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.
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.
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.
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.
Recombinant humanized IgG1 monoclonal antibody targeting HER2 (ErbB2); administered IV (4 mg/kg loading then 2 mg/kg weekly, or 8 mg/kg loading then 6 mg/kg every 3 weeks). Binds the HER2 extracellular domain, inhibits receptor activation/dimerization and shedding, suppresses PI3K/AKT/mTOR and RAS/RAF/MEK/ERK signaling, and induces ADCC via FcγR-bearing immune effector cells.
Humanized IgG1 monoclonal antibody targeting HER2 (ErbB2); binds the extracellular domain to block receptor activation and dimerization and inhibit shedding, thereby suppressing downstream PI3K/AKT/mTOR and RAS/RAF/MEK/ERK signaling, while engaging FcγR-expressing immune cells to mediate ADCC against HER2-overexpressing tumor cells.
Binds HER2 and recruits FcγR-expressing effector cells (e.g., NK cells) to kill target cells via ADCC; minor CDC/apoptosis may occur.
Allogeneic, gene-engineered natural killer cell therapy expressing a chimeric antigen receptor targeting Trop-2 (TACSTD2) to enable antigen-specific NK activation and cytotoxicity against Trop2-positive tumor cells in relapsed/refractory NSCLC.
Allogeneic, gene-engineered natural killer cells expressing a chimeric antigen receptor for Trop-2 (TACSTD2) recognize Trop-2–positive tumor cells and induce antigen-dependent NK activation, resulting in perforin/granzyme-mediated cytotoxicity and cytokine release to kill Trop-2–expressing NSCLC cells.
CAR-NK cells recognize Trop-2 on target cells and kill them via antigen-dependent activation with perforin/granzyme-mediated cytotoxicity (with cytokine release).