Autologous peripheral blood mononuclear cells (primarily T cells) activated ex vivo with IL-2 and OKT3 and coated with OKT3 and elotuzumab to generate bispecific antibody–armed T cells targeting SLAMF7+ multiple myeloma.
Autologous PBMCs (primarily T cells) are activated ex vivo with IL-2/OKT3 and coated with OKT3 (anti‑CD3) plus elotuzumab (anti‑SLAMF7), creating bispecific antibody–armed T cells that bridge CD3 on T cells to SLAMF7 on myeloma cells, forming an immune synapse and redirecting T‑cell cytotoxicity against SLAMF7+ multiple myeloma.
NO
INDIRECT
Anti-CD3 (OKT3) binds CD3ε on T cells to activate and link them to SLAMF7+ myeloma via elotuzumab; CD3+ T cells act as effectors and kill SLAMF7-expressing tumor cells via immune synapse and perforin/granzyme release, not the CD3+ cells themselves.
Humanized monoclonal antibody targeting SLAMF7/CS1, used to arm T cells by binding SLAMF7 on myeloma cells to facilitate immune synapse formation.
Humanized IgG1 monoclonal antibody targeting SLAMF7/CS1. By binding SLAMF7 on multiple myeloma cells and engaging Fcγ receptors on NK cells, it triggers antibody-dependent cellular cytotoxicity (ADCC) and can co-activate NK cells via SLAMF7 signaling, leading to immune-mediated killing of SLAMF7+ myeloma cells.
YES
DIRECT
Elotuzumab binds SLAMF7 on myeloma cells and its Fc engages Fcγ receptors on NK cells to trigger ADCC, while also co-activating NK cells via SLAMF7 signaling, leading to lysis of SLAMF7+ cells.
Anti-CD3 monoclonal antibody used to activate T cells ex vivo and to coat cells, engaging CD3/TCR signaling to redirect T-cell cytotoxicity.
Anti-CD3 monoclonal antibody that binds the CD3 complex on T cells to trigger TCR signaling and activation; when used to coat/arm T cells (often alongside a tumor-targeting antibody), it engages CD3 to form an immune synapse and redirects T-cell cytotoxicity toward antigen-positive targets.
NO
INDIRECT
The antibody binds CD3 on T cells to activate and redirect them; the activated T cells then kill antigen-positive target cells (e.g., via perforin/granzyme), not the CD3+ T cells themselves.
HER2-directed antibody–drug conjugate: a humanized anti‑HER2 IgG1 linked to monomethyl auristatin E (MMAE). Binds HER2 on tumor cells, internalizes, and releases MMAE to disrupt microtubules, causing mitotic arrest/apoptosis; may also mediate ADCC and bystander killing.
HER2-targeted antibody-drug conjugate: a humanized anti-HER2 IgG1 linked to the microtubule toxin MMAE. After binding HER2 and internalization, it releases MMAE to inhibit microtubule polymerization, causing mitotic arrest and apoptosis; may also mediate ADCC and bystander killing.
YES
DIRECT
The ADC binds HER2, is internalized, and releases MMAE intracellularly to inhibit microtubules, causing mitotic arrest and apoptosis; it may also trigger ADCC and bystander killing.
HER2-directed antibody–drug conjugate: a humanized anti‑HER2 IgG1 linked to monomethyl auristatin E (MMAE). Binds HER2 on tumor cells, internalizes, and releases MMAE to disrupt microtubules, causing mitotic arrest/apoptosis; may also mediate ADCC and bystander killing.
HER2-targeted antibody-drug conjugate: a humanized anti-HER2 IgG1 linked to the microtubule toxin MMAE. After binding HER2 and internalization, it releases MMAE to inhibit microtubule polymerization, causing mitotic arrest and apoptosis; may also mediate ADCC and bystander killing.
NO
INDIRECT
Disitamab vedotin targets HER2, is internalized, and releases MMAE, which binds the β‑tubulin vinca site to block microtubule polymerization, causing mitotic arrest and apoptosis; ADCC/bystander effects may contribute.