A humanized IgG4 bispecific T-cell–redirecting antibody targeting CD3 on T cells and BCMA on malignant plasma cells; it crosslinks T cells to BCMA+ cells to activate TCR/CD3 signaling and cytotoxicity, leading to lysis of BCMA-expressing myeloma cells.
Humanized IgG4 bispecific antibody that binds CD3 on T cells and BCMA on malignant plasma cells, crosslinking T cells to BCMA+ myeloma cells to trigger TCR/CD3 activation and T‑cell cytotoxicity, leading to targeted lysis of BCMA‑expressing cells.
NO
INDIRECT
CD3 binding serves to recruit/activate T cells; it does not target CD3+ cells for killing. Activated T cells then kill BCMA-expressing tumor cells (perforin/granzyme after TCR/CD3 engagement).
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.
YES
DIRECT
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.
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.
NO
INDIRECT
T-DM1 targets HER2 on the cell surface; after HER2-mediated internalization, the DM1 payload binds beta-tubulin to disrupt microtubules, causing mitotic arrest and apoptosis in HER2-positive cells. Beta-tubulin expression itself is not the basis for targeting.
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.
YES
DIRECT
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.
YES
DIRECT
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).