Back

Discovery of first-in-class inhibitors of the TRF1-TIN2 protein-protein interaction by fragment screening

Casale, G.; Liu, M.; Le Bihan, Y.-V.; Inian, O.; Stammers, E.; Caldwell, J.; van Montfort, R. L. M.; Collins, I.; Guettler, S.

2025-02-16 biochemistry
10.1101/2025.02.14.638354 bioRxiv
Show abstract

TRF1 is a subunit of the shelterin complex that binds to and protects the linear ends of chromosomes known as telomeres. Both genetic deletion and chemical inhibition of TRF1 have been shown to block the growth of lung carcinoma, glioblastoma, and renal cell carcinoma in mice without affecting mouse survival or tissue function, making TRF1 a potential therapeutic target in cancer1-3. Here, we report the discovery of a series of fragment hits that bind at the interface between the TRFH domain of TRF1 (TRF1TRFH) and a peptide of TIN2 (TIN2TBM), an interaction essential for the recruitment of TRF1 to shelterin, using X-ray crystallography (XChem) and ligand-observed NMR (LO-NMR) fragment screening. We discovered a first-in-class inhibitor of the TRF1-TIN2 interaction (compound 40) that binds to TRF1TRFH with a KD of 29 M (95% CI: 20 - 41 M), displaces a TIN2 probe with an IC50 of 67 {+/-} 28 M, and expels TRF1 from purified shelterin. Aided by a novel crystal system of TRF1TRFH, we characterised fragments binding in a hotspot at the TRF1-TIN2 interface which will serve as a starting point for the structure-guided development of potent inhibitors of TRF1 protein-protein interactions to disrupt shelterin complex assembly.

Matching journals

The top 6 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.