Autologous gene-modified T-cell therapy engineered to express a chimeric antigen receptor targeting mesothelin (MSLN) on ovarian cancer cells. CAR engagement activates CD3ζ/costimulatory signaling, inducing cytokine release and perforin/granzyme-mediated cytotoxicity. Administered as a single IV infusion in dose-escalation cohorts (1×10^6, 3×10^6, 1×10^7, 2×10^7 cells/kg) for advanced, platinum-resistant, MSLN-positive ovarian cancer.
Autologous T cells are engineered to express a chimeric antigen receptor that recognizes mesothelin on tumor cells. CAR engagement activates CD3ζ and costimulatory signaling, inducing T‑cell activation, cytokine release, and perforin/granzyme‑mediated cytotoxic killing of mesothelin‑positive ovarian cancer cells.
CAR-T cells bind mesothelin on target cells, triggering CD3ζ/costimulatory signaling and killing via perforin–granzyme–mediated cytolysis (and Fas/FasL apoptosis).
Fc-enhanced anti-CTLA-4 monoclonal antibody (AGEN1181) designed to deplete intratumoral regulatory T cells via FcγR/ADCC and enhance T-cell priming.
Fc‑engineered anti‑CTLA‑4 IgG1 monoclonal antibody that blocks CTLA‑4–mediated inhibitory signaling to enhance T‑cell priming/activation and engages Fcγ receptors to promote ADCC‑mediated depletion of intratumoral regulatory T cells, thereby augmenting antitumor cytotoxic T‑cell responses.
Binds CTLA-4 on T cells (especially intratumoral Tregs) and engages Fcγ receptor–bearing effector cells to mediate ADCC/ADCP, depleting CTLA-4–expressing cells.
An anti-TROP2 antibody-drug conjugate composed of a TROP2-targeting monoclonal antibody linked via a cleavable peptide to the topoisomerase I inhibitor exatecan; binds TROP2 on tumor cells, is internalized, and releases exatecan to induce DNA damage, S-phase arrest, and apoptosis.
TROP2-targeting antibody-drug conjugate that binds TROP2 on tumor cells, is internalized, and releases the topoisomerase I inhibitor exatecan via a cleavable linker; the released payload inhibits TOP1, causing DNA damage, S-phase arrest, and apoptosis in TROP2-expressing tumor cells.
ADC binds TROP2 on tumor cells, is internalized, and releases the TOP1 inhibitor exatecan, causing DNA damage, S-phase arrest, and apoptosis of TROP2-expressing cells.
Chimeric anti‑CD20 monoclonal antibody that binds CD20 on B cells, mediating ADCC, complement‑dependent cytotoxicity, and apoptosis.
Chimeric anti‑CD20 monoclonal antibody that binds CD20 on B cells and depletes them by inducing antibody‑dependent cellular cytotoxicity, complement‑dependent cytotoxicity, and apoptosis.
Rituximab binds CD20 on B cells and induces killing via Fc-mediated ADCC by immune effector cells and complement-dependent cytotoxicity; CD20 crosslinking can also trigger apoptosis.
A humanized IgG4 bispecific T-cell–redirecting antibody targeting CD3 on T cells and BCMA on malignant plasma cells; it crosslinks T cells to BCMA+ cells to activate TCR/CD3 signaling and cytotoxicity, leading to lysis of BCMA-expressing myeloma cells.
Humanized IgG4 bispecific antibody that binds CD3 on T cells and BCMA on malignant plasma cells, crosslinking T cells to BCMA+ myeloma cells to trigger TCR/CD3 activation and T‑cell cytotoxicity, leading to targeted lysis of BCMA‑expressing cells.
Bispecific antibody binds BCMA on target cells and CD3 on T cells, crosslinking to activate TCR/CD3 signaling and T-cell degranulation, leading to perforin/granzyme-mediated lysis of BCMA-expressing cells.