Murine IgG1 anti-CD66 (CEACAM) monoclonal antibody conjugated with the beta-emitting radionuclide Yttrium-90 to deliver targeted radiation to CD66+ myeloid/granulocytic cells in bone marrow and spleen for marrow-directed myeloablation.
Murine IgG1 anti-CD66 (CEACAM) monoclonal antibody conjugated to the beta-emitting radionuclide Yttrium-90; upon binding CD66+ myeloid/granulocytic cells in bone marrow and spleen, it delivers localized radiation that induces DNA damage and cell death, effecting marrow-directed myeloablation and reducing leukemic burden with limited exposure to other tissues.
NO
INDIRECT
This Y-90–labeled anti-CD66 antibody targets granulocytic/myeloid CD66 antigens (e.g., CEACAM6/8), not CEACAM5 (CEA). Only cells bound by the antibody receive beta radiation and are killed via DNA damage; CEACAM5+ cells are not targeted.
An antibody–drug conjugate (POLIVY) consisting of a humanized anti‑CD79b IgG1 monoclonal antibody linked to the cytotoxic payload monomethyl auristatin E (MMAE), a microtubule inhibitor. It binds CD79b on B cells, is internalized, and releases MMAE intracellularly to disrupt microtubules, leading to mitotic arrest and apoptosis of malignant B cells in DLBCL.
Humanized anti‑CD79b IgG1 antibody conjugated via a protease‑cleavable linker to monomethyl auristatin E (MMAE). After binding CD79b on B cells and internalization, MMAE is released intracellularly, inhibits tubulin polymerization, induces G2/M mitotic arrest, and triggers apoptosis of malignant B cells.
YES
DIRECT
The ADC binds CD79b on B cells, is internalized, and releases MMAE intracellularly; MMAE inhibits tubulin polymerization, causing G2/M arrest and apoptosis of the target cell.
An antibody–drug conjugate (POLIVY) consisting of a humanized anti‑CD79b IgG1 monoclonal antibody linked to the cytotoxic payload monomethyl auristatin E (MMAE), a microtubule inhibitor. It binds CD79b on B cells, is internalized, and releases MMAE intracellularly to disrupt microtubules, leading to mitotic arrest and apoptosis of malignant B cells in DLBCL.
Humanized anti‑CD79b IgG1 antibody conjugated via a protease‑cleavable linker to monomethyl auristatin E (MMAE). After binding CD79b on B cells and internalization, MMAE is released intracellularly, inhibits tubulin polymerization, induces G2/M mitotic arrest, and triggers apoptosis of malignant B cells.
NO
INDIRECT
The ADC binds CD79b on B cells, is internalized, and releases MMAE, which binds beta-tubulin (vinca site) to inhibit microtubule polymerization, causing G2/M arrest and apoptosis. Tubulin expression alone does not target cells for killing.
Anti-CD2 monoclonal antibody (also known as TCD601) used peri-transplant for in vivo T-cell depletion to reduce GVHD and graft failure; targets CD2 on T and NK cells.
Humanized IgG1 anti‑CD2 monoclonal antibody that binds CD2 on T and NK cells and induces immune‑mediated cytotoxicity (ADCC/CDC), depleting CD2+ lymphocytes and suppressing T‑cell activity to reduce GVHD and graft rejection.
YES
DIRECT
Siplizumab binds CD2 on target cells and recruits immune effectors via its Fc to trigger ADCC and complement-dependent cytotoxicity, leading to lysis/depletion of CD2+ cells.
Autologous T lymphocytes genetically engineered to express a chimeric antigen receptor targeting CD19 on B cells; administered as cellular immunotherapy for B‑cell malignancies.
Autologous T lymphocytes engineered to express a chimeric antigen receptor that recognizes CD19 on B cells. CAR signaling via CD3ζ and costimulatory domains (e.g., 4-1BB or CD28) upon CD19 binding triggers T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytolysis of CD19-positive malignant B cells, frequently causing B-cell aplasia.
YES
DIRECT
CAR T cells bind CD19 on target cells, form an immune synapse, and induce killing via perforin/granzyme release (and death receptor signaling), leading to apoptosis of CD19-positive cells.