Special Issue "Animal Toxins Targeting Ion Channels Involved in Pain"
Deadline for manuscript submissions: closed (30 June 2012)
Prof. Dr. Glenn F. King
Division of Chemistry & Structural Biology, Institute for Molecular Bioscience, The University of Queensland, St. Lucia, QLD 4072, Australia
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Fax: +61 7 3346-2101
Interests: venoms-based drug discovery; venoms-based insecticide discovery; venom evolution; ion channel blockers; acid-sensing ion channels; voltage-gated sodium channels; chronic pain; stroke; NMR structural biology
Normal pain is a key adaptive response that serves to limit our exposure to potentially damaging or life-threatening events. In contrast, aberrant long-lasting pain transforms this adaptive response into a debilitating and often poorly managed disease. In 2007, global sales of pain medications totalled $34 billion, highlighting the pervasive nature of this medical condition. Unfortunately, very few drugs are available for the treatment of chronic pain, and most of these have limited efficacy and undesirable side-effects.
A variety of ion channels and receptors are involved sensing pain, including voltage-gated sodium (NaV) channels, voltage-gated calcium (CaV) channels, transient receptor potential (TRP) channels, acid-sensing ion channels (ASICs), and GABAB, P2X, and nicotinic acetylcholine (nAChR) receptors. In many cases, peptides derived from animal venoms are the most potent and selective modulators of these channels and receptors. As a result, venom peptides have been used extensively for characterizing these channels and receptors, and for their validation as analgesic targets. Moreover, some of these venom peptides are being developed as therapeutics. One venom peptide (Prialt®) has been approved by the FDA for the treatment of chronic pain, while several others are undergoing clinical trials (Xen2174 and CBSB004) or are in various stages of preclinical development. The aim of this special edition of Toxins is to review the potential of venom-derived peptides as leads for the development of novel analgesics.
Articles for this special edition are by invitation only. Authors wishing to submit an article to the special edition should submit a synopsis of no more than 250 words to either of the guest editors for consideration. The article must be aligned with the topic and preference will be given to toxins with potential as therapeutics or as leads for therapeutic development, or toxins that have facilitated the validation of novel analgesic targets.
Prof. Glenn King
Dr. Lachlan Rash
- chronic pain
- cone snail
- inflammatory pain
- neuropathic pain