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Updated: Mar 13, 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

Anti-TNF Therapy.

Irina Udalova¹, Claudia Monaco¹, Jagdeep Nanchahal¹

¹Kennedy Institute of Rheumatology, NDORMS, University of Oxford, Botnar Research Centre, Headington, Oxford OX3 7LD, United Kingdom.

Microbiology Spectrum

|October 12, 2016

Summary

This summary is machine-generated.

Tumor necrosis factor (TNF) is a key cytokine in host defense, but prolonged production is linked to inflammatory diseases like rheumatoid arthritis. Anti-TNF therapies offer benefits but have limitations, with potential applications in other conditions.

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Area of Science:

Immunology
Cytokine Biology
Inflammatory Diseases

Background:

Tumor necrosis factor (TNF) is a critical cytokine produced by macrophages, essential for host defense.
Rapid release of TNF occurs after injury, but sustained production is associated with chronic inflammatory conditions.
The role of TNF in diseases such as rheumatoid arthritis, Crohn's disease, and psoriasis is well-established.

Purpose of the Study:

To review the discovery and development of anti-TNF therapies.
To discuss the benefits and limitations of current anti-TNF treatments.
To explore the potential of anti-TNF therapy in non-inflammatory diseases and novel strategies for TNF synthesis inhibition.

Main Methods:

Literature review of anti-TNF therapy discovery.
Analysis of clinical benefits and limitations of anti-TNF treatments.
Discussion of emerging applications and therapeutic targets for TNF modulation.

Main Results:

Anti-TNF therapies have demonstrated significant efficacy in treating chronic inflammatory diseases.
Limitations of anti-TNF therapy include potential side effects and incomplete response in some patients.
Emerging research suggests potential benefits in cardiovascular diseases and fibrosis, alongside strategies to block TNF synthesis.

Conclusions:

Anti-TNF therapy represents a major advancement in managing inflammatory diseases.
Further research is needed to optimize anti-TNF treatments and expand their therapeutic scope.
Targeting TNF synthesis offers a promising avenue for future therapeutic interventions.