A HER2-targeted antibody–drug conjugate (RC48) that binds HER2 on tumor cells, is internalized, and releases the cytotoxic microtubule inhibitor MMAE via a cleavable linker to disrupt mitosis and induce apoptosis.
HER2-targeted antibody-drug conjugate: Disitamab binds HER2 on tumor cells, is internalized, and a cleavable linker releases monomethyl auristatin E (MMAE), which inhibits microtubule polymerization, causing G2/M arrest and apoptosis.
NO
INDIRECT
The ADC targets HER2 for uptake; once internalized, it releases MMAE that binds beta‑tubulin to disrupt microtubules and induce G2/M arrest and apoptosis. Tubulin expression alone does not lead to targeted killing.
Genetically engineered CAR T-cell therapy that expresses dual chimeric antigen receptors targeting CD19 and CD22 to recognize and kill malignant B-ALL cells; administered intravenously at 1.0×10^6–10.0×10^6 CAR T cells/kg.
Genetically engineered T cells expressing dual chimeric antigen receptors targeting CD19 and CD22; antigen binding triggers CAR signaling (CD3ζ with costimulatory domains) to activate, expand, and mediate cytotoxic killing of malignant B‑ALL cells, mitigating antigen escape seen with single‑antigen CARs.
YES
DIRECT
CAR T cells bind CD19 via the CAR, activate, and directly lyse target cells through perforin/granzyme-mediated cytotoxicity (and Fas–FasL apoptosis).
Genetically engineered CAR T-cell therapy that expresses dual chimeric antigen receptors targeting CD19 and CD22 to recognize and kill malignant B-ALL cells; administered intravenously at 1.0×10^6–10.0×10^6 CAR T cells/kg.
Genetically engineered T cells expressing dual chimeric antigen receptors targeting CD19 and CD22; antigen binding triggers CAR signaling (CD3ζ with costimulatory domains) to activate, expand, and mediate cytotoxic killing of malignant B‑ALL cells, mitigating antigen escape seen with single‑antigen CARs.
YES
DIRECT
CAR T cells bind CD22 on target cells, triggering CD3ζ/costimulatory signaling that activates cytotoxic T-cell functions (perforin/granzyme release and death-receptor pathways) to lyse CD22+ cells.
Autologous, gene-modified CAR-T cell therapy targeting Claudin 18.2 (CLDN18.2); administered as a single infusion to mediate T-cell cytotoxicity against CLDN18.2-positive tumors.
Autologous T cells are engineered ex vivo to express a chimeric antigen receptor specific for Claudin 18.2 (CLDN18.2). Upon binding CLDN18.2 on tumor cells, CAR signaling (CD3zeta with costimulatory domains) activates T-cell proliferation, cytokine release, and perforin/granzyme-mediated cytotoxicity, enabling targeted killing of CLDN18.2-positive tumors after a single infusion.
YES
DIRECT
Autologous CAR-T cells bind CLDN18.2 on target cells and, upon CAR signaling, kill them via perforin/granzyme-mediated cytolysis (with cytokine release).
Autologous chimeric antigen receptor T-cell therapy engineered to express an anti-CEACAM5 (CEA/CD66e) CAR; upon binding to CEA on tumor cells, CAR signaling activates T-cell cytotoxicity and cytokine release. Administered intravenously or intraperitoneally.
Autologous T cells are engineered to express a chimeric antigen receptor targeting CEACAM5 (CEA). Upon binding CEA on tumor cells, CAR signaling (CD3ζ with costimulatory domains) activates T-cell cytotoxicity, proliferation, and cytokine release, leading to perforin/granzyme-mediated killing of CEA-positive cells.
YES
DIRECT
Anti-CEA CAR T cells bind CEACAM5 on target cells; CAR signaling activates T-cell cytotoxicity leading to perforin/granzyme-mediated lysis (and Fas/FasL apoptosis) of CEA-positive cells.