Long-acting broadly neutralizing anti–HIV-1 human IgG1 monoclonal antibody with LS Fc mutations for extended half-life; targets the gp120 V3 glycan (N332) supersite to neutralize virus and block entry, and engages Fcγ receptor–mediated effector functions (ADCC, phagocytosis) to eliminate Env-expressing infected cells and reduce the intact proviral reservoir.
A long-acting broadly neutralizing human IgG1 monoclonal antibody with LS Fc mutations that extend half-life; it binds the HIV-1 Env gp120 V3 glycan (N332) supersite to neutralize virions and block viral entry, and engages Fcγ receptors to mediate ADCC and phagocytosis of Env-expressing infected cells, aiming to reduce the intact proviral reservoir.
NO
INDIRECT
The antibody binds HIV-1 Env on infected cells and uses its Fc to engage Fcγ receptors (including CD32a) on effector cells, triggering ADCC/phagocytosis that kills Env-expressing cells; CD32a+ cells are not the targets and are not directly killed.
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.
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
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).