Anti-CD117 (c-Kit) monoclonal antibody used in conditioning to deplete/disable recipient hematopoietic stem and progenitor cells and facilitate donor engraftment.
Humanized anti-CD117 (c-Kit) monoclonal antibody that blocks stem cell factor (SCF) binding/signaling on hematopoietic stem and progenitor cells, depleting/functional disabling them to create marrow niche space and facilitate donor engraftment during conditioning.
YES
INDIRECT
Blocks SCF–c-Kit signaling on hematopoietic stem/progenitor cells, removing survival signals and causing apoptosis/depletion; Fc-mediated clearance may contribute.
Anti-CD52 monoclonal antibody for lymphodepletion to reduce rejection and graft-versus-host disease.
Humanized anti-CD52 IgG1 monoclonal antibody that binds CD52 on B and T lymphocytes (and some monocytes, macrophages, NK cells), inducing cell depletion via complement-dependent cytotoxicity and Fc-mediated ADCC, producing profound lymphodepletion to reduce rejection and graft-versus-host disease.
YES
DIRECT
Alemtuzumab binds CD52 on target cells and induces complement-dependent cytotoxicity and Fc-mediated effector killing (ADCC/ADCP), leading to lysis and depletion of CD52+ cells.
Chimeric IgG1 monoclonal antibody against TNF-α; neutralizes soluble and transmembrane TNF-α, can induce apoptosis of activated effector T cells/monocytes, and suppresses NF-κB–driven cytokines.
Chimeric IgG1 monoclonal antibody that binds and neutralizes soluble and transmembrane TNF-alpha, blocking TNF signaling; can induce apoptosis of activated effector T cells/monocytes and suppress NF-kB–driven proinflammatory cytokines to reduce inflammation.
NO
INDIRECT
Infliximab binds and neutralizes soluble TNF-α to block TNFR signaling; it does not directly kill cells via this target. Direct cytotoxicity occurs only when binding transmembrane TNF (reverse signaling/ADCC/CDC), not soluble TNF.
Chimeric IgG1 monoclonal antibody against TNF-α; neutralizes soluble and transmembrane TNF-α, can induce apoptosis of activated effector T cells/monocytes, and suppresses NF-κB–driven cytokines.
Chimeric IgG1 monoclonal antibody that binds and neutralizes soluble and transmembrane TNF-alpha, blocking TNF signaling; can induce apoptosis of activated effector T cells/monocytes and suppress NF-kB–driven proinflammatory cytokines to reduce inflammation.
YES
DIRECT
Infliximab binds transmembrane TNF on target cells; its IgG1 Fc mediates ADCC and complement-dependent cytotoxicity, and tmTNF reverse signaling can induce apoptosis of activated TNF+ T cells/monocytes.
An antibody–drug conjugate (brand name BESPONSA) composed of a humanized anti‑CD22 IgG4 monoclonal antibody linked to the cytotoxic antibiotic calicheamicin; binds CD22 on B‑lineage lymphoblasts, is internalized, and releases calicheamicin to induce DNA double‑strand breaks leading to apoptosis.
CD22-directed antibody-drug conjugate; the anti-CD22 IgG4 binds CD22 on B-lineage cells, is internalized, and releases the calicheamicin payload, which binds DNA and induces double-strand breaks leading to apoptosis.
NO
INDIRECT
The ADC targets CD22 on B cells for internalization; once inside, calicheamicin binds the DNA minor groove to cause double-strand breaks and apoptosis. DNA is the payload’s intracellular binding site, not the selective target for cell killing.