Engineered natural killer cells expressing an NKG2D-based chimeric antigen receptor; administered via endoscopic ultrasound–guided intratumoral injection plus two intravenous infusions to recognize NKG2D ligands (e.g., MICA, MICB, ULBP family) and induce NK-mediated cytotoxicity.
Engineered NK cells expressing an NKG2D-based chimeric antigen receptor bind NKG2D ligands (e.g., MICA, MICB, ULBP family) on tumor cells, triggering NK activation and cytotoxicity (perforin/granzyme release, cytokine production) to kill cancer cells.
YES
DIRECT
NKG2D CAR-NK cells bind MICA on target cells, triggering NK activation and degranulation to kill via perforin/granzyme-mediated cytotoxicity (with possible death receptor signaling).
Engineered natural killer cells expressing an NKG2D-based chimeric antigen receptor; administered via endoscopic ultrasound–guided intratumoral injection plus two intravenous infusions to recognize NKG2D ligands (e.g., MICA, MICB, ULBP family) and induce NK-mediated cytotoxicity.
Engineered NK cells expressing an NKG2D-based chimeric antigen receptor bind NKG2D ligands (e.g., MICA, MICB, ULBP family) on tumor cells, triggering NK activation and cytotoxicity (perforin/granzyme release, cytokine production) to kill cancer cells.
YES
DIRECT
NKG2D CAR–engineered NK cells bind MICB on target cells, triggering NK activation and cytolysis via perforin/granzyme release (and death-receptor pathways), leading to apoptosis of MICB-expressing cells.
Engineered natural killer cells expressing an NKG2D-based chimeric antigen receptor; administered via endoscopic ultrasound–guided intratumoral injection plus two intravenous infusions to recognize NKG2D ligands (e.g., MICA, MICB, ULBP family) and induce NK-mediated cytotoxicity.
Engineered NK cells expressing an NKG2D-based chimeric antigen receptor bind NKG2D ligands (e.g., MICA, MICB, ULBP family) on tumor cells, triggering NK activation and cytotoxicity (perforin/granzyme release, cytokine production) to kill cancer cells.
YES
DIRECT
NKG2D CAR-NK cells bind ULBP1 on target cells, activating NK degranulation (perforin/granzyme) and inducing target cell lysis/apoptosis.
A recombinant human broadly neutralizing monoclonal antibody that binds the HIV-1 Env gp120 CD4-binding site to block virus–CD4 interaction and entry; neutralizes diverse HIV-1 strains and can mediate Fc-dependent effector functions (ADCC/ADCP). The LS Fc mutations enhance FcRn binding and extend serum half-life.
Recombinant human broadly neutralizing monoclonal antibody that binds the HIV-1 Env gp120 CD4-binding site, blocking gp120–CD4 interaction and viral entry; neutralizes diverse HIV-1 strains and can engage Fc-dependent effector functions (ADCC/ADCP) against infected cells. LS Fc mutations enhance FcRn binding to extend serum half-life.
NO
INDIRECT
3BNC117-LS binds HIV-1 Env gp120 on infected cells and recruits FcγR-expressing effector cells (e.g., via CD16/CD32a) to mediate ADCC/ADCP against gp120+ infected cells. Cells expressing CD32a are effector cells and are not targeted or killed by the antibody.
Engineered natural killer cells expressing an NKG2D-based chimeric antigen receptor; administered via endoscopic ultrasound–guided intratumoral injection plus two intravenous infusions to recognize NKG2D ligands (e.g., MICA, MICB, ULBP family) and induce NK-mediated cytotoxicity.
Engineered NK cells expressing an NKG2D-based chimeric antigen receptor bind NKG2D ligands (e.g., MICA, MICB, ULBP family) on tumor cells, triggering NK activation and cytotoxicity (perforin/granzyme release, cytokine production) to kill cancer cells.
YES
DIRECT
NKG2D CAR-NK cells bind ULBP2 on target cells, triggering NK activation and degranulation (perforin/granzyme–mediated apoptosis), with possible contribution from death receptor pathways (FasL/TRAIL).