Multicomponent Stapling of Glucagon‐Like Peptide‐1 Enables Receptor‐Guided PROTAC Delivery
Achieving cell-selective targeted protein degradation remains a major challenge for translating proteolysis-targeting chimeras (PROTACs) into therapeutics. Although pancreatic β-cells are well vascularised and readily accessible to circulating peptides, selective receptor-mediated drug delivery remains challenging. Here, we exploit the glucagon-like peptide-1 receptor (GLP-1R) as a β-cell-specific entry route and report, for the first time, a multicomponent stapled glucagon-like peptide-1 (GLP-1) analogue constructed by tryptophan-mediated multicomponent Petasis reaction (TMPR). This modular stapling strategy affords a conformationally stabilised GLP-1 peptide bearing a chemically orthogonal handle for late-stage conjugation, displaying markedly enhanced α-helicity and improved receptor potency, compared with the wild-type peptide. Linking this improved analogue to a bromodomain-containing protein 4 (BRD4)-directed degrader furnishes the first GLP-1-guided PROTAC, which retains GLP-1R agonism and induces selective BRD4 degradation in GLP-1R-positive cells, consistent with receptor-guided uptake and intracellular activation of the degrader payload. Together, these results provide strong proof-of-concept evidence that a TMPR-stapled GLP-1 peptide can serve as a β-cell-directed delivery platform for receptor-defined protein degradation.
Authors
- Soňa Krajčovičová (ORCID: https://orcid.org/0000-0003-0139-2360)
- David R. Spring (ORCID: https://orcid.org/0000-0001-7355-2824)
- Graeme Davies
- H M Bolt
- Jan L. Venne
- Jefferson Revell
Institutions
- University of Cambridge (GB)
- The Francis Crick Institute (GB)
- Palacký University Olomouc (CZ)
Publication Details
- Journal
- Angewandte Chemie International Edition
- Published
- 2026-06-12
- DOI
- https://doi.org/10.1002/anie.9595531
- Primary Topic
- Protein Degradation and Inhibitors
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- Grantová Agentura České Republiky
- Medical Research Council