CT-P13 is a chimeric human–murine IgG1 monoclonal antibody biosimilar to infliximab (Remicade). It is an anti–TNF-α mAb that binds soluble and transmembrane TNF-α, blocking TNFR1/TNFR2 signaling, reducing NF-κB/MAPK pathway activation and downstream pro‑inflammatory cytokines (e.g., IL‑1, IL‑6) and adhesion molecules; it can induce apoptosis and CDC/ADCC against TNF‑expressing cells. Administered intravenously (IV) or subcutaneously (SC).
Chimeric IgG1 monoclonal antibody biosimilar to infliximab that binds soluble and transmembrane TNF-α, neutralizing TNF-α and preventing TNFR1/TNFR2 signaling. This reduces NF-κB/MAPK pathway activation and downstream pro‑inflammatory cytokines and adhesion molecules; can also induce apoptosis and mediate CDC/ADCC against TNF‑expressing cells.
YES
DIRECT
By binding transmembrane TNF-α, CT-P13 triggers reverse-signaling apoptosis and engages Fc-mediated effector functions (ADCC via NK cells and CDC), killing TNF-α–expressing cells.
Oral small-molecule BCL-2 inhibitor that restores mitochondrial apoptosis in leukemic blasts.
Selective oral BCL-2 inhibitor (BH3 mimetic) that binds the hydrophobic groove of BCL-2, blocks its anti-apoptotic function, and restores mitochondrial apoptosis in malignant cells; minimal BCL-XL inhibition.
YES
DIRECT
Venetoclax directly inhibits BCL-2 (BH3 mimetic), freeing pro-apoptotic proteins to activate BAX/BAK, inducing mitochondrial outer membrane permeabilization, caspase activation, and apoptosis of BCL-2–dependent cells.
Murine-derived, second-generation chimeric antigen receptor T cells targeting CD19 with 4-1BB costimulation for targeted killing and T-cell persistence.
Autologous T cells engineered to express a murine-derived anti-CD19 chimeric antigen receptor with 4-1BB costimulation and CD3z signaling; upon binding CD19 on B cells, the CAR triggers MHC-independent T-cell activation, proliferation, cytokine release, and cytolytic killing, with 4-1BB enhancing T-cell persistence.
YES
DIRECT
CAR binding to CD19 activates the engineered T cell to kill target cells via perforin/granzyme-mediated cytolysis (and Fas–FasL), MHC-independently.
IgG-based bispecific T-cell–engaging monoclonal antibody (anti-CD20 × anti-CD3) that redirects cytotoxic T cells to deplete CD20+ B cells.
IgG-based bispecific antibody that binds CD20 on B cells and CD3 on T cells, bringing them into proximity to activate T cells and induce perforin/granzyme-mediated lysis of CD20+ malignant (and normal) B cells.
YES
DIRECT
Bispecific antibody bridges CD3 on T cells to CD20 on target cells, activating T cells to deliver perforin/granzyme-mediated lysis of CD20+ cells.
IgG-based bispecific T-cell–engaging monoclonal antibody (anti-CD20 × anti-CD3) that redirects cytotoxic T cells to deplete CD20+ B cells.
IgG-based bispecific antibody that binds CD20 on B cells and CD3 on T cells, bringing them into proximity to activate T cells and induce perforin/granzyme-mediated lysis of CD20+ malignant (and normal) B cells.
NO
INDIRECT
CD3 on T cells is engaged to activate T cells; activated T cells kill CD20+ B cells via perforin/granzyme-mediated cytolysis. CD3-expressing T cells are not the targets of killing.