Medication Class Introduction

Anti-tumor necrosis factor (TNF) medications are a class of biologics introduced in the 1990s that are used in the treatment of inflammatory bowel disease (IBD) in appropriate patients.¹ They are monoclonal antibodies that target and inhibit the TNF-α cytokine, a protein involved in the gastrointestinal tract inflammatory process.² TNF-α plays a key role in the immune response and pathogenesis of IBD.

Biosimilars are monoclonal antibodies that have highly similar clinical characteristics to an FDA-approved reference product.³ There are anti-TNF biosimilars available on the US market.

IBD Treatment Landscape^1,4–13

JAK=Janus kinase; S1P=sphingosine-1-phosphate; TNF=tumor necrosis factor.

Role in IBD Pathogenesis

TNF-α levels may be elevated in patients with IBD.² TNF-α binds to 2 types of receptors: TNF receptor 1 (TNFR1) and TNF receptor 2 (TNFR2).^2,14 Once bound to these receptors, TNF-α activates intracellular signaling pathways, inducing expression of pro-inflammatory cytokines. Increased production of these pro-inflammatory cytokines is associated with the inflammatory response that occurs in IBD.²

DNA=deoxyribonucleic acid; TNF-α=tumor necrosis factor alpha; TNFR1/2=tumor necrosis factor receptor 1 or 2.

Mechanism of Action in IBD

Anti-TNF medications are monoclonal antibodies that bind to TNF-α and prevent binding to TNFR1 and TNFR2, which inhibits activation of intracellular signaling pathways.^2,14,15 This results in decreased levels of the pro-inflammatory cytokines that cause inflammation in the intestines in patients with IBD.^2,14,15

DNA=deoxyribonucleic acid; TNF-α=tumor necrosis factor alpha; TNFR1/2=tumor necrosis factor receptor 1 or 2.