Anti-EGFR antibody-drug conjugate that binds EGFR, internalizes, and releases the microtubule-disrupting payload MMAE, causing mitotic arrest and apoptosis; the IgG1 backbone may also mediate ADCC.
MRG003 is an anti-EGFR IgG1 antibody–drug conjugate that binds EGFR on tumor cells, is internalized, and releases the cytotoxic payload MMAE, which inhibits tubulin polymerization, causing G2/M mitotic arrest and apoptosis; the IgG1 backbone may also mediate ADCC.
YES
DIRECT
The anti-EGFR ADC binds EGFR on tumor cells, is internalized, and releases MMAE, which inhibits tubulin polymerization causing G2/M arrest and apoptosis; the IgG1 Fc may also trigger ADCC.
An intravenous, every-2-weeks protein biologic CAR T-cell engager that binds the anti-CD19 CAR on previously infused CAR T cells and simultaneously binds antigens on malignant B cells, bridging them to form an immune synapse to reactivate and expand residual CD19-CAR T cells and redirect them to tumor cells.
Intravenous bispecific fusion protein that binds the anti‑CD19 CAR on previously infused CD19 CAR T cells and simultaneously binds antigens on malignant B cells, bridging them to form an immune synapse. This reactivates and expands residual CAR T cells and redirects their cytotoxicity toward B‑cell tumors.
NO
INDIRECT
ALETA-001 binds the anti-CD19 CAR on infused CAR T cells and antigens on malignant B cells, bridging them to form an immune synapse that activates/expands CAR T cells, which then kill B-cell tumors via T-cell cytotoxicity (perforin/granzyme). The CAR T cells (the target-expressing cells) are not killed.
An intravenous, every-2-weeks protein biologic CAR T-cell engager that binds the anti-CD19 CAR on previously infused CAR T cells and simultaneously binds antigens on malignant B cells, bridging them to form an immune synapse to reactivate and expand residual CD19-CAR T cells and redirect them to tumor cells.
Intravenous bispecific fusion protein that binds the anti‑CD19 CAR on previously infused CD19 CAR T cells and simultaneously binds antigens on malignant B cells, bridging them to form an immune synapse. This reactivates and expands residual CAR T cells and redirects their cytotoxicity toward B‑cell tumors.
YES
DIRECT
ALETA-001 bridges anti-CD19 CAR T cells to malignant B cells by binding their surface antigens, forming an immune synapse that reactivates CAR T cells and triggers perforin/granzyme-mediated cytotoxic killing of the antigen-expressing tumor cells.
Antibody-drug conjugate that binds a tumor surface antigen, is internalized, and releases a topoisomerase I inhibitor payload to induce DNA damage and tumor-cell death.
Anti-TROP-2 IgG1 antibody-drug conjugate that binds TROP-2 on tumor cells, is internalized, and via a cleavable linker releases an exatecan-derived topoisomerase I inhibitor (SHR9265), leading to Topo I inhibition, DNA damage, replication arrest, and apoptosis.
YES
DIRECT
The ADC binds TROP-2 on tumor cells, is internalized, and releases an exatecan-derived topoisomerase I inhibitor (SHR9265), causing DNA damage, replication arrest, and apoptosis of the target-expressing cells.
Antibody-drug conjugate that binds a tumor surface antigen, is internalized, and releases a topoisomerase I inhibitor payload to induce DNA damage and tumor-cell death.
Anti-TROP-2 IgG1 antibody-drug conjugate that binds TROP-2 on tumor cells, is internalized, and via a cleavable linker releases an exatecan-derived topoisomerase I inhibitor (SHR9265), leading to Topo I inhibition, DNA damage, replication arrest, and apoptosis.
NO
INDIRECT
The ADC binds TROP-2 on tumor cells, is internalized, and releases a topoisomerase I inhibitor (SHR9265) that causes DNA damage and apoptosis. Topoisomerase I is the intracellular enzymatic target of the payload, not the binding target; killing is driven by TROP-2–mediated delivery, not by Topo I expression per se.