Humanized monoclonal antibody targeting the HER2 extracellular dimerization domain (subdomain II); blocks HER2 heterodimerization, especially HER2/HER3, thereby inhibiting downstream PI3K/AKT and MAPK signaling and leading to tumor cell growth inhibition and apoptosis (with potential ADCC contribution).
YES
DIRECT
Pertuzumab binds HER2, blocks HER2 dimerization and survival signaling to induce apoptosis, and its Fc engages Fcγ receptor–bearing immune cells to mediate ADCC against HER2-expressing cells.
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.
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
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.
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.
NO
INDIRECT
The ADC targets CEACAM5, is internalized, and releases DM4, which binds beta-tubulin to inhibit microtubule polymerization, causing mitotic arrest and apoptosis. Beta-tubulin is not the targeting antigen, so its expression alone does not confer direct killing.