Antibody–drug conjugate targeting TROP-2 that delivers SN-38 (govitecan), a topoisomerase I inhibitor; internalization and linker cleavage release the cytotoxic payload with potential bystander effect.
Humanized anti–TROP-2 monoclonal antibody conjugated to SN-38 (topoisomerase I inhibitor). Binding to TROP-2 triggers internalization; linker cleavage releases SN-38, stabilizing Topo I–DNA complexes to cause DNA breaks and apoptosis, with potential membrane-permeable bystander killing.
Anti–TROP-2 antibody–drug conjugate binds TROP-2, is internalized, and releases SN-38, a topoisomerase I inhibitor, causing DNA damage and apoptosis in target cells (with potential bystander effect).
An anti-HER2 antibody–drug conjugate administered IV every 6 weeks (2.2 mg/kg). The monoclonal antibody targets HER2, is internalized, and releases the auristatin-derived microtubule inhibitor Amberstatin-269 to disrupt tubulin polymerization, causing G2/M arrest and apoptosis; the antibody component may also inhibit HER2 signaling and mediate ADCC.
HER2-targeted monoclonal antibody-drug conjugate. After binding HER2 and internalization, it releases an auristatin (MMAF analog) payload that inhibits microtubule polymerization, causing G2/M arrest and apoptosis; the antibody component may also inhibit HER2 signaling and mediate antibody-dependent cellular cytotoxicity (ADCC).
ARX788 binds HER2, is internalized, and releases an MMAF analog that inhibits microtubule polymerization, causing G2/M arrest and apoptosis; the antibody may also recruit ADCC.
Antibody–drug conjugate targeting HER2 that delivers DXd, a membrane-permeable topoisomerase I inhibitor via a cathepsin-cleavable linker; enables receptor-mediated internalization and bystander effect.
HER2-targeted monoclonal antibody (trastuzumab) linked via a cathepsin-cleavable linker to deruxtecan (DXd), a membrane-permeable topoisomerase I inhibitor. Binding to HER2 triggers receptor-mediated internalization; linker cleavage releases DXd, which stabilizes Top1–DNA complexes, inhibiting DNA replication and inducing apoptosis. Also mediates bystander killing and antibody-dependent cell-mediated cytotoxicity (ADCC).
The ADC binds HER2, is internalized, and releases the topoisomerase I inhibitor deruxtecan (DXd) after linker cleavage, causing DNA replication inhibition and apoptosis; it can also trigger ADCC and bystander killing.
Autologous patient T cells genetically engineered to express a chimeric antigen receptor that co-recognizes CD38 and CS1 (SLAMF7) on myeloma cells, triggering T-cell cytotoxicity to treat relapsed/refractory multiple myeloma.
Autologous T cells are engineered to express a dual-target chimeric antigen receptor that co-recognizes CD38 and CS1 (SLAMF7) on myeloma cells; antigen binding activates CAR signaling (CD3zeta with costimulation), triggering perforin/granzyme release and cytokine-mediated killing of CD38+ and/or CS1+ malignant plasma cells, reducing antigen-loss escape.
CAR T cells bind CD38 on target cells; CAR signaling triggers T‑cell degranulation with perforin/granzyme release (and death‑receptor/cytokine effects), causing apoptosis/lysis of CD38+ cells.
Autologous patient T cells genetically engineered to express a chimeric antigen receptor that co-recognizes CD38 and CS1 (SLAMF7) on myeloma cells, triggering T-cell cytotoxicity to treat relapsed/refractory multiple myeloma.
Autologous T cells are engineered to express a dual-target chimeric antigen receptor that co-recognizes CD38 and CS1 (SLAMF7) on myeloma cells; antigen binding activates CAR signaling (CD3zeta with costimulation), triggering perforin/granzyme release and cytokine-mediated killing of CD38+ and/or CS1+ malignant plasma cells, reducing antigen-loss escape.
CAR T cells recognize CS1 (SLAMF7) on target cells; CAR signaling activates T-cell cytotoxicity with perforin/granzyme release (and cytokine-mediated apoptosis), killing CS1+ cells.