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Related Experiment Video

Updated: May 18, 2026

Determination of the Relative Potency of an Anti-TNF Monoclonal Antibody (mAb) by Neutralizing TNF Using an In Vitro Bioanalytical Method
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Determination of the Relative Potency of an Anti-TNF Monoclonal Antibody (mAb) by Neutralizing TNF Using an In Vitro Bioanalytical Method

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Tumor necrosis factors blocking agents: analogies and differences.

Maurizio Benucci1, Gianantonio Saviola, Mariangela Manfredi

  • 1Rheumatology Unit, Department of Internal Medicine, Hospital di S. Giovanni di Dio, Azienda Sanitaria di Firenze, Italy. maubenucci@tiscali.it

Acta Bio-Medica : Atenei Parmensis
|September 18, 2012
PubMed
Summary

Five anti-tumor necrosis factor (TNF) agents for rheumatoid arthritis (RA) show varied effects on TNF-alpha-producing cells. Understanding these differences in transmembrane TNF-alpha interactions is key to explaining their distinct clinical efficacy.

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In Vitro Methods for Comparing Target Binding and CDC Induction Between Therapeutic Antibodies: Applications in Biosimilarity Analysis

Published on: May 4, 2017

Area of Science:

  • Immunology
  • Pharmacology
  • Rheumatology

Background:

  • Five anti-tumor necrosis factor (TNF) agents are approved for rheumatoid arthritis (RA).
  • These agents neutralize soluble TNF-alpha but have differential effects on transmembrane TNF-alpha-expressing cells.
  • Variations in affinity, avidity, and cellular effects like apoptosis and cytotoxicity exist among these agents.

Purpose of the Study:

  • To review the biological interactions between transmembrane TNF-alpha and anti-TNF agents.
  • To elucidate the basis for differential clinical efficacy among approved anti-TNF therapies for RA.

Main Methods:

  • Comparative analysis of anti-TNF agent properties.
  • Review of studies detailing cellular effects (apoptosis, CDC, ACDC) and gene expression changes.
  • Examination of affinity and avidity differences for soluble and transmembrane TNF-alpha.

Main Results:

  • Anti-TNF agents exhibit distinct binding affinities and avidities for soluble and transmembrane TNF-alpha.
  • Differential effects on cell apoptosis, complement-dependent cytotoxicity (CDC), and antibody-dependent cell-mediated cytotoxicity (ACDC) were observed.
  • Significant gene expression alterations were noted across all evaluated anti-TNF agents.

Conclusions:

  • The interaction of anti-TNF agents with transmembrane TNF-alpha is a critical factor in their therapeutic effects.
  • Understanding these molecular and cellular differences can explain the varying clinical outcomes in RA patients treated with these agents.