Off-the-shelf (allogeneic) CD7-directed chimeric antigen receptor T-cell (CAR-T) therapy; single intravenous dose of 2 x 10^8 CAR+ T cells engineered to express a CD7-binding CAR with CD3zeta/co-stimulatory signaling domains, inducing cytotoxic killing of CD7+ malignant T cells in relapsed/refractory T-ALL/LBL.
Off-the-shelf (allogeneic) T cells engineered to express a CD7-binding chimeric antigen receptor with CD3zeta and costimulatory signaling domains. Upon binding CD7 on malignant T cells, the CAR triggers T-cell activation, cytokine release, and perforin/granzyme-mediated cytotoxicity, leading to selective killing of CD7-positive leukemic/lymphoblastic cells.
YES
DIRECT
CD7-directed CAR-T cells bind CD7 on target cells, become activated, and kill via perforin/granzyme-mediated cytotoxicity (and related T cell effector mechanisms).
Patient-derived T cells primed and expanded ex vivo against individualized tumor neoantigens using autologous antigen-presenting cells, then infused intravenously to mediate TCR-dependent cytotoxicity against neoantigen-expressing cancer cells.
Autologous T cells are primed and expanded ex vivo against patient-specific tumor neoantigens and, after infusion, use their endogenous TCRs to recognize neoantigen peptides presented by MHC on tumor cells, inducing cytotoxic killing via perforin/granzyme and antitumor cytokine release.
YES
DIRECT
Neoantigen-specific TCRs recognize the patient-specific peptide–HLA class I complex on tumor cells, triggering cytotoxic T lymphocyte killing via perforin/granzyme (and Fas–FasL)–mediated apoptosis.
Patient-derived T cells primed and expanded ex vivo against individualized tumor neoantigens using autologous antigen-presenting cells, then infused intravenously to mediate TCR-dependent cytotoxicity against neoantigen-expressing cancer cells.
Autologous T cells are primed and expanded ex vivo against patient-specific tumor neoantigens and, after infusion, use their endogenous TCRs to recognize neoantigen peptides presented by MHC on tumor cells, inducing cytotoxic killing via perforin/granzyme and antitumor cytokine release.
YES
DIRECT
Infused neoantigen-specific T cells use endogenous TCRs to recognize the neoantigen–HLA class II complex on target cells and kill them via perforin/granzyme-mediated cytolysis (and Fas–FasL), inducing apoptosis.
Type II, glycoengineered anti-CD20 monoclonal antibody that depletes CD20+ B cells via ADCC and direct cell death to suppress pathogenic humoral immunity.
Type II, glycoengineered anti-CD20 IgG1 that binds CD20 on B cells and, via enhanced FcγRIIIa engagement, induces potent antibody-dependent cellular cytotoxicity and direct (caspase-independent) cell death, depleting CD20+ B cells to suppress pathogenic humoral immunity.
YES
DIRECT
Obinutuzumab binds CD20 on B cells; its Fc engages FcγRIIIa to trigger NK cell–mediated ADCC (and phagocytosis) and also induces direct, caspase-independent cell death; some complement-mediated lysis may occur.
Fully humanized IgG1 antibody-drug conjugate targeting B7-H3 (CD276); binds B7-H3 on tumor cells, is internalized, and releases a cytotoxic payload to induce tumor-cell death, with potential Fc effector activity.
Fully human IgG1 ADC targeting B7-H3 (CD276); after binding to B7-H3 on tumor cells and internalization, it releases a topoisomerase inhibitor payload that inhibits DNA topoisomerase activity, blocking DNA replication and inducing cell-cycle arrest and apoptosis; the IgG1 Fc may also elicit effector functions such as ADCC/CDC.
YES
DIRECT
ADC binds B7-H3 on target cells, is internalized, and releases a topoisomerase inhibitor that blocks DNA replication leading to cell-cycle arrest and apoptosis; the IgG1 Fc can also trigger ADCC/CDC against B7-H3–expressing cells.