A HER2-targeting antibody–drug conjugate consisting of a human monoclonal antibody linked to the microtubule inhibitor monomethyl auristatin F (MMAF). It binds HER2 (ERBB2), is internalized, and releases MMAF to disrupt tubulin polymerization, leading to cell-cycle arrest and apoptosis.
HER2-targeted antibody–drug conjugate that binds HER2 (ERBB2) on tumor cells, is internalized, and releases the microtubule inhibitor monomethyl auristatin F (MMAF) via linker cleavage, inhibiting tubulin polymerization and inducing G2/M arrest and apoptosis.
YES
DIRECT
The ADC binds HER2 on the tumor cell, is internalized, and releases MMAF intracellularly, inhibiting tubulin polymerization and causing G2/M arrest and apoptosis of the HER2-expressing cell.
A HER2-targeting antibody–drug conjugate consisting of a human monoclonal antibody linked to the microtubule inhibitor monomethyl auristatin F (MMAF). It binds HER2 (ERBB2), is internalized, and releases MMAF to disrupt tubulin polymerization, leading to cell-cycle arrest and apoptosis.
HER2-targeted antibody–drug conjugate that binds HER2 (ERBB2) on tumor cells, is internalized, and releases the microtubule inhibitor monomethyl auristatin F (MMAF) via linker cleavage, inhibiting tubulin polymerization and inducing G2/M arrest and apoptosis.
NO
INDIRECT
The ADC binds HER2 on tumor cells, is internalized, and releases MMAF, which then inhibits beta-tubulin polymerization, causing G2/M arrest and apoptosis. Beta-tubulin-expressing cells are not targeted unless they are HER2+ and receive the payload.
Autologous CMV-specific T cells genetically modified to express an anti-CD19 chimeric antigen receptor (CAR); given IV after lymphodepletion to kill CD19+ malignant B cells, with native CMV specificity enabling TCR-mediated boosting by the CMV vaccine.
Autologous CMV-specific T cells engineered to express an anti-CD19 chimeric antigen receptor. The CAR targets CD19 on malignant B cells to activate T-cell cytotoxicity and kill CD19+ cells; the native CMV TCR specificity allows boosting of expansion and persistence upon CMV antigen/vaccine stimulation.
YES
DIRECT
Anti-CD19 CAR T cells recognize CD19 on target cells and induce T-cell cytotoxicity, killing CD19+ cells via perforin/granzyme-mediated lysis (and related effector pathways).
Autologous CMV-specific T cells genetically modified to express an anti-CD19 chimeric antigen receptor (CAR); given IV after lymphodepletion to kill CD19+ malignant B cells, with native CMV specificity enabling TCR-mediated boosting by the CMV vaccine.
Autologous CMV-specific T cells engineered to express an anti-CD19 chimeric antigen receptor. The CAR targets CD19 on malignant B cells to activate T-cell cytotoxicity and kill CD19+ cells; the native CMV TCR specificity allows boosting of expansion and persistence upon CMV antigen/vaccine stimulation.
NO
INDIRECT
CMV peptide–HLA engagement of the native TCR is used to boost expansion/persistence; killing is triggered by the anti-CD19 CAR against CD19+ cells via perforin/granzyme-mediated cytotoxicity.
Autologous, gene-engineered T cells expressing a dual chimeric antigen receptor targeting BCMA (TNFRSF17) and GPRC5D on myeloma cells to activate T-cell cytotoxicity and eliminate malignant plasma cells.
Autologous T cells are gene-engineered to express dual chimeric antigen receptors recognizing BCMA (TNFRSF17) and GPRC5D on myeloma cells. Binding triggers CAR signaling (CD3z with costimulatory domains), activating T-cell proliferation, cytokine release, and perforin/granzyme-mediated cytotoxicity to eliminate malignant plasma cells while reducing antigen escape.
YES
DIRECT
CAR-T cells bind BCMA via their CAR, become activated (CD3ζ/costimulatory signaling), form a cytolytic synapse, and kill BCMA+ cells by perforin/granzyme–mediated apoptosis (and potentially Fas–FasL).