Backbone cyclization turns a venom peptide into a stable and equipotent ligand at both muscle and neuronal nicotinic receptors

Journal Publication ResearchOnline@JCU
Giribaldi, Julien;Haufe, Yves;Evans, Evans R.J.;Amar, Muriel;Durner, Anna;Schmidt, Casey;Faucherre, Adèle;Moha Ou Maati, Hamid;Enjalbal, Christine;Molgó, Jordi;Servent, Denis;Wilson, David T.;Daly, Norelle L.;Nicke, Annette
Abstract

Venom peptides are promising drug leads, but their therapeutic use is often limited by stability and bioavailability issues. In this study, we designed cyclic analogues of α-conotoxin CIA, a potent muscle nicotinic acetylcholine receptor (nAChR) blocker with a significantly lower affinity at the neuronal α3β2 subtype. Remarkably, all analogues retained the low nanomolar activity of native CIA toward muscle-type nAChRs but showed greatly improved resistance to degradation in human serum and, surprisingly, displayed up to 52-fold higher potency for the α3β2 neuronal nAChR subtype (IC50 1.3 nM). Comparison of nuclear magnetic resonance-derived structures revealed some differences that might explain the gain of potency at α3β2 nAChRs. All peptides were highly paralytic when injected into adult zebrafish and bath-applied to zebrafish larvae, suggesting barrier-crossing capabilities and efficient uptake. Finally, these cyclic CIA analogues were shown to be unique pharmacological tools to investigate the contribution of the presynaptic α3β2 nAChR subtype to the train-of-four fade.

Journal

Journal of Medicinal Chemistry

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Volume

63

ISBN/ISSN

1520-4804

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Issue

21

Pages Count

11

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Publisher

American Chemical Society

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EISSN

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DOI

10.1021/acs.jmedchem.0c00957