An autologous BCMA-directed chimeric antigen receptor T-cell (CAR-T) therapy in which a patient's T cells are gene-modified to express a CAR targeting BCMA, leading to T-cell activation, cytokine release, expansion, and targeted cytotoxic killing of malignant plasma cells in multiple myeloma.
Autologous T cells are genetically engineered to express a chimeric antigen receptor targeting BCMA on malignant plasma cells; antigen engagement activates the T cells, inducing cytokine release, clonal expansion, and targeted cytotoxic killing of multiple myeloma cells.
BCMA-specific CAR T cells bind BCMA on target cells, become activated, and kill via perforin/granzyme-mediated cytolysis and apoptosis (with contribution from Fas–FasL).
Fully human IgG1 anti-CD20 monoclonal antibody immunotherapy administered subcutaneously; depletes CD20+ B lymphocytes via CDC, ADCC, and apoptosis, reducing naive and memory B cells while sparing stem cells and plasma cells.
Fully human IgG1 anti-CD20 monoclonal antibody that binds CD20 on B lymphocytes and depletes them via complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC), and apoptosis, reducing naive and memory B cells while sparing hematopoietic stem cells and plasma cells.
Ofatumumab binds CD20 on B cells, triggers complement-dependent cytotoxicity (CDC) and Fc-mediated ADCC/ADCP by NK cells/macrophages, and can induce apoptosis of the bound cells.
Humanized, defucosylated IgG1 monoclonal antibody (KW-0761) targeting CCR4; depletes CCR4+ malignant T cells and Tregs by blocking CCR4–chemokine signaling and inducing potent ADCC via NK cells.
Humanized, defucosylated IgG1 monoclonal antibody against CCR4 (CD194) that blocks CCR4–chemokine signaling (e.g., CCL17/TARC, CCL22/MDC) and induces potent FcγRIIIa-dependent ADCC by NK cells to deplete CCR4+ malignant T cells and regulatory T cells, reducing tumor burden and Treg-mediated immunosuppression.
Mogamulizumab binds CCR4 on target cells and engages FcγRIIIa on NK cells, inducing potent ADCC that kills CCR4+ cells (depleting CCR4+ malignant T cells and Tregs).
A CRISPR/Cas9-edited, allogeneic B7-H3 (CD276)–targeted chimeric antigen receptor (CAR) T-cell therapy administered intrapleurally; engineered T cells recognize B7-H3 on tumor cells to induce antigen-dependent T-cell activation, cytokine release, and cytotoxic killing.
CRISPR/Cas9-edited, allogeneic T cells engineered to express a B7-H3 (CD276)–specific chimeric antigen receptor. Upon binding B7-H3 on tumor cells, the CAR activates T-cell signaling, leading to cytokine release and targeted cytotoxic killing; gene edits support allogeneic use and minimize alloreactivity. Administered intrapleurally to treat pleural tumors.
B7-H3-specific CAR T cells bind B7-H3 on target cells, activate, and directly kill them via perforin/granzyme-mediated cytolysis (and Fas/FasL), with cytokine release.
Chimeric IgG1 anti–TNF-α monoclonal antibody that binds soluble and transmembrane TNF-α to inhibit TNFR1/2 signaling, thereby reducing NF-κB/MAPK activation, pro-inflammatory cytokines (e.g., IL-1, IL-6), adhesion molecule expression, and leukocyte trafficking; can induce apoptosis/ADCC of TNF-expressing cells.
Chimeric IgG1 monoclonal antibody against TNF-alpha that binds soluble and transmembrane TNF-alpha to block TNFR1/2 signaling, suppressing NF-kB/MAPK pathways, pro-inflammatory cytokines, adhesion molecules, and leukocyte trafficking; can also mediate ADCC/complement effects and apoptosis of TNF-expressing cells.
Binds transmembrane TNF-α and, via IgG1 Fc, triggers ADCC and complement-dependent lysis; also induces apoptosis through reverse (outside-in) signaling in tmTNF-expressing cells.