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.
NO
INDIRECT
HS-20093 binds B7-H3 on tumor cells, is internalized, and releases a payload that inhibits DNA topoisomerase I, causing DNA damage and apoptosis. Expression of topoisomerase I alone does not lead to targeting or killing; killing requires B7-H3-mediated delivery.
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.
YES
DIRECT
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.
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.
NO
INDIRECT
Belantamab mafodotin binds BCMA on target cells, is internalized, and releases MMAF to inhibit tubulin and disrupt microtubules, inducing apoptosis; Fc effector functions add ADCC/ADCP. Cells are not killed simply for expressing tubulin.
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.
NO
INDIRECT
CD16 is on NK effector cells; the TriKE uses CD16 to engage and IL-15 to activate/expand NK cells, which then kill CD33+ target myeloid cells via NK-mediated cytotoxicity (perforin/granzyme), not CD16+ 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.
YES
DIRECT
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.