An antibody–drug conjugate targeting Trop-2 that delivers SN-38 (the active metabolite of irinotecan), a topoisomerase I inhibitor; internalization and linker cleavage release SN-38 to induce DNA damage and tumor cell death, with a potential bystander effect.
Humanized anti-Trop-2 monoclonal antibody linked via a cleavable linker to SN-38 (active metabolite of irinotecan). After Trop-2 binding and internalization, linker cleavage releases SN-38, which inhibits topoisomerase I by stabilizing Topo I-DNA cleavage complexes, causing DNA damage, replication arrest, and apoptosis; extracellular release can produce a bystander killing effect.
ADC binds TROP-2, is internalized, and releases SN-38 via linker cleavage; SN-38 inhibits topoisomerase I, causing DNA damage and apoptosis (with possible bystander killing from extracellular SN-38).
Autologous CAR-T cell therapy in which patient T cells are engineered to express a chimeric antigen receptor using the BAFF (BLyS) ligand as the binding domain, enabling multi-antigen recognition of BAFF-R, BCMA, and TACI to target malignant plasma cells in relapsed/refractory multiple myeloma.
Autologous T cells are engineered to express a BAFF (BLyS) ligand–based chimeric antigen receptor that binds BAFF-R, BCMA, and TACI on malignant plasma/B-lineage cells. Antigen engagement activates CAR signaling to drive T‑cell proliferation and targeted cytotoxicity (perforin/granzyme and cytokine-mediated killing), providing multi-antigen recognition to reduce antigen escape in relapsed/refractory multiple myeloma.
BAFF-ligand CAR-T cells bind BAFF-R on target cells, activate the CAR, and kill targets via T-cell cytotoxic pathways (perforin/granzyme release and cytokine-mediated apoptosis).
Autologous CAR-T cell therapy in which patient T cells are engineered to express a chimeric antigen receptor using the BAFF (BLyS) ligand as the binding domain, enabling multi-antigen recognition of BAFF-R, BCMA, and TACI to target malignant plasma cells in relapsed/refractory multiple myeloma.
Autologous T cells are engineered to express a BAFF (BLyS) ligand–based chimeric antigen receptor that binds BAFF-R, BCMA, and TACI on malignant plasma/B-lineage cells. Antigen engagement activates CAR signaling to drive T‑cell proliferation and targeted cytotoxicity (perforin/granzyme and cytokine-mediated killing), providing multi-antigen recognition to reduce antigen escape in relapsed/refractory multiple myeloma.
BAFF-ligand CAR-T cells bind BCMA on target cells, triggering CAR signaling and T-cell cytotoxicity via perforin/granzyme release and cytokine/Fas-mediated apoptosis.
Autologous CAR-T cell therapy in which patient T cells are engineered to express a chimeric antigen receptor using the BAFF (BLyS) ligand as the binding domain, enabling multi-antigen recognition of BAFF-R, BCMA, and TACI to target malignant plasma cells in relapsed/refractory multiple myeloma.
Autologous T cells are engineered to express a BAFF (BLyS) ligand–based chimeric antigen receptor that binds BAFF-R, BCMA, and TACI on malignant plasma/B-lineage cells. Antigen engagement activates CAR signaling to drive T‑cell proliferation and targeted cytotoxicity (perforin/granzyme and cytokine-mediated killing), providing multi-antigen recognition to reduce antigen escape in relapsed/refractory multiple myeloma.
BAFF-ligand CAR-T cells bind TACI on target cells, activate CAR signaling, form a cytolytic synapse, and kill via perforin/granzyme release and cytokine-mediated cytotoxicity.
PSMA-targeted small-molecule radioligand linked to lutetium-177 that binds PSMA, is internalized, and emits beta particles to deliver localized radiation and induce tumor cell DNA damage.
PSMA-targeted small-molecule/peptide radioligand (vipivotide tetraxetan) chelated to lutetium-177 that binds PSMA on prostate cancer cells, is internalized, and delivers beta-particle radiation, causing DNA double-strand breaks and tumor cell death, with potential short-range bystander effects; minor gamma emissions enable imaging.
PSMA-binding radioligand is internalized and delivers Lu-177 beta-particle radiation, causing DNA double-strand breaks and death of PSMA-expressing cells (with short-range bystander/crossfire effects).