Development of G Protein-Coupled Receptor 183 Benzimidazole Antagonists Utilizing a Core-Hopping Approach
G protein-coupled receptor 183 (GPR183, EBI2) has emerged as a promising therapeutic target for neuropathic pain due to its role in neuroinflammatory signaling. Previously, our group identified SAE-14 as a potent GPR183 antagonist and lead scaffold for analgesic development. To further explore the structural requirements for receptor antagonism, a ligand-based core-hopping strategy was employed to identify novel chemotypes derived from SAE-14. Virtual screening identified a trisubstituted benzimidazole scaffold as a promising candidate for further investigation. A focused series of benzimidazole analogs was synthesized and evaluated for inhibition of 7α,25-dihydroxycholesterol (7α,25-OHC)-induced GPR183 activation using calcium mobilization assays. Several compounds exhibited potent antagonistic activity, with four analogs demonstrating comparable potency relative to SAE-14. The most active compounds displayed IC50 values of 15.7, 15.8, 18.0, and 19.3 nM. Structure–activity relationship studies revealed that both electron-rich aromatic substituents and heteroaromatic moieties were well tolerated within the benzimidazole scaffold. These findings identify benzimidazole as a novel scaffold for GPR183 antagonism, expand the chemical space surrounding GPR183 inhibitors, and provide a foundation for future lead optimization efforts.
Authors
- Vanja Kalajdzic
- Israel Olayide (ORCID: https://orcid.org/0009-0002-0082-1522)
- Christopher Kent Arnatt (ORCID: https://orcid.org/0000-0002-9445-4796)
- Daniela Salvemini (ORCID: https://orcid.org/0000-0002-0612-4448)
- Angelina Ellis (ORCID: https://orcid.org/0009-0005-4225-9306)
Institutions
- Saint Louis University (US)
Publication Details
- Journal
- Molecules
- Published
- 2026-09-29
- DOI
- https://doi.org/10.3390/molecules31193469
- Primary Topic
- Receptor Mechanisms and Signaling
- Type
- article
- Field-Weighted Citation Impact
- 0.00