title: No gain, no pain: NaV1.7 as an analgesic target.
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.
authors.affiliation: Institute for Molecular Bioscience, The University of Queensland , St Lucia, QLD 4072, Australia.
authors.forename: Glenn F
authors.initials: GF
authors.lastname: King
authors.forename: Irina
authors.initials: I
authors.lastname: Vetter
mesh_terms: D000700:Analgesics / Q000494:pharmacology / Q000627:therapeutic use*; D000818:Animals; D006801:Humans; D062556:NAV1.7 Voltage-Gated Sodium Channel / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D010146:Pain / Q000188:drug therapy* / Q000235:genetics; D011984:Sensory Receptor Cells / Q000187:drug effects; D026941:Sodium Channel Blockers / Q000494:pharmacology / Q000627:therapeutic use
chemical_list: D000700:Analgesics; D062556:NAV1.7 Voltage-Gated Sodium Channel; C486866:SCN9A protein, human; D026941:Sodium Channel Blockers
keywords: Chronic pain; NaV1.7; analgesic; monoclonal antibody; nociceptor; sensory neuron