Human CD20 Antibody - Rituximab IgG1NQ Isotype

Anti-human CD20 antibody - Human IgG1fut (low effector functions)

Anti-hCD20-hIgG1NQ is a Rituximab biosimilar antibody with a mutated constant region of the human IgG1 isotype.
Rituximab is a mouse/human chimeric monoclonal antibody that targets the CD20 antigen found on the surface of malignant and normal B lymphocytes. Binding of rituximab to CD20 results in cell destruction through different mechanisms, including direct signaling of apoptosis, complement activation, and cell-mediated cytotoxicity. Rituximab has been approved by the FDA to treat various lymphoid malignancies, including B-cell non-Hodgkin's lymphoma and B-cell chronic lymphocytic leukemia.

Anti-hCD20-hIgG1NQ contains a N-glycosylation mutation of the constant region of the human IgG1, where potential asparagine (N) glycosylation sites are substituted by glutamine (Q) residue,s resulting in the production of a non-glycosylated antibody. Glycosylation of an antibody does not affect antigen binding but is essential for Fc receptor-mediated activity [1]. In non-glycosylated antibodies, the effector mechanisms mediated through the Fc receptor types (FcgRI, FcgRII, FcgRIII) and the C1q component of complement are severely compromised or ablated [2].

Anti-hCD20-hIgG1NQ was generated by recombinant DNA technology. It has been produced in Chinese hamster ovary (CHO) cells and purified by affinity chromatography with protein G.

More isotypes of this antibody are available and can be used for comparison of biological activities such as ADCC (see below or in the 'upon request' section). InvivoGen also provides type I and type II anti-hCD20 mAbs featuring the variable regions of Ofatumumab or Obinutuzumab, with either native or engineered Fc regions.

References:

1. Arnold J. et al., 2007. The impact of glycosylation on the biological function and structure of human immunoglobulins. Annu Rev Immunol 25:21-50.
2. Jefferis R., 2009. Glycosylation as a strategy to improve antibody-based therapeutics. Nat Rev Drug Discov. 8(3):226-34.