# GB20-5A8-31, an anti-TL1A antibody for treating inflammatory bowel disease

## TL;DR

A new antibody, GB20-5A8-31, shows strong potential for treating inflammatory bowel disease by targeting TL1A with high affinity and effectiveness.

## Contribution

GB20-5A8-31 is a novel anti-TL1A antibody with ultra-high affinity, potent anti-inflammatory effects, and favorable biophysical properties for IBD treatment.

## Key findings

- GB20-5A8-31 has ultra-high affinity (KD = 5.11×10–11 M) for human TL1A and inhibits TL1A signaling effectively.
- The antibody shows potent anti-inflammatory and anti-fibrotic effects in rat and mouse IBD models.
- GB20-5A8-31 has an extended half-life (T1/2 = 248.54 h) and favorable properties for high-concentration formulations.

## Abstract

Inflammatory bowel disease (IBD) remains a critical unmet medical challenge, with a substantial number of patients experiencing ineffective treatment or therapeutic failure over time. Here, GB20-5A8-31, a novel anti-TNF-like ligand 1A (TL1A) antibody, was engineered for high potency and superior developability. GB20-5A8–31 exhibited ultra-high affinity (KD = 5.11×10–11 M) for human TL1A, potent inhibition of TL1A signaling in vitro. Meanwhile, GB20-5A8–31 demonstrated potent anti-inflammatory effects and anti-fibrotic tendencies in both the 2,4,6-trinitro-benzenesulfonic acid-induced rat and dextran sulfate-induced hTLIA-transgenic mouse acute IBD models. Its favorable pharmacokinetic profile, including an extended half-life (T1/2 = 248.54 h) in hFcRn-transgenic Sprague-Dawley rats, supports sustained target engagement. Crucially, GB20-5A8–31 exhibits advantageous biophysical properties—including high stability, solubility, and low aggregation—which facilitate the development of high-concentration formulations aimed at improving patient compliance. In summary, these findings indicate that GB20-5A8–31 is a therapeutic candidate for IBD with promising preclinical efficacy and the potential to advance to the Chemistry, Manufacturing and Controls research.