Recombinant humanized IgG1 monoclonal antibody targeting HER2 (ErbB2); administered IV (4 mg/kg loading then 2 mg/kg weekly, or 8 mg/kg loading then 6 mg/kg every 3 weeks). Binds the HER2 extracellular domain, inhibits receptor activation/dimerization and shedding, suppresses PI3K/AKT/mTOR and RAS/RAF/MEK/ERK signaling, and induces ADCC via FcγR-bearing immune effector cells.
Humanized IgG1 monoclonal antibody targeting HER2 (ErbB2); binds the extracellular domain to block receptor activation and dimerization and inhibit shedding, thereby suppressing downstream PI3K/AKT/mTOR and RAS/RAF/MEK/ERK signaling, while engaging FcγR-expressing immune cells to mediate ADCC against HER2-overexpressing tumor cells.
YES
DIRECT
Binds HER2 and recruits FcγR-expressing effector cells (e.g., NK cells) to kill target cells via ADCC; minor CDC/apoptosis may occur.
Allogeneic, gene-engineered natural killer cell therapy expressing a chimeric antigen receptor targeting Trop-2 (TACSTD2) to enable antigen-specific NK activation and cytotoxicity against Trop2-positive tumor cells in relapsed/refractory NSCLC.
Allogeneic, gene-engineered natural killer cells expressing a chimeric antigen receptor for Trop-2 (TACSTD2) recognize Trop-2–positive tumor cells and induce antigen-dependent NK activation, resulting in perforin/granzyme-mediated cytotoxicity and cytokine release to kill Trop-2–expressing NSCLC cells.
YES
DIRECT
CAR-NK cells recognize Trop-2 on target cells and kill them via antigen-dependent activation with perforin/granzyme-mediated cytotoxicity (with cytokine release).
Allogeneic, off-the-shelf CD19-targeted CAR-T cell therapy (also referred to as REVO-UWD-19 or UWD-CD19) designed to bind CD19 on B cells and mediate T-cell activation and cytotoxic killing; administered as a single infusion.
Allogeneic T cells engineered with a CD19-directed chimeric antigen receptor bind CD19 on malignant B cells, triggering T‑cell activation, cytokine release, and cytotoxic killing that clears CD19+ cells (with expected on‑target B‑cell aplasia).
YES
DIRECT
CD19-directed CAR-T cells bind CD19 on target B cells, triggering T-cell activation and cytotoxic killing via perforin/granzyme release and death receptor pathways, leading to apoptosis/lysis of CD19+ cells.
An antibody-drug conjugate composed of a humanized anti-HER2 monoclonal antibody (disitamab) linked via a cleavable linker to the microtubule-disrupting payload monomethyl auristatin E (MMAE). After binding HER2 on tumor cells, the ADC is internalized and MMAE is released to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; additional effects may include ADCC and a bystander effect.
Humanized anti-HER2 monoclonal antibody (disitamab) delivers the microtubule toxin MMAE via a cleavable linker. After binding HER2, the ADC is internalized and MMAE is released in lysosomes to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; may also induce Fc-mediated ADCC and a membrane-permeable bystander effect.
YES
DIRECT
Anti-HER2 ADC binds HER2, is internalized, and releases MMAE in lysosomes to inhibit microtubule polymerization, causing G2/M arrest and apoptosis (with possible ADCC and bystander effects).
An antibody-drug conjugate composed of a humanized anti-HER2 monoclonal antibody (disitamab) linked via a cleavable linker to the microtubule-disrupting payload monomethyl auristatin E (MMAE). After binding HER2 on tumor cells, the ADC is internalized and MMAE is released to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; additional effects may include ADCC and a bystander effect.
Humanized anti-HER2 monoclonal antibody (disitamab) delivers the microtubule toxin MMAE via a cleavable linker. After binding HER2, the ADC is internalized and MMAE is released in lysosomes to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; may also induce Fc-mediated ADCC and a membrane-permeable bystander effect.
YES
INDIRECT
After HER2 binding and internalization, the ADC releases MMAE, which binds the vinca site on beta-tubulin, inhibits microtubule polymerization, and induces G2/M arrest and apoptosis; killing depends on HER2-mediated delivery (with possible bystander effect).