An intravenous, fully humanized IgG1 antibody–drug conjugate targeting B7-H3 (CD276). Upon binding and internalization into B7-H3–expressing tumor cells, it releases a cytotoxic payload to induce direct tumor cell killing. Tested as 10 mg/kg monotherapy in advanced solid tumors including recurrent/metastatic HNSCC.
Fully humanized IgG1 ADC that binds B7-H3 (CD276) on tumor cells, is internalized, and releases a topoisomerase inhibitor payload, inhibiting DNA topoisomerase activity to block DNA replication and induce cell cycle arrest and apoptosis in B7-H3–expressing cancer cells.
ADC binds B7-H3 on tumor cells, is internalized, and releases a topoisomerase inhibitor payload that blocks DNA replication, causing cell cycle arrest and apoptosis of B7-H3–expressing cells.
Anti-BCMA antibody–drug conjugate: a humanized, afucosylated IgG1 monoclonal antibody targeting BCMA linked to the microtubule inhibitor MMAF; induces apoptosis upon internalization and leverages Fc-mediated ADCC/ADCP to deplete plasmablasts/plasma cells and reduce pathogenic autoantibodies.
Humanized, afucosylated anti-BCMA IgG1 linked to the microtubule inhibitor MMAF. Binds BCMA on plasmablasts/plasma cells, is internalized, and releases MMAF to disrupt microtubules and induce apoptosis. Afucosylated Fc enhances FcγR engagement to drive ADCC/ADCP, depleting BCMA+ antibody-secreting cells and reducing pathogenic autoantibodies.
Belantamab mafodotin binds BCMA on target cells, is internalized, and releases the MMAF payload to disrupt microtubules and induce apoptosis; its afucosylated Fc also engages FcγRs to trigger ADCC/ADCP against BCMA+ cells.
An engineered trispecific NK cell engager (TriKE) composed of anti-CD16, an IL-15 moiety, and anti-CD33 domains; designed to bridge NK cells via CD16 to induce cytotoxicity, deliver IL-15 to expand/sustain NK cells via JAK/STAT signaling, and target CD33+ leukemic blasts and myeloid-derived suppressor cells; administered as a single-agent continuous infusion in 28-day cycles.
Engineered TriKE that binds CD16 on NK cells and CD33 on target myeloid cells to form an immune synapse and trigger NK-mediated cytotoxicity; includes an IL-15 moiety to activate and expand NK cells via JAK/STAT signaling, enhancing sustained killing of CD33+ leukemic blasts and MDSCs.
TriKE bridges NK cells (via CD16) to CD33+ target cells, forming an immune synapse that triggers NK degranulation (perforin/granzymes) and killing; the IL-15 moiety activates/expands NK cells via JAK/STAT to enhance sustained cytotoxicity.
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 express NKG2D that binds MICA on target cells, activating an immune synapse and inducing perforin/granzyme-mediated apoptosis (with supportive cytokine release).
An anti-HER2 antibody-drug conjugate (RC48-ADC) in which a humanized anti-HER2 monoclonal antibody delivers the microtubule-disrupting payload monomethyl auristatin E (MMAE) via a cleavable linker; after HER2 binding and internalization, MMAE is released to induce G2/M arrest and apoptosis, with possible bystander effect and Fc-mediated ADCC.
Humanized anti‑HER2 monoclonal antibody binds HER2 on tumor cells, is internalized, and a cleavable linker releases MMAE, which binds tubulin to inhibit microtubule polymerization, causing G2/M arrest and apoptosis; may exert a bystander effect and engage Fc-mediated ADCC.
Anti-HER2 ADC binds HER2, is internalized, and releases MMAE via a cleavable linker; MMAE inhibits microtubule polymerization leading to G2/M arrest and apoptosis (with possible Fc-mediated ADCC and bystander effect).