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Related Experiment Video

Updated: Jun 26, 2026

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

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

Published on: September 16, 2017

Differences in binding and effector functions between classes of TNF antagonists.

Taruna Arora¹, Rupa Padaki, Ling Liu

¹Amgen Inc., One Amgen Center Drive, Thousand Oaks, CA 91320-1799, USA. tarora@amgen.com

|January 9, 2009

Summary

This summary is machine-generated.

Anti-tumor necrosis factor-alpha (TNF-alpha) monoclonal antibodies (mAbs) show greater binding to Fc receptors and mediate more potent cell death than etanercept, potentially explaining clinical differences.

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An ELISA Based Binding and Competition Method to Rapidly Determine Ligand-receptor Interactions

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Last Updated: Jun 26, 2026

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

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

Published on: September 16, 2017

An ELISA Based Binding and Competition Method to Rapidly Determine Ligand-receptor Interactions

An ELISA Based Binding and Competition Method to Rapidly Determine Ligand-receptor Interactions

Published on: March 14, 2016

Area of Science:

Immunology
Pharmacology
Biochemistry

Background:

Two main classes of Food and Drug Administration-approved biologic agents target tumor necrosis factor-alpha (TNF-alpha): anti-TNF monoclonal antibodies (mAbs) and soluble TNF receptors.
Adalimumab and infliximab are anti-TNF mAbs, while etanercept is a soluble TNF receptor.

Purpose of the Study:

To investigate the binding capabilities of TNF antagonists to Fc receptors (FcgammaRs) and C1q.
To evaluate the in vitro efficacy of TNF antagonists in mediating Ab-dependent cellular cytotoxicity (ADCC) and complement-mediated cytotoxicity (CDC) against cells expressing membrane-bound TNF (mTNF).

Main Methods:

In vitro assessment of TNF antagonist binding to FcgammaRs (FcgammaRI, FcgammaRIIa, FcgammaRIIIa, FcgammaRIIb) and C1q.
Measurement of ADCC and CDC induced by TNF antagonists against mTNF-expressing cells.

Main Results:

Both anti-TNF mAbs and etanercept exhibited low-level binding to FcgammaRs without exogenous TNF.
Upon TNF addition, mAbs demonstrated significantly increased FcgammaR binding, particularly to FcgammaRII and FcgammaRIII, whereas etanercept did not.
Infliximab and adalimumab induced significantly higher levels of ADCC and CDC compared to etanercept in the presence of TNF.
mAbs bound C1q in the presence of TNF, but etanercept did not bind C1q under any tested conditions.

Conclusions:

Differences in FcgammaR and C1q binding may contribute to the varying clinical efficacy and safety profiles of TNF antagonists.
Anti-TNF mAbs exhibit superior Fc-mediated effector functions (ADCC and CDC) compared to etanercept.
The interaction of TNF antagonists with Fc receptors and complement system components is crucial for their cytotoxic activity.