Patient-derived T cells genetically engineered to express a chimeric antigen receptor targeting BCMA (TNFRSF17); administered intravenously at 2–4 × 10^6 BCMA CAR+ T cells/kg to eliminate residual multiple myeloma via CAR-mediated T-cell cytotoxicity and cytokine release.
Autologous T cells are genetically engineered to express a chimeric antigen receptor targeting BCMA; upon binding BCMA on myeloma/plasma cells, the CAR activates the T cells to deliver targeted cytotoxicity and cytokine release, killing BCMA-positive malignant cells and clearing residual disease.
BCMA-specific CAR-T cells bind BCMA on target cells, become activated, and directly kill them via perforin/granzyme-mediated cytolysis and Fas–FasL apoptosis, with supportive cytokine release.
A humanized anti-HER2 IgG1 monoclonal antibody that inhibits HER2 signaling and dimerization and mediates antibody-dependent cellular cytotoxicity (ADCC).
Humanized anti-HER2 IgG1 monoclonal antibody that binds the HER2 extracellular domain, inhibits receptor dimerization and downstream MAPK/PI3K-AKT signaling, and mediates antibody-dependent cellular cytotoxicity (ADCC) by engaging immune effector cells against HER2-overexpressing tumor cells.
Trastuzumab binds HER2 on tumor cells and engages Fcγ receptor–bearing immune cells (e.g., NK cells) to induce antibody-dependent cellular cytotoxicity; it may also contribute via complement activation and HER2 signaling blockade leading to apoptosis.
Oral small-molecule BH3-mimetic BCL-2 inhibitor that induces intrinsic apoptosis in BCL-2–dependent myeloma (notably t(11;14)).
Selective BH3-mimetic BCL-2 inhibitor that binds the hydrophobic groove of BCL-2, neutralizing its anti-apoptotic function and freeing pro-apoptotic proteins to activate BAX/BAK, induce mitochondrial outer membrane permeabilization, and trigger caspase-dependent intrinsic apoptosis. Spares BCL-XL, reducing thrombocytopenia risk. Particularly effective in BCL-2–dependent tumors such as t(11;14) multiple myeloma.
Venetoclax binds and inhibits BCL-2, releasing pro-apoptotic BH3 proteins to activate BAX/BAK, cause mitochondrial outer membrane permeabilization, caspase activation, and intrinsic apoptosis of BCL-2–dependent cells.
Anti-CD38 IgG1 monoclonal antibody that targets CD38 on myeloma and immune cells, mediating ADCC, CDC, ADCP, and immunomodulation.
Unconjugated anti-CD38 IgG1 monoclonal antibody that binds CD38 on myeloma and immune cells, inducing Fc-mediated antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and antibody-dependent cellular phagocytosis (ADCP); also depletes CD38+ immunosuppressive cells (Tregs, Bregs, MDSCs), enhancing antitumor immunity.
Daratumumab binds CD38 on target cells and engages immune effectors via its Fc to mediate NK cell ADCC, complement-dependent cytotoxicity (CDC), and macrophage antibody-dependent cellular phagocytosis (ADCP), leading to lysis and clearance of CD38+ cells.
An autologous anti-mesothelin CAR T-cell therapy. Patient T cells are engineered ex vivo using circular mRNA to transiently express a mesothelin-targeting chimeric antigen receptor (no genomic integration) and administered by IV infusion weekly ×4 (dose escalation 1×10^8 to 2×10^9 cells). The CAR engages mesothelin on tumor cells to drive HLA-independent T-cell activation, cytotoxicity, cytokine release, and proliferation.
Autologous T cells are engineered ex vivo with circular mRNA to transiently express a mesothelin-targeting chimeric antigen receptor. Upon binding mesothelin on tumor cells, the CAR delivers HLA-independent activation signals (CD3ζ-based), triggering T‑cell cytotoxicity (perforin/granzyme), cytokine release, and clonal expansion without genomic integration.
Anti-mesothelin CAR T cells bind mesothelin and, via CD3zeta signaling, directly lyse target cells through perforin/granzyme-mediated cytotoxicity (with cytokine release).