Poster Presentation 11th Australian Peptide Conference 2015

Comparison of structural conformation and stability of native and mutated ω-conotoxins (#178)

David Armstrong 1 2 , Andreas Brust 2 , Richard J Lewis 2 , K. Johan Rosengren 1
  1. School of Biomedical Sciences, The University of Queensland, Brisbane, QLD, Australia
  2. Institute for Molecular Biosciences , The University of Queensland, Brisbane, QLD, Australia

The University of Queensland, 1School of Biomedical Sciences and 2Institute for Molecular Bioscience, Brisbane, QLD 4072, Australia.

The disulphide-rich peptide toxins found in the venom of cone snails, referred to as conotoxins, have a well known potential as drug leads in neuropharmacology due to their selectivity and potency for a wide range of voltage and ligand gated ion-channels and other membrane receptors.

The ω-conotoxin family is of pharmacological interest due to their inhibition of the neuronal (N)-type voltage gated calcium channels (VGCCs) that are involved in nociception. The activity and selectivity for subtypes of VGCCs varies between different members of the ω-family. The recently discovered CVIF and CVIE ω-conotoxins are of particular interest due to exhibiting reversible block of N-type VGCCs.[1]

To aid the drug development process an understanding of the structure activity relationships of ω-conotoxins is critical. Here we have resolved the NMR structures of CVIE and CVIF and revisited the structures of several other native or mutated ω-conotoxins. Using both homonuclear and heteronuclear NMR data recorded at natural abundance to achieve high-resolution structures we are able to assess and compare structural conformation and flexibility in detail. The differences in key structural characteristics of ω-conotoxins can be analysed in conjunction with pharmacological activities to develop comprehensive structural activity relationships to guide the design of future analogues.

  1. Berecki, G., et al., Analgesic ω-conotoxins CVIE and CVIF selectively and voltage-dependently block recombinant and native N-type calcium channels. Molecular pharmacology, 2010. 77(2): p. 139-148.