Investigational EGFR×CD28 bispecific antibody that binds EGFR on tumor cells and CD28 on T cells to provide conditional costimulation and amplify T-cell activation with PD-1 blockade.
Dalmitamig (REGN7075) is a bispecific antibody that binds EGFR on tumor cells and CD28 on T cells, delivering tumor-targeted CD28 costimulation to enhance and redirect T-cell activation and cytotoxicity against EGFR-expressing tumor cells, with synergy alongside PD-1 blockade.
The EGFR×CD28 bispecific binds EGFR on tumor cells and CD28 on T cells, providing localized costimulation that activates and redirects CTLs to kill EGFR-expressing cells via perforin/granzyme-mediated cytotoxicity.
An autologous, genetically engineered Tmod CAR T-cell therapy with a dual-receptor logic gate: an activator CAR targets carcinoembryonic antigen (CEA) and a blocker receptor recognizes HLA-A*02 on normal cells. The cells activate only in CEA-positive tumor cells lacking HLA-A*02 (AND-NOT gating) to spare normal CEA-expressing tissues. Investigated post-lymphodepletion for CEA+ solid tumors with HLA-A*02 loss of heterozygosity.
Autologous T cells engineered with a dual-receptor logic gate: an activating CAR targets CEA to trigger cytotoxicity, while an HLA-A*02–specific inhibitory receptor (LIR-1–based) blocks activation on HLA-A*02–positive normal cells. This AND-NOT gating enables killing only of CEA-positive tumor cells that have lost HLA-A*02. An shRNA against B2M reduces HLA class I expression on the engineered T cells.
Engineered CAR T cells bind CEA via the activator CAR and directly kill CEA+ tumor cells (perforin/granzyme-mediated lysis); activation is blocked on HLA-A*02–positive cells by the inhibitory receptor.
Antibody–drug conjugate targeting CD79b on B cells; after internalization releases MMAE (microtubule inhibitor) causing cell-cycle arrest and apoptosis.
CD79b-targeted monoclonal antibody delivers the microtubule inhibitor MMAE via a cleavable linker; after binding and internalization in B cells, MMAE is released to inhibit tubulin polymerization, causing G2/M cell-cycle arrest and apoptosis of malignant B cells.
ADC binds CD79b on B cells, is internalized, linker is cleaved to release MMAE, which inhibits tubulin polymerization causing G2/M arrest and apoptosis.
Chimeric anti-CD20 monoclonal antibody that depletes B cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and direct apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20+ cells via complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC), and direct induction of apoptosis.
Rituximab binds CD20 on B cells and triggers killing via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity (through FcγR-expressing effector cells), and direct induction of apoptosis upon CD20 crosslinking.
Anti-CCR8 monoclonal antibody that depletes CCR8+ tumor-infiltrating regulatory T cells via ADCC to reprogram the tumor microenvironment.
Anti-CCR8 monoclonal antibody that binds CCR8 on tumor-infiltrating regulatory T cells, blocks CCL1–CCR8 signaling, and induces Fc-mediated ADCC to deplete CCR8+ Tregs, reducing immunosuppression and enhancing antitumor immunity.
Antibody binds CCR8 on Tregs and engages Fcγ receptors on NK cells/macrophages to mediate ADCC, depleting CCR8+ cells.