Anti-CD19 monoclonal antibody that depletes B-lineage cells, including plasmablasts, to reduce autoantibody production.
Humanized, afucosylated anti-CD19 IgG1 monoclonal antibody that binds CD19 on B-lineage cells (including plasmablasts) and depletes them via enhanced Fc-mediated ADCC, thereby reducing pathogenic autoantibody production.
YES
DIRECT
The anti-CD19 IgG1 binds CD19 on B-lineage cells and recruits FcγR-expressing effector cells to mediate antibody-dependent cellular cytotoxicity (and phagocytosis), depleting CD19+ cells; complement activation may also contribute.
A chimeric IgG1 anti–TNF-α monoclonal antibody biosimilar to infliximab. Binds soluble and transmembrane TNF-α to block TNFR1/2 signaling and downstream NF-κB/MAPK pathways, reducing proinflammatory cytokines (e.g., IL-1, IL-6) and adhesion molecules; can induce apoptosis and Fc-mediated cytotoxicity of TNF-expressing immune cells. Administered subcutaneously (120 mg every 2 weeks) or intravenously (5–10 mg/kg every 8 weeks) for maintenance therapy in Crohn’s disease.
Chimeric IgG1 anti–TNF-alpha monoclonal antibody (biosimilar to infliximab) that binds soluble and transmembrane TNF-alpha, neutralizing TNFR1/2 signaling and downstream NF-kB/MAPK pathways; reduces proinflammatory cytokines and adhesion molecules and can induce apoptosis and Fc-mediated cytotoxicity of TNF-expressing immune cells.
YES
DIRECT
The IgG1 antibody binds transmembrane TNF on cells and can trigger apoptosis via reverse signaling and mediate Fc-dependent ADCC/CDC by effector cells/complement, killing TNF-expressing immune cells (neutralization of soluble TNF does not kill cells).
Anti-CD20 monoclonal antibody that depletes CD20+ B cells via antibody-dependent cellular cytotoxicity, complement activation, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes them via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
YES
DIRECT
Rituximab binds CD20 on B cells and eliminates them via Fc-mediated ADCC by effector cells, complement-dependent cytotoxicity (CDC), and direct apoptosis signaling.
Oral small-molecule BCL-2 inhibitor that promotes mitochondrial apoptosis in malignant B cells.
Selective oral BCL-2 inhibitor that mimics BH3-only proteins and binds the BCL-2 hydrophobic groove, blocking its anti-apoptotic function and restoring intrinsic (mitochondrial) apoptosis in BCL-2–dependent tumor cells; spares BCL-XL compared with navitoclax.
YES
DIRECT
Venetoclax inhibits anti-apoptotic BCL-2, releasing BH3 activators to trigger BAX/BAK activation, mitochondrial outer membrane permeabilization, cytochrome c release, and caspase-dependent apoptosis in BCL-2–dependent cells.
Multi-antigen DNA vaccine (nucleic acid immunotherapy) encoding CMV antigens IE-1+pp65 (fusion) and gB, each fused to LAMP1 to enhance MHC II presentation and cross-presentation to MHC I, intended to elicit CMV-specific CD4+ and CD8+ T-cell responses against CMV-expressing GBM cells.
Off‑the‑shelf plasmid DNA vaccine encoding CMV IE‑1/pp65 (fusion) and gB, each fused to LAMP1. Following intramuscular delivery with electroporation, plasmids are taken up by antigen‑presenting cells; LAMP1 targets antigens to lysosomes to enhance MHC II presentation with cross‑presentation on MHC I, inducing CMV‑specific CD4+ and CD8+ T‑cell responses to recognize and kill CMV‑expressing GBM cells.
YES
INDIRECT
The DNA vaccine primes CMV IE1-specific CD8+ T cells that recognize IE1 peptides on MHC I of CMV-expressing tumor cells and lyse them via perforin/granzyme-mediated cytotoxicity (with CD4+ T-cell help).