No Gain, No Pain: NaV1.7 as an Analgesic Target | Zendy

Glenn F. King | Zendy; Irina Vetter | Zendy

AI Assistant Blog Pricing

Home ZAIA Blog

Open Access

No Gain, No Pain: Na_V1.7 as an Analgesic Target

Author(s) -

Glenn F. King,

Irina Vetter

Publication year - 2014

Publication title -

acs chemical neuroscience

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.158

H-Index - 69

ISSN - 1948-7193

DOI - 10.1021/cn500171p

Subject(s) - analgesic , sodium channel , limiting , addiction , ion channel , medicine , neuroscience , sensory system , pharmacology , analgesic agents , psychology , chemistry , sodium , receptor , mechanical engineering , organic chemistry , engineering

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.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research