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ACS Chem Neurosci. 2014 Sep 17;5(9):749-51. doi: 10.1021/cn500171p. Epub 2014 Aug 11.

No gain, no pain: NaV1.7 as an analgesic target.

Author information

1
Institute for Molecular Bioscience, The University of Queensland , St Lucia, QLD 4072, Australia.

Abstract

Chronic pain is one of the most complex and difficult to manage clinical problems, with the therapeutic utility of current-generation analgesics restricted by problems such as dose-limiting side effects, tolerance, and the potential for addiction. The voltage-gated sodium channel NaV1.7 plays a key role in setting the threshold for action potential generation in primary sensory neurons, and humans that lack this channel are completely insensitive to pain. In this Viewpoint, we examine the potential of NaV1.7 as an analgesic target a well as the challenges involved in developing therapeutically useful subtype-selective inhibitors of this ion channel.

KEYWORDS:

Chronic pain; NaV1.7; analgesic; monoclonal antibody; nociceptor; sensory neuron

PMID:
25111714
DOI:
10.1021/cn500171p
[Indexed for MEDLINE]

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