Autologous T cells genetically engineered to express a chimeric antigen receptor targeting CD7, enabling recognition and cytotoxic elimination of CD7-expressing malignant hematologic cells (e.g., T-ALL, CD7+ AML); on-target T-cell aplasia may occur.
Autologous T cells engineered to express an anti‑CD7 chimeric antigen receptor bind CD7 on malignant hematologic cells, triggering CAR signaling (CD3ζ with co‑stimulation) to activate, proliferate, release cytokines, and mediate cytotoxic killing; on‑target T‑cell aplasia can occur due to CD7 expression on normal T cells.
Anti-CD7 CAR-T cells bind CD7 on target cells, activate via CAR signaling, and kill through perforin/granzyme-mediated cytolysis (and death receptor pathways), eliminating CD7+ cells.
Gene-modified cellular immunotherapy consisting of chimeric antigen receptor–engineered natural killer (NK) cells targeting mesothelin; administered by IV infusion every 2 weeks with dose escalation for advanced mesothelin-positive triple-negative breast cancer.
Chimeric antigen receptor–engineered natural killer (NK) cells targeting mesothelin; CAR binding to mesothelin on tumor cells triggers NK activation, leading to cytotoxic degranulation (perforin/granzyme) and cytokine release, causing lysis of mesothelin‑positive cancer cells.
CAR-engineered NK cells bind mesothelin on target cells, triggering NK activation and cytotoxic degranulation (perforin/granzyme) leading to apoptosis/lysis, with cytokine release contributing.
An antibody–drug conjugate targeting CEACAM5, consisting of an anti-CEACAM5 monoclonal antibody linked to the maytansinoid payload DM4 (ravtansine). After binding CEACAM5 on tumor cells, it is internalized and releases DM4 to inhibit tubulin polymerization, causing mitotic arrest and apoptosis.
Tusamitamab ravtansine is an anti-CEACAM5 monoclonal antibody linked to the maytansinoid payload DM4 (ravtansine). After binding CEACAM5 on tumor cells, the ADC is internalized and releases DM4 intracellularly, where it inhibits tubulin polymerization, leading to mitotic arrest and apoptosis of CEACAM5-positive tumor cells.
The ADC binds CEACAM5 on target cells, is internalized, and releases the DM4 payload, which inhibits tubulin polymerization, leading to mitotic arrest and apoptosis of CEACAM5-positive cells.
A humanized monoclonal antibody–drug conjugate targeting DLK1; after binding DLK1 on tumor cells, it is internalized and releases a cytotoxic payload to induce targeted tumor cell death. Evaluated in DLK1-expressing neuroendocrine neoplasms and adrenocortical carcinoma.
Humanized IgG1 antibody targeting DLK1 linked via a cleavable linker to a pyrrolobenzodiazepine (PBD) dimer; after binding DLK1 on tumor cells, the ADC is internalized and cathepsin-mediated cleavage releases the PBD payload, which creates DNA interstrand cross-links, inhibiting cell division and killing DLK1-expressing cancer cells.
After binding DLK1, the ADC is internalized and linker cleavage releases a PBD dimer that creates DNA interstrand cross-links, blocking replication and killing the DLK1-expressing cell.
Izalontamab brengitecan (BMS-986507), an EGFR/HER3-directed bispecific antibody–drug conjugate that internalizes upon binding and releases the topoisomerase I inhibitor brengitecan to induce DNA strand breaks and bystander killing.
Bispecific EGFR/HER3-targeting antibody-drug conjugate that binds EGFR and HER3 on tumor cells, internalizes, and releases the topoisomerase I inhibitor brengitecan to induce DNA strand breaks, leading to tumor cell death and bystander killing.
The ADC binds EGFR (and HER3) on tumor cells, is internalized, and releases the topoisomerase I inhibitor brengitecan, causing DNA strand breaks and cell death, with bystander killing of nearby cells.