One of the many breakthroughs to result from the extensive study of GPCR structure and function is the wide recognition that, in addition to the orthosteric site traditionally targeted by drug discovery programs, potentially all GPCRs contain topographically-distinct allosteric binding sites that can be targeted by novel therapeutic agents.1 Such ligands have the potential to elicit a more fine-tuned, highly selective response than their orthosteric counterparts, and are hence avidly pursued by drug discovery programs.
This project aims to elucidate the binding site of a subtype-selective, orally bioavailable allosteric ligand, BQCA,2 at the M1 muscarinic acetylcholine receptor (M1 mAChR); a CNS target of therapeutic interest for the treatment of the cognitive deficits associated with Alzheimer’s disease and schizophrenia.3 Ultimately, this will provide invaluable information for efficiently guiding rational drug design of optimised BQCA analogues as putative clinical candidates.
Four novel rationally-designed analogues of BQCA were synthesised; each containing different functionalities capable of reacting covalently with a nucleophilic amino acid residue of the target protein. These analogues were pharmacologically evaluated for the preservation of both allosteric binding and functional activation at M1 mAChR-expressing Chinese hamster ovary cells using radioligand binding and ERK1/2 phosphorylation assays. Saturation radioligand binding assays were employed to evaluate potential irreversible interaction.
The allosteric binding and functional properties of BQCA were preserved to varying extents in all four analogues. Data from saturation radioligand binding experiments with one analogue, MIPS1262, suggest that an irreversible interaction with the receptor has been successfully formed.
MIPS1262 will serve as a useful structural probe to identify the BQCA binding site; either by analyzing the ligand-receptor complex to determine the amino acid residue involved in the irreversible interaction, thereby informing computational modelling of the binding site, or, ideally, by co-crystallisation with the M1 mAChR.