Chimeric monoclonal antibody targeting CD20 to deplete malignant B cells.
Chimeric anti-CD20 IgG1 monoclonal antibody that binds CD20 on pre‑B and mature B cells and depletes CD20+ cells via antibody‑dependent cellular cytotoxicity (ADCC), complement‑dependent cytotoxicity (CDC), and apoptosis induction.
Rituximab binds CD20 on B cells; its Fc region engages Fcγ receptor–bearing effector cells to mediate ADCC and phagocytosis, and it activates complement for CDC, with additional apoptosis induction upon crosslinking.
Autologous, genetically modified dual-target CAR T-cell therapy (also known as AZD0120) engineered to express CARs against BCMA and CD19; administered as a single infusion. Antigen engagement activates CAR signaling (CD3ζ with co-stimulation), driving T-cell cytotoxicity (immune synapse formation, perforin/granzyme release, cytokine secretion) to eliminate malignant plasma cells/B-lineage cells and mitigate antigen escape.
Autologous T cells genetically modified to express dual CARs against BCMA and CD19. Antigen engagement triggers CD3ζ/co-stimulatory signaling, activating cytotoxic T-cell functions (immune synapse formation, perforin/granzyme release, cytokine secretion) to eliminate malignant plasma cells and B-lineage cells. Dual targeting reduces antigen escape by covering both BCMA- and CD19-expressing tumor populations.
BCMA-specific CAR T cells bind BCMA on target cells, form an immune synapse, and induce apoptosis via perforin/granzyme release and death-receptor signaling.
Autologous, genetically modified dual-target CAR T-cell therapy (also known as AZD0120) engineered to express CARs against BCMA and CD19; administered as a single infusion. Antigen engagement activates CAR signaling (CD3ζ with co-stimulation), driving T-cell cytotoxicity (immune synapse formation, perforin/granzyme release, cytokine secretion) to eliminate malignant plasma cells/B-lineage cells and mitigate antigen escape.
Autologous T cells genetically modified to express dual CARs against BCMA and CD19. Antigen engagement triggers CD3ζ/co-stimulatory signaling, activating cytotoxic T-cell functions (immune synapse formation, perforin/granzyme release, cytokine secretion) to eliminate malignant plasma cells and B-lineage cells. Dual targeting reduces antigen escape by covering both BCMA- and CD19-expressing tumor populations.
GC012F CAR T cells bind CD19 on target cells, form an immune synapse, and kill via perforin/granzyme release (and death-receptor pathways) following CAR activation.
Gene-modified natural killer (NK) cells engineered to express a chimeric antigen receptor based on NKG2D, enabling recognition of stress-induced ligands (MICA, MICB, ULBP family) on tumor cells and triggering NK cytotoxicity and cytokine release; infused after lymphodepleting chemotherapy to promote expansion and persistence.
Gene‑modified natural killer cells expressing an NKG2D‑based chimeric antigen receptor recognize stress‑induced ligands (MICA, MICB, ULBP family) on tumor cells, triggering NK activation, perforin/granzyme‑mediated cytotoxicity, and cytokine release; lymphodepleting chemotherapy is used to enhance CAR‑NK expansion and persistence.
NKG2D CAR-NK cells bind MICA via the NKG2D-based CAR, activating NK cytotoxicity and killing target cells through perforin/granzyme-mediated apoptosis (with cytokine release).
Gene-modified natural killer (NK) cells engineered to express a chimeric antigen receptor based on NKG2D, enabling recognition of stress-induced ligands (MICA, MICB, ULBP family) on tumor cells and triggering NK cytotoxicity and cytokine release; infused after lymphodepleting chemotherapy to promote expansion and persistence.
Gene‑modified natural killer cells expressing an NKG2D‑based chimeric antigen receptor recognize stress‑induced ligands (MICA, MICB, ULBP family) on tumor cells, triggering NK activation, perforin/granzyme‑mediated cytotoxicity, and cytokine release; lymphodepleting chemotherapy is used to enhance CAR‑NK expansion and persistence.
NKG2D CAR-NK cells recognize MICB on target cells, triggering NK activation and perforin/granzyme-mediated cytolysis (with possible death receptor signaling), killing the MICB+ cells.