Tregalizumab Overview

Introduction of Tregalizumab

Tregalizumab represents a novel, humanized, anti-human CD4 IgG1κ monoclonal antibody (mAb) derived from a murine predecessor B-F5 by complementarity-determining region (CDR) grafting and subcloning. It binds to a unique epitope of CD4 in the IgG-like C2 type 1 domain on the opposite side of the binding region for other known ligands, including other anti-CD4 mAbs, gp120, and major histocompatibility complex (MHC) class II. Tregalizumab was developed by AbbVie/Biotest GA for the treatment of autoimmune diseases, e.g., rheumatoid arthritis.

Mechanism of Action of Tregalizumab

As a specialized subpopulation of regulatory T cells (Tregs), CD4⁺ T cells are essential for maintaining peripheral tolerance and preventing autoimmunity. The immunomodulatory effects of Tregs depend on their activation status. Tregalizumab is able to selectively activate the suppressive properties of Tregs by binding to CD4 and activation of signaling downstream pathways, resulting the increasing of cyclic adenosine monophosphate (cAMP), latency-associated peptide (LAP), and transforming growth factor-β (TGF-β). Due to binding to a unique, conformational epitope on domain 2 of the CD4 molecule, tregalizumab induces a unique phosphorylation of T-cell receptor complex-associated signaling molecules. This is sufficient to activate the function of Tregs without activating effector T cells. Furthermore, Tregalizumab does not induce the release of pro-inflammatory cytokines.

Fig.1 Mechanism of action of tregalizumab

What We Provide

Therapeutic Antibody

Tregalizumab

We provide high-quality Tregalizumab for use in WB, FC, IP, ELISA, Neut, FuncS, IF and most other immunological methods. For lab research use only, not for diagnostic, therapeutic or any in vivo human use.

For research use only. Not intended for any clinical use.