HER2-targeted antibody-drug conjugate that binds HER2, is internalized, and releases MMAE (a microtubule inhibitor) to induce cytotoxicity with potential bystander effect.
HER2-targeted antibody-drug conjugate that binds HER2 on tumor cells, is internalized, and releases the microtubule inhibitor MMAE after linker cleavage, causing microtubule disruption, G2/M cell-cycle arrest, and apoptosis; membrane-permeable payload enables a bystander killing effect.
NO
INDIRECT
RC48 targets HER2 on tumor cells; after internalization it releases MMAE, which binds the vinca domain of beta-tubulin to disrupt microtubules and induce apoptosis. Beta-tubulin expression alone does not confer targeting; killing requires HER2-mediated delivery (with possible bystander killing from diffused payload).
Third-generation, irreversible EGFR tyrosine kinase inhibitor that covalently binds the ATP site of mutant EGFR (including T790M), suppresses downstream signaling (e.g., MAPK/PI3K-AKT), and induces tumor cell death while relatively sparing wild-type EGFR.
YES
DIRECT
Irreversible inhibition of mutant EGFR kinase (including T790M) suppresses MAPK/PI3K-AKT signaling, leading to apoptosis of EGFR-dependent tumor cells while relatively sparing wild-type EGFR.
A bispecific T-cell engager (BiTE) antibody construct that binds CD19 on B-lineage leukemia cells and CD3 on T cells to redirect endogenous T cells to kill CD19+ blasts; administered by continuous IV infusion (28 days on, 14 days off) for up to 5 cycles.
A bispecific anti-CD19/anti-CD3 antibody that bridges CD19+ B cells and T cells, engaging the TCR via CD3 to form an immune synapse and activate T cells, leading to perforin/granzyme-mediated killing of CD19-expressing blasts and B-cell depletion.
YES
DIRECT
Blinatumomab bridges CD19 on target cells to CD3 on T cells, activating T cells to form an immune synapse and kill CD19+ cells via perforin/granzyme-mediated cytolysis.
A bispecific T-cell engager (BiTE) antibody construct that binds CD19 on B-lineage leukemia cells and CD3 on T cells to redirect endogenous T cells to kill CD19+ blasts; administered by continuous IV infusion (28 days on, 14 days off) for up to 5 cycles.
A bispecific anti-CD19/anti-CD3 antibody that bridges CD19+ B cells and T cells, engaging the TCR via CD3 to form an immune synapse and activate T cells, leading to perforin/granzyme-mediated killing of CD19-expressing blasts and B-cell depletion.
NO
INDIRECT
Blinatumomab binds CD3ε on T cells and CD19 on B cells to form an immune synapse, activating T cells to release perforin/granzyme and kill CD19+ cells; CD3+ T cells are effectors, not killed.
An anti-HER2 antibody–drug conjugate (RC48-ADC) that binds HER2 on tumor cells, is internalized, and releases the microtubule inhibitor MMAE to disrupt tubulin and induce cell-cycle arrest/apoptosis; Fc functions may add ADCC against HER2-positive cells.
Humanized anti‑HER2 IgG1 antibody linked to the microtubule inhibitor MMAE. After binding HER2 on tumor cells, the ADC is internalized and releases MMAE to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; Fc-mediated effector functions may add ADCC against HER2-expressing cells.
YES
DIRECT
ADC binds HER2 on tumor cells, is internalized, and releases MMAE intracellularly to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; Fc effector functions may add ADCC against HER2-expressing cells.