SCN10A

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SCN10A

A gene on chromosome 3p22.2 that encodes a voltage-gated sodium ion channel, which is an integral membrane glycoprotein. It is responsible for the initial rising phase of the action potential in most excitable cells.
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Selective NaV1.8 Inhibitors for the Treatment of Pain: Data are expected in the first half of 2019 from a Phase 2b dose-ranging study evaluating the NaV1.8 inhibitor VX-150 using an oral formulation in patients with acute pain following bunionectomy surgery.
Vertex Pharmaceuticals Incorporated announced positive results of a Phase 2 study of the investigational NaV1.8 inhibitor VX-150 in patients with pain caused by small fiber neuropathy.
Two types of VGSCs, Nav1.7 and Nav1.8, are known to contribute to pain transduction in nociceptive neurons [21, 22].
Xia, "Nav1.7 and Nav1.8: diabetes-induced changes in primary sensory neurons in rats," Journal of Neurogastroenterology and Motility, vol.
Furthermore, the expression levels of the nociceptive channels Nav1.7 and Nav1.8 increased in chronic pain in mice (Figures 2(c) and 2(d), 135.86 [+ or -] 12.99% and 139.16 [+ or -] 16.03%, n = 8), which were reduced by EA and TRPV1 deletions but not in the sham treated group (Figures 2(c) and 2(d), n = 8).
Su et al., "Electroacupuncture reduces carrageenan- and CFA-induced inflammatory pain accompanied by changing the expression of Nav1.7 and Nav1.8, rather than Nav1.9, in mice dorsal root ganglia," Evidence-Based Complementary and Alternative Medicine, vol.
By use of a patch clamp, we evaluated the effects of menthol application on tetrodotoxin (TTX)-resistant Nav1.8 and Nav1.9 channel subtypes in DRG neurons, and on TTX-sensitive Na() channels in immortalized DRG neuron-derived F11 cells.
[16] Similar results were obtained in another study performed in relation to the Nav1.8 immunoexpression.
The specific isoforms Nav1.8 and Nav1.9 play a key role in the generation and maintenance of inflammatory pain.
A large variety of Nav subtypes from DRG cells, including tetrodotoxin- (TTX-) sensitive channels Nav1.1, Nav1.2, Nav1.6, and Nav1.7 and TTX-resistant channels Nav1.8 and Nav1.9, have been evaluated for involvement in epilepsy [35, 36].
Hyperexcited ectopic impulses are generated by the expression of various voltage-gated sodium channels, such as Nav1.3, Nav1.7, and Nav1.8 [20].