Universal chimeric natural killer receptor–modified T cells engineered to dual-target NKG2D and NKp44 (NCR2) ligands on tumors, triggering T-cell cytotoxicity and cytokine release.
T cells engineered with NK receptor–based chimeric receptors that dual-target ligands for NKG2D and NKp44 (NCR2) on tumor cells; ligand engagement triggers T‑cell activation signaling to drive cytotoxic killing and cytokine release, addressing antigen heterogeneity in solid tumors.
YES
DIRECT
ULBP6 is an NKG2D ligand; binding to the NKG2D-based chimeric receptor on the engineered T cells activates them to kill target cells via perforin/granzyme-mediated cytolysis and apoptosis, with cytokine release.
Universal chimeric natural killer receptor–modified T cells engineered to dual-target NKG2D and NKp44 (NCR2) ligands on tumors, triggering T-cell cytotoxicity and cytokine release.
T cells engineered with NK receptor–based chimeric receptors that dual-target ligands for NKG2D and NKp44 (NCR2) on tumor cells; ligand engagement triggers T‑cell activation signaling to drive cytotoxic killing and cytokine release, addressing antigen heterogeneity in solid tumors.
YES
DIRECT
Engineered T cells bearing NK receptor–based chimeric receptors bind NKp44 ligands on tumor cells, triggering T-cell activation and perforin/granzyme-mediated cytolysis (with cytokine release).
Human IgG1 anti-PD-L1 monoclonal antibody immune checkpoint inhibitor that blocks PD-1/PD-L1 and PD-L1/CD80 interactions and can trigger ADCC to enhance T-cell and NK-cell activity.
Human IgG1 anti-PD-L1 checkpoint-blocking monoclonal antibody that prevents PD-L1 interaction with PD-1 and CD80, releasing PD-1-mediated inhibitory signaling to restore T-cell function; Fc-competent IgG1 also triggers antibody-dependent cellular cytotoxicity against PD-L1-expressing cells, enhancing T-cell and NK-cell antitumor activity.
YES
DIRECT
Avelumab binds PD-L1 on target cells and, via its IgG1 Fc, engages FcγR on NK cells/macrophages to trigger antibody-dependent cellular cytotoxicity (ADCC), killing PD-L1–expressing cells.
An antibody-drug conjugate (Blenrep) consisting of a humanized anti-BCMA IgG1 monoclonal antibody linked to the microtubule toxin MMAF; binds BCMA on myeloma cells, is internalized, and releases MMAF to disrupt microtubules and induce apoptosis; can also engage immune effector functions (ADCC/ADCP).
Belantamab mafodotin is an anti-BCMA IgG1 antibody-drug conjugate that binds BCMA on myeloma cells, is internalized, and releases the auristatin payload MMAF to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; the afucosylated Fc can also mediate ADCC/ADCP.
YES
DIRECT
ADC binds BCMA, is internalized, and releases MMAF to inhibit tubulin, causing G2/M arrest and apoptosis; afucosylated Fc also triggers ADCC/ADCP.
An antibody-drug conjugate (Blenrep) consisting of a humanized anti-BCMA IgG1 monoclonal antibody linked to the microtubule toxin MMAF; binds BCMA on myeloma cells, is internalized, and releases MMAF to disrupt microtubules and induce apoptosis; can also engage immune effector functions (ADCC/ADCP).
Belantamab mafodotin is an anti-BCMA IgG1 antibody-drug conjugate that binds BCMA on myeloma cells, is internalized, and releases the auristatin payload MMAF to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; the afucosylated Fc can also mediate ADCC/ADCP.
NO
INDIRECT
The ADC binds BCMA (not beta‑tubulin), is internalized, then releases MMAF that binds the beta‑tubulin vinca domain to inhibit microtubule polymerization, causing G2/M arrest and apoptosis; Fc can also trigger ADCC/ADCP after BCMA binding.