Target intelligence / Profile preview

Sodium channel protein type 7 subunit alpha (NaV1.7) (NaV1.7)

Target
NaV1.7
Molecular classification
Ion channel, Voltage-gated sodium channel
01

Overview

Sodium channel protein type 7 subunit alpha (NaV1.7) is a voltage-gated sodium channel predominantly expressed in peripheral neurons, including those in the dental pulp. It plays a central role in the initiation and propagation of action potentials, especially in nociceptors, and is implicated in the pathophysiology of pain, hyperalgesia, and pulpitis. Changes in expression or function of NaV1.7, as well as NaV1.8, drive pain hypersensitivity following injury or inflammation. These channels represent validated therapeutic targets for managing dental pain and related neuropathic pain conditions. Selective inhibitors are in development, aiming to block painful signaling while minimizing systemic effects.

Other names
SCN9ASodium channel Nav1.7Voltage-gated sodium channel type IX alpha subunit
02

Mechanism of action

Inhibition of sodium influx, which suppresses action potential propagation and neuronal excitability; Blockade can reduce or eliminate pain signaling from pulp tissue

03

Biological functions

Action potential generationSensory neuron excitabilityPain transduction
04

Disease associations

Inflammation (especially pulpitis)Neuropathic painPain hypersensitivity
05

Safety considerations

Broad sodium channel blockade may cause unwanted systemic effects (e.g., numbness, motor impairment)Target specificity is critical to avoid CNS side effects
06

Interacting drugs

Tetrodotoxin (inhibits some VGSCs, but NaV1.7 is tetrodotoxin-sensitive; NaV1.8 is resistant)

2 more in the full profile.

07

Biomarkers

NaV1.7 and NaV1.8 immunoreactivity in dental pulp tissue (distinguishing painful from non-painful pulpitis)

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