An antibody–drug conjugate combining trastuzumab (humanized anti-HER2 IgG1) with the maytansinoid DM1 payload; binds HER2/ERBB2 to inhibit signaling, promote receptor internalization, and mediate ADCC, while the DM1 component disrupts microtubules leading to mitotic arrest and apoptosis.
Humanized anti-HER2 IgG1 (trastuzumab) targets HER2/ERBB2, inhibiting HER2 signaling, promoting receptor internalization, and mediating ADCC. The conjugated maytansinoid payload (DM1) is internalized and released to disrupt microtubules, causing mitotic arrest and apoptosis in HER2-overexpressing tumor cells.
T-DM1 binds HER2 on target cells, is internalized, and releases the DM1 payload that disrupts microtubules, causing mitotic arrest and apoptosis; its Fc can also mediate ADCC.
Subcutaneous anti-CD38 IgG1 monoclonal antibody inducing ADCC/CDC and apoptosis, and depleting CD38+ immunosuppressive cells.
Human IgG1k monoclonal antibody against CD38 that binds CD38 on myeloma and other CD38+ cells, inducing direct apoptosis and immune effector–mediated killing (ADCC, ADCP, CDC) and depleting CD38+ immunosuppressive cells (Tregs, Bregs, MDSCs), leading to antitumor activity.
Binds CD38 and triggers immune effector killing (ADCC, ADCP, CDC) and can induce direct apoptosis of CD38+ cells.
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.
The ADC binds HER2, is internalized, and releases MMAE after linker cleavage; MMAE disrupts microtubules, causing G2/M arrest and apoptosis (with a membrane-permeable payload enabling a bystander effect).
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.
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.
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.