Gene-modified natural killer (NK) cells engineered to express an NKG2D-based chimeric antigen receptor (CAR) that recognizes NKG2D ligands (MICA, MICB, ULBP family) on tumor cells, activating NK cytotoxicity for treatment of relapsed/refractory multiple myeloma.
Gene‑modified NK cells expressing an NKG2D‑based CAR recognize stress‑induced NKG2D ligands (MICA, MICB, ULBP family) on tumor cells. CAR signaling activates NK cytotoxic functions, inducing degranulation (perforin/granzyme), cytokine‑mediated killing, and apoptosis of malignant cells, targeting relapsed/refractory multiple myeloma.
NKG2D CAR-engineered NK cells recognize ULBP3 on target cells, become activated, and kill via degranulation with perforin/granzymes leading to apoptosis.
Disitamab vedotin is an anti-HER2 monoclonal antibody conjugated to the microtubule inhibitor MMAE. It binds HER2 on tumor cells, is internalized, and releases MMAE via a protease-cleavable linker in lysosomes, leading to microtubule disruption, G2/M cell-cycle arrest, and apoptotic cell death; the antibody component may also contribute to antitumor activity via Fc-mediated effector functions.
HER2-targeted ADC binds HER2, is internalized, and releases MMAE via protease-cleavable linker; MMAE disrupts microtubules causing G2/M arrest and apoptosis. Fc-mediated ADCC may also contribute.
First-in-human, intravenous investigational immunotherapy; precise target/mechanism not disclosed in the registry. PK/PD and preliminary antitumor activity are being characterized.
Humanized IgG1 bispecific checkpoint antibody targeting TIGIT and PVRIG (CD112R). Blocks TIGIT–CD155/CD112 and PVRIG–CD112 interactions, shifting signaling toward CD226 co-stimulation to activate CD8+ T cells and NK cells. Also leverages Fc effector function to deplete TIGIT+ regulatory T cells, enhancing antitumor immunity.
The IgG1 Fc engages Fc-gamma receptor effector cells (e.g., NK cells, macrophages) to mediate ADCC/ADCP (and possibly CDC), depleting TIGIT-expressing regulatory T cells.
First-in-human, intravenous investigational immunotherapy; precise target/mechanism not disclosed in the registry. PK/PD and preliminary antitumor activity are being characterized.
Humanized IgG1 bispecific checkpoint antibody targeting TIGIT and PVRIG (CD112R). Blocks TIGIT–CD155/CD112 and PVRIG–CD112 interactions, shifting signaling toward CD226 co-stimulation to activate CD8+ T cells and NK cells. Also leverages Fc effector function to deplete TIGIT+ regulatory T cells, enhancing antitumor immunity.
IgG1 Fc-mediated effector function (ADCC/ADCP) can deplete PVRIG-expressing (TIGIT+) regulatory T cells bound by the antibody; effector T/NK cells are activated rather than depleted.
Autologous T cells genetically engineered to express a chimeric antigen receptor targeting CD19 on B-lineage malignant cells; used for CD19-positive lymphoproliferative disorders. CAR engagement triggers T-cell activation and cytotoxicity.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that recognizes CD19 on B-lineage malignant cells; CAR engagement triggers CD3ζ and costimulatory signaling (e.g., CD28 or 4-1BB), leading to T-cell activation, proliferation, cytokine release, and targeted cytotoxic killing of CD19-positive cancer cells.
CAR binding to CD19 activates engineered T cells (via CD3ζ and costimulatory domains), leading to targeted killing of CD19+ cells through perforin/granzyme release and Fas–FasL–mediated apoptosis.