Autologous patient-derived CD4+/CD8+ T cells (LMY-920) gene-modified via a non-viral transposon to express a BAFF-ligand chimeric antigen receptor targeting BAFF-R/BR3, TACI, and BCMA to eliminate malignant B cells; dosed at 1–8×10^6 CAR+ cells/kg following lymphodepletion.
Autologous CD4+/CD8+ T cells engineered via a non-viral transposon to express a BAFF-ligand chimeric antigen receptor that binds BAFF family receptors (BAFF-R/BR3, TACI, BCMA) on malignant B cells; antigen engagement activates the CAR T cells to proliferate, secrete cytotoxic mediators/cytokines, and kill the target B cells.
BAFF-ligand CAR-T cells bind TACI on target cells, activating the CAR T cells to release perforin/granzymes and induce apoptotic killing of the TACI-expressing cells.
Autologous patient-derived CD4+/CD8+ T cells (LMY-920) gene-modified via a non-viral transposon to express a BAFF-ligand chimeric antigen receptor targeting BAFF-R/BR3, TACI, and BCMA to eliminate malignant B cells; dosed at 1–8×10^6 CAR+ cells/kg following lymphodepletion.
Autologous CD4+/CD8+ T cells engineered via a non-viral transposon to express a BAFF-ligand chimeric antigen receptor that binds BAFF family receptors (BAFF-R/BR3, TACI, BCMA) on malignant B cells; antigen engagement activates the CAR T cells to proliferate, secrete cytotoxic mediators/cytokines, and kill the target B cells.
BAFF-ligand CAR-T cells recognize BCMA on target cells, become activated, and kill via perforin/granzyme cytolysis and death-receptor (e.g., Fas/TRAIL) pathways with cytokine-mediated effects.
CD79b-directed antibody–drug conjugate that delivers monomethyl auristatin E (MMAE), a microtubule inhibitor, to B cells to induce apoptosis.
CD79b-directed antibody–drug conjugate that binds CD79b on B cells, is internalized, and releases monomethyl auristatin E (MMAE) via a cleavable linker; MMAE inhibits tubulin polymerization, causing G2/M arrest and apoptosis of CD79b-positive malignant B cells.
The ADC binds CD79b on B cells, is internalized, and releases MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptosis of CD79b-positive cells.
Chimeric anti-CD20 monoclonal antibody that depletes B cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes them via complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC), and induction of apoptosis.
Rituximab binds CD20 on B cells and triggers complement-dependent cytotoxicity and Fc-mediated ADCC, and can also induce apoptosis of the target cells.
A B7-H3–targeted antibody–drug conjugate consisting of a human IgG1 monoclonal antibody to B7-H3 (CD276) linked to a deruxtecan payload (exatecan-derived topoisomerase I inhibitor); binding to B7-H3 leads to internalization and release of the payload, causing topo-I–mediated DNA damage and apoptosis with potential bystander effect.
B7-H3–targeted IgG1 antibody–drug conjugate; the antibody binds B7-H3 (CD276) on tumor cells, is internalized, and a cleavable linker releases a deruxtecan (exatecan-derived) topoisomerase I inhibitor payload that causes DNA damage and apoptosis, with potential bystander cytotoxicity.
ADC binds B7-H3 on target cells, is internalized, and releases a deruxtecan topoisomerase I inhibitor that induces DNA damage leading to apoptosis (with possible bystander killing).