Allogeneic, multiplex base-edited anti-CD7 CAR-T cell therapy with edits in TRAC, CD7, PDCD1 (PD-1), and CD52 to target CD7+ malignant T cells, reduce GVHD and fratricide, resist alemtuzumab, and enhance antitumor activity.
Allogeneic, multiplex base-edited anti-CD7 CAR T cells that bind CD7 on malignant T cells and mediate targeted cytotoxicity. Edits knock out TRAC (removes TCR to reduce GVHD), CD7 (prevents fratricide), PDCD1/PD-1 (limits checkpoint inhibition to enhance activity), and CD52 (confers resistance to alemtuzumab during conditioning), enabling effective killing of CD7+ T-cell malignancies.
YES
DIRECT
Anti-CD7 CAR T cells recognize CD7 on target cells and kill them via T-cell effector functions, primarily perforin/granzyme-mediated cytolysis and death receptor signaling.
Allogeneic, multiplex base-edited anti-CD7 CAR-T cell therapy with edits in TRAC, CD7, PDCD1 (PD-1), and CD52 to target CD7+ malignant T cells, reduce GVHD and fratricide, resist alemtuzumab, and enhance antitumor activity.
Allogeneic, multiplex base-edited anti-CD7 CAR T cells that bind CD7 on malignant T cells and mediate targeted cytotoxicity. Edits knock out TRAC (removes TCR to reduce GVHD), CD7 (prevents fratricide), PDCD1/PD-1 (limits checkpoint inhibition to enhance activity), and CD52 (confers resistance to alemtuzumab during conditioning), enabling effective killing of CD7+ T-cell malignancies.
NO
INDIRECT
PD-1 is not a cytotoxic target of BEAM-201; PDCD1 (PD-1) is knocked out in the CAR T cells to prevent inhibition. BEAM-201 kills CD7-expressing cells via CAR engagement of CD7 and T-cell cytotoxic mechanisms (perforin/granzyme), not via PD-1.
Allogeneic, multiplex base-edited anti-CD7 CAR-T cell therapy with edits in TRAC, CD7, PDCD1 (PD-1), and CD52 to target CD7+ malignant T cells, reduce GVHD and fratricide, resist alemtuzumab, and enhance antitumor activity.
Allogeneic, multiplex base-edited anti-CD7 CAR T cells that bind CD7 on malignant T cells and mediate targeted cytotoxicity. Edits knock out TRAC (removes TCR to reduce GVHD), CD7 (prevents fratricide), PDCD1/PD-1 (limits checkpoint inhibition to enhance activity), and CD52 (confers resistance to alemtuzumab during conditioning), enabling effective killing of CD7+ T-cell malignancies.
NO
INDIRECT
TRAC is not targeted for killing; it is knocked out in the CAR T cells to remove their endogenous TCR. BEAM-201 kills CD7-expressing cells via CAR-mediated T-cell cytotoxicity (perforin/granzyme).
Allogeneic, multiplex base-edited anti-CD7 CAR-T cell therapy with edits in TRAC, CD7, PDCD1 (PD-1), and CD52 to target CD7+ malignant T cells, reduce GVHD and fratricide, resist alemtuzumab, and enhance antitumor activity.
Allogeneic, multiplex base-edited anti-CD7 CAR T cells that bind CD7 on malignant T cells and mediate targeted cytotoxicity. Edits knock out TRAC (removes TCR to reduce GVHD), CD7 (prevents fratricide), PDCD1/PD-1 (limits checkpoint inhibition to enhance activity), and CD52 (confers resistance to alemtuzumab during conditioning), enabling effective killing of CD7+ T-cell malignancies.
NO
INDIRECT
BEAM-201 CAR-T cells target CD7, not CD52. CD52 is knocked out in the CAR-T cells to resist anti-CD52 conditioning (alemtuzumab); any killing of CD52+ cells is due to alemtuzumab, not BEAM-201.
Anti-CD52 monoclonal antibody used for lymphodepletion to enhance CAR-T cell engraftment.
Humanized anti-CD52 IgG1 monoclonal antibody that binds CD52 on lymphocytes and other leukocytes and mediates complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity, depleting CD52+ cells; used here for lymphodepletion to enhance CAR-T engraftment (with BEAM-201 edited to resist alemtuzumab).
YES
DIRECT
Alemtuzumab binds CD52 on leukocytes and triggers complement-dependent cytotoxicity and Fc receptor–mediated antibody-dependent cellular cytotoxicity by NK cells/macrophages, lysing CD52+ cells.