TL1A

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Ligands
TL1A (Human)

GtoPdb Ligand ID: 5071

Synonyms: Tumor necrosis factor ligand superfamily member 15, membrane form

Compound class: Endogenous peptide in human, mouse or rat

Comment: TL1A occurs as both membrane‐bound and soluble forms. It principally functions as a negative modulator of epithelial cell proliferation.
Inhibiting the TL1A/death receptor 3 (TNFRSF25) pathway has been proposed as mechanism to treat inflammatory bowel disease [1]. In addition, TL1A has been associated with tumourigenesis and progression of some gastrointestinal malignancies [3,5,9], making it a target of interest for the development of novel anti-cancer drugs, and profibrotic processes.
TL1A is also an endogenous ligand for decoy receptor 3 (DcR3; TNFRSF6B).

Species: Human

No information available.

No information available.

Summary of Clinical Use
TL1A is being evaluated as a therapeutic target as a novel mechanism for ulcerative colitis treatment [8]. Afimkibart (RG6631; Roche, formerly RVT-3101 and PF-06480605) was the first-in-class TL1A blocking monoclonal antibody. It inhibits pro-inflammatory cytokine production by T cell subsets [1]. Other anti-TL1A clinical candidates include duvakitug (TEV-48574; Teva/Sanofi) and tulisokibart (PRA023, MK-7240; Prometheus Biosciences/Merck). As of March 2026 afimkibart, duvakitug and tulisokibart were all in phase 3 trials.

Summary of Clinical Use

TL1A is being evaluated as a therapeutic target as a novel mechanism for ulcerative colitis treatment [8]. Afimkibart (RG6631; Roche, formerly RVT-3101 and PF-06480605) was the first-in-class TL1A blocking monoclonal antibody. It inhibits pro-inflammatory cytokine production by T cell subsets [1]. Other anti-TL1A clinical candidates include duvakitug (TEV-48574; Teva/Sanofi) and tulisokibart (PRA023, MK-7240; Prometheus Biosciences/Merck). As of March 2026 afimkibart, duvakitug and tulisokibart were all in phase 3 trials.