Hypoimmune, allogeneic CD22-directed CAR T-cell therapy; donor-derived T cells engineered with an anti-CD22 chimeric antigen receptor to target CD22+ B cells, designed to evade host immune rejection and enhance persistence.
Allogeneic T cells engineered with an anti-CD22 chimeric antigen receptor recognize CD22 on malignant B cells and mediate cytotoxic killing. Hypoimmune edits disrupt MHC class I/II and add CD47 to evade host innate and adaptive immune rejection, enhancing persistence.
Anti-CD22 CAR T cells recognize CD22 on target B cells and induce cytotoxic killing via T-cell effector functions, primarily perforin/granzyme–mediated apoptosis (and death-receptor pathways).
Humanized, afucosylated IgG1 monoclonal antibody (KW-0761) targeting CCR4 that induces ADCC via NK-cell Fcγ receptors, depleting CCR4+ T cells including HTLV-1–infected clones and regulatory T cells, and modulating the CCR4–CCL17/CCL22 axis.
Humanized, afucosylated IgG1 monoclonal antibody targeting CCR4; blocks CCR4-chemokine signaling and triggers enhanced ADCC via NK-cell Fc-gamma receptors, leading to depletion of CCR4+ T cells (including HTLV-1–infected clones and regulatory T cells) and modulation of the CCL17/CCL22 axis.
Mogamulizumab binds CCR4 on target cells and its afucosylated IgG1 Fc engages NK-cell FcγRIIIa to trigger antibody‑dependent cellular cytotoxicity (ADCC), causing lysis/apoptosis of CCR4+ cells.
An intratumorally injected, replication-competent oncolytic herpes simplex virus type 2 engineered to secrete a PD-L1×CD3 bispecific T-cell engager. Mechanisms include tumor-selective oncolysis, in situ innate immune activation (TLR/cGAS–STING, type I IFN), and local T-cell redirection via the secreted PD-L1/CD3 bispecific antibody, potentially also blocking PD-1/PD-L1 signaling.
Intratumoral, replication-competent HSV-2 (ICP34.5/ICP47-deleted) selectively infects and replicates in tumor cells, causing oncolysis and antigen release; viral PAMPs trigger local innate sensing (TLR, cGAS-STING) and type I IFN to inflame the tumor; infected cells secrete a PD-L1×CD3 bispecific antibody that binds PD-L1 on tumor/myeloid cells and CD3 on T cells, redirecting T cells for cytotoxic killing and concurrently blocking PD-1/PD-L1 signaling to relieve T-cell inhibition.
Infected tumor cells secrete a PD-L1×CD3 bispecific that binds PD-L1 on target cells and CD3 on T cells, creating an immune synapse that triggers T‑cell cytotoxicity (perforin/granzyme) and concurrently blocks PD‑1/PD‑L1 signaling; thus PD‑L1+ cells are directly killed by redirected T cells.
Autologous patient T cells genetically engineered to express a chimeric antigen receptor targeting glypican-2 (GPC2) for treatment of relapsed/refractory high-risk neuroblastoma and metastatic retinoblastoma; CAR engagement induces T-cell activation, cytokine release, and cytotoxic killing of GPC2-positive tumor cells, including stem-like compartments.
Autologous T cells engineered with a chimeric antigen receptor targeting glypican-2 (GPC2). CAR binding to GPC2 activates CD3zeta and costimulatory signaling, leading to T-cell activation, cytokine release, proliferation, and targeted cytotoxic killing of GPC2-positive tumor cells (neuroblastoma/retinoblastoma), including stem-like compartments.
GPC2-specific CAR engagement activates T cells to kill GPC2-positive cells via perforin/granzyme-mediated cytolysis and apoptosis pathways (e.g., Fas–FasL).
An antibody–drug conjugate consisting of a humanized anti–Trop-2 IgG1 monoclonal antibody linked to the topoisomerase I inhibitor SN-38; delivers SN-38 to Trop-2–expressing tumor cells to induce DNA damage and apoptosis and may enhance radiosensitivity.
Humanized anti–Trop-2 IgG1 antibody–drug conjugate linked to SN-38. After binding Trop-2 on tumor cells and internalization, SN-38 is released to inhibit topoisomerase I, stabilizing Topo I–DNA complexes, causing DNA breaks, blocking replication, and inducing apoptosis; may enhance radiosensitivity.
Antibody–drug conjugate binds TROP2, is internalized, and releases SN-38 (topoisomerase I inhibitor), causing DNA damage, replication arrest, and apoptosis of the target cell.