
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.
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.
CD19-directed CAR T cells bind CD19 on target B cells, become activated, and kill them via perforin/granzyme-mediated cytolysis (and apoptosis).