An anti-HER2 antibody–drug conjugate (RC48) that binds HER2, is internalized, and releases the microtubule toxin MMAE to disrupt microtubules, causing G2/M arrest and apoptosis; may also mediate ADCC and a bystander effect.
HER2-targeted ADC that binds HER2, is internalized, and releases MMAE to inhibit tubulin polymerization, leading to G2/M arrest and apoptosis; may also trigger ADCC and a bystander killing effect.
YES
INDIRECT
The HER2-targeted ADC is internalized into HER2+ cells and releases MMAE, which binds the vinca domain on β-tubulin to inhibit microtubule polymerization, causing G2/M arrest and apoptosis; released MMAE can also produce a bystander killing effect.
Humanized IgG1 monoclonal antibody targeting EGFR (ErbB1); blocks ligand binding, inhibits MAPK/ERK and PI3K/AKT signaling, can trigger ADCC, and enhances radiosensitization of EGFR-expressing tumor cells.
Humanized IgG1 monoclonal antibody that binds EGFR (ErbB1), blocks ligand binding and receptor activation, suppressing downstream MAPK/ERK and PI3K/AKT signaling; can engage ADCC and enhances radiosensitization of EGFR-expressing tumor cells, leading to growth inhibition.
YES
DIRECT
Anti-EGFR IgG1 mAb binds EGFR on target cells, blocks survival signaling (promoting growth arrest/apoptosis) and recruits FcγR+ effector cells to mediate ADCC against EGFR-expressing cells.
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.
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
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.