A bispecific antibody–drug conjugate targeting EGFR and HER3 that delivers a camptothecin-class topoisomerase I inhibitor payload (brengitecan) to induce DNA damage and tumor cell death.
Bispecific EGFR/HER3-targeted antibody–drug conjugate that binds EGFR- and HER3-expressing tumor cells, is internalized, and releases a camptothecin-class topoisomerase I inhibitor (brengitecan) to induce DNA damage and tumor cell death, with potential bystander effect.
The bispecific ADC binds EGFR on tumor cells, is internalized, and releases the camptothecin-class topoisomerase I inhibitor brengitecan, causing DNA damage and apoptosis (with potential bystander effect).
A bispecific antibody–drug conjugate targeting EGFR and HER3 that delivers a camptothecin-class topoisomerase I inhibitor payload (brengitecan) to induce DNA damage and tumor cell death.
Bispecific EGFR/HER3-targeted antibody–drug conjugate that binds EGFR- and HER3-expressing tumor cells, is internalized, and releases a camptothecin-class topoisomerase I inhibitor (brengitecan) to induce DNA damage and tumor cell death, with potential bystander effect.
The bispecific ADC binds HER3 on target cells, is internalized, and releases the topoisomerase I inhibitor brengitecan, causing DNA damage and cell death (with potential bystander effect).
Autologous, genetically engineered anti-CD19 chimeric antigen receptor (CAR) T-cell therapy that co-expresses and secretes human interleukin-18 (armored CAR). Designed for relapsed/refractory CD19+ non-Hodgkin lymphomas to mediate antigen-specific cytotoxicity against B-cell malignancies, while IL-18 enhances CAR-T expansion/persistence and induces a Th1-skewed proinflammatory environment (enhancing IFN-γ and activating NK cells and macrophages). Administered as a single IV infusion with dose escalation.
Autologous T cells engineered to express an anti-CD19 chimeric antigen receptor and to secrete IL-18. CAR engagement of CD19 on B-cell malignancies triggers antigen-specific T-cell activation and cytolysis, while IL-18 secretion enhances CAR-T expansion and persistence and creates a Th1-skewed proinflammatory milieu, increasing IFN-γ and activating NK cells and macrophages.
Anti-CD19 CAR T cells bind CD19, activate, and kill target cells via perforin/granzyme-mediated cytolysis (with IL-18 enhancing CAR-T expansion and activity).
Autologous (or donor-derived) T cells genetically modified to express an anti-CD19 chimeric antigen receptor that binds CD19 on B-lineage cells and activates T-cell cytotoxicity to eliminate CD19+ leukemic blasts; induces B-cell aplasia.
Autologous or donor-derived T cells are engineered to express an anti‑CD19 chimeric antigen receptor. Binding to CD19 on B‑lineage cells activates CAR signaling (CD3ζ with costimulatory domains), driving T‑cell proliferation, cytokine release, and perforin/granzyme‑mediated cytotoxicity to eradicate CD19+ leukemic blasts, resulting in on‑target B‑cell aplasia.
Anti-CD19 CAR T cells bind CD19 on target cells, become activated, and kill them via perforin/granzyme-mediated cytolysis (and apoptosis), leading to on-target B-cell depletion.
Autologous whole-tumor cell vaccine designed to prime and expand neoantigen-specific T-cell responses in newly diagnosed GBM.
Autologous T cells are primed in vivo by a personalized whole-tumor cell vaccine to generate neoantigen-reactive clones, then collected by leukapheresis, activated and expanded ex vivo, and reinfused to recognize patient-specific neoantigens on GBM cells and kill them via TCR-mediated cytotoxic activity; low-dose IL-2 supports T-cell survival and proliferation.
Adoptively transferred neoantigen-specific T cells recognize the patient-specific peptide–MHC I via their TCR and kill target cells through perforin/granzyme release and Fas/FasL-mediated apoptosis.