Autologous, genetically engineered convertible CAR T-cell therapy expressing an inert NKG2D-based receptor; requires an adaptor (MicAbody) to engage tumor targets and activate T cells.
Autologous T cells engineered with an inert NKG2D-based convertible CAR that requires an adaptor antibody (MA-20/ASP101G MicAbody). The adaptor binds CD20 on tumor cells and presents a ULBP2 ligand to the CAR, triggering T-cell activation and cytotoxicity against CD20-positive B-cell malignancies; without the adaptor, the CAR T cells remain inactive.
NO
INDIRECT
ULBP2 is the ligand on the adaptor that binds the NKG2D-based convertible CAR to activate T cells only when the adaptor also binds CD20 on tumor cells; the CAR T cells then kill CD20+ cells, not ULBP2-expressing 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.
NO
INDIRECT
I-DXd targets B7-H3 on tumor cells, is internalized, and releases a deruxtecan payload that inhibits topoisomerase I to cause DNA damage and apoptosis; Topoisomerase I is not the antigen targeted by the drug.
Arlocabtagene autoleucel (BMS-986393; arlo-cel) is an autologous anti-GPRC5D CAR T-cell therapy that redirects patient T cells to recognize and kill GPRC5D-expressing myeloma cells.
Autologous T cells engineered to express a chimeric antigen receptor targeting GPRC5D. After reinfusion, the CAR T cells bind GPRC5D on myeloma cells, become activated, proliferate, release cytotoxic mediators and cytokines, and selectively lyse GPRC5D-expressing tumor cells.
YES
DIRECT
Anti-GPRC5D CAR T cells bind GPRC5D on target cells, become activated, and kill them via T‑cell cytotoxic mechanisms (perforin/granzyme-mediated apoptosis and related effector functions).
Alnuctamab (BMS-986349; CC-93269) is a BCMA×CD3 bispecific T-cell–engaging antibody that links CD3 on T cells to BCMA on myeloma cells to trigger T-cell cytotoxicity.
Bispecific T‑cell–engaging antibody that binds BCMA on myeloma cells and CD3 on T cells, bringing them into proximity to activate and redirect cytotoxic T cells to kill BCMA‑expressing tumor cells (e.g., via immune synapse formation and perforin/granzyme release).
YES
DIRECT
The BCMA×CD3 bispecific engages T cells via CD3 and binds BCMA on target cells, forming an immune synapse and activating T-cell cytotoxicity (perforin/granzyme-mediated lysis) against BCMA-expressing cells.
Alnuctamab (BMS-986349; CC-93269) is a BCMA×CD3 bispecific T-cell–engaging antibody that links CD3 on T cells to BCMA on myeloma cells to trigger T-cell cytotoxicity.
Bispecific T‑cell–engaging antibody that binds BCMA on myeloma cells and CD3 on T cells, bringing them into proximity to activate and redirect cytotoxic T cells to kill BCMA‑expressing tumor cells (e.g., via immune synapse formation and perforin/granzyme release).
NO
INDIRECT
Alnuctamab binds CD3 on T cells to engage and activate them against BCMA+ tumor cells; T cells kill BCMA-expressing cells via immune synapse formation and perforin/granzyme release. CD3+ cells are not targeted for killing.