Humanized IgG1 anti-HER2 monoclonal antibody that binds HER2, inhibits downstream signaling (PI3K/AKT, MAPK), reduces receptor dimerization, and mediates ADCC.
Humanized IgG1 monoclonal antibody targeting HER2; binds HER2 on tumor cells, inhibits receptor dimerization and downstream PI3K/AKT and MAPK signaling, and engages Fcγ receptors to trigger antibody-dependent cellular cytotoxicity (ADCC).
Trastuzumab binds HER2 on target cells and its Fc engages Fcγ receptors on NK cells and other effectors to trigger antibody‑dependent cellular cytotoxicity (ADCC); may also activate complement; additionally inhibits HER2 signaling (primarily cytostatic).
Adoptive γδ T‑cell therapy using Vγ9Vδ2 T cells expanded from healthy donors and administered intraventricularly/intracavitary via an Ommaya reservoir. These innate‑like cytotoxic lymphocytes recognize tumor phosphoantigens via BTN3A1/BTN2A1 independent of MHC, triggering perforin/granzyme‑mediated killing and cytokine release; they can also respond via NKG2D and mediate ADCC.
Allogeneic Vγ9Vδ2 T cells recognize tumor-derived phosphoantigens generated by dysregulated mevalonate metabolism via BTN3A1/BTN2A1 in an MHC-independent manner, triggering perforin/granzyme-mediated cytotoxicity and cytokine release. They also respond to stress ligands through NKG2D and can mediate ADCC.
Vγ9Vδ2 T cells engage ULBP2 via their NKG2D receptor, triggering immune synapse formation and perforin/granzyme-mediated cytotoxic killing of the target cell.
A fully humanized IgG1 antibody-drug conjugate (ADC) targeting B7-H3 (CD276); it binds B7-H3 on tumor cells, is internalized, and releases a cytotoxic payload to induce targeted tumor cell death. Administered intravenously every 3 weeks.
B7-H3–targeted IgG1 antibody-drug conjugate that binds CD276 on tumor cells, is internalized, and releases a topoisomerase inhibitor payload to inhibit DNA topoisomerase activity, causing replication arrest and apoptosis in B7-H3–expressing tumor cells.
The anti–B7-H3 ADC binds CD276 on target cells, is internalized, and releases a topoisomerase inhibitor payload that blocks DNA topoisomerase activity, causing replication arrest, DNA damage, and apoptosis of B7-H3–expressing cells.
Humanized IgG1 monoclonal antibody targeting IL-5 receptor alpha (IL-5Rα); depletes eosinophils (and basophils) primarily via antibody-dependent cell-mediated cytotoxicity (ADCC) by engaging NK cells, thereby inhibiting IL-5/IL-5R signaling and eosinophil survival.
Afucosylated humanized IgG1 monoclonal antibody targeting IL-5 receptor alpha (IL-5Ralpha); binds IL-5Ralpha on eosinophils/basophils and induces their depletion via Fc-mediated ADCC through NK cells, thereby blocking IL-5 signaling and reducing eosinophil survival and inflammation.
Benralizumab binds IL-5Rα on eosinophils/basophils and engages NK cells via its afucosylated Fc (FcγRIIIa), triggering potent ADCC that lyses/induces apoptosis of IL-5Rα+ cells.
Trop-2–directed antibody–drug conjugate that delivers SN-38 (a topoisomerase I inhibitor) to Trop-2–expressing tumor cells and nearby cells (bystander effect), causing DNA damage.
Trop-2–targeted antibody–drug conjugate that binds Trop-2 on tumor cells, is internalized, and releases SN-38 (a topoisomerase I inhibitor). SN-38 stabilizes Topo I–DNA complexes, causing DNA strand breaks, replication arrest, and apoptosis; the membrane-permeable payload also produces a bystander killing effect.
ADC binds TROP-2 on tumor cells, is internalized, and releases SN-38; SN-38 inhibits topoisomerase I, causing DNA strand breaks, replication arrest, and apoptosis (with additional bystander killing due to payload permeability).