Anti-CD38 monoclonal antibody that targets malignant plasma cells; mediates ADCC, CDC, ADCP, and immune modulation.
Human IgG1κ anti-CD38 monoclonal antibody that binds CD38 on malignant plasma cells, inducing immune effector–mediated killing (ADCC, CDC) and phagocytosis (ADCP), and depleting CD38-positive immunosuppressive cells (Tregs, B cells, MDSCs) to enhance antitumor immunity.
YES
DIRECT
Anti-CD38 IgG1 binds CD38 on target cells and recruits immune effectors via its Fc domain, causing NK cell–mediated ADCC, macrophage-mediated ADCP, and complement-dependent cytotoxicity (CDC); may also induce apoptosis upon crosslinking.
Adoptive γδ T‑cell therapy using Vγ9Vδ2 T cells expanded from healthy donors and administered intraventricularly/intracavitary via an Ommaya reservoir. These innate‑like cytotoxic lymphocytes recognize tumor phosphoantigens via BTN3A1/BTN2A1 independent of MHC, triggering perforin/granzyme‑mediated killing and cytokine release; they can also respond via NKG2D and mediate ADCC.
Allogeneic Vγ9Vδ2 T cells recognize tumor-derived phosphoantigens generated by dysregulated mevalonate metabolism via BTN3A1/BTN2A1 in an MHC-independent manner, triggering perforin/granzyme-mediated cytotoxicity and cytokine release. They also respond to stress ligands through NKG2D and can mediate ADCC.
YES
DIRECT
Vγ9Vδ2 T cells expressing CD16 (FcγRIIIa) bind IgG Fc on opsonized tumor cells, triggering ADCC and perforin/granzyme-mediated killing.
Bispecific T-cell engager antibody targeting BCMA on plasma cells and CD3 on T cells to redirect T-cell cytotoxicity.
Bispecific humanized monoclonal antibody that binds BCMA on plasma cells and CD3 on T cells, cross-linking them to form an immune synapse and redirect T-cell cytotoxicity, leading to T-cell activation and lysis of BCMA-expressing malignant plasma cells.
YES
DIRECT
Teclistamab binds BCMA on target cells and CD3 on T cells, forming an immune synapse that redirects T-cell killing via perforin/granzyme-mediated lysis of BCMA-expressing cells.
Bispecific T-cell engager antibody targeting BCMA on plasma cells and CD3 on T cells to redirect T-cell cytotoxicity.
Bispecific humanized monoclonal antibody that binds BCMA on plasma cells and CD3 on T cells, cross-linking them to form an immune synapse and redirect T-cell cytotoxicity, leading to T-cell activation and lysis of BCMA-expressing malignant plasma cells.
NO
INDIRECT
Teclistamab binds CD3 on T cells to engage and activate them to kill BCMA-expressing malignant plasma cells via redirected T-cell cytotoxicity (perforin/granzyme); CD3+ T cells are not targeted for killing.
Humanized IgG1 monoclonal antibody targeting the HER2 extracellular dimerization domain; prevents HER2 dimerization—especially HER2/HER3—thereby blocking downstream PI3K/AKT/MAPK signaling to inhibit tumor growth and promote apoptosis; can also mediate ADCC.
YES
DIRECT
Pertuzumab binds HER2, blocks HER2/HER3 signaling to trigger apoptosis, and its IgG1 Fc engages FcγR+ effector cells (e.g., NK cells) to mediate ADCC (±CDC), killing HER2+ cells.