The NaV1.8-Collapsin Response Mediator Protein 5 Interaction Regulates NaV1.8 Membrane Localization and Nociception

Nociceptor action potential firing is a tightly balanced mechanism whose dysregulation contributes to chronic pain. During the establishment of persistent pain, increased function of the voltage gated sodium channels NaV1.7 and NaV1.8 led to facilitated or spontaneous activity in sensory neurons. While pharmacological inhibition of NaV1.7 is becoming encumbered with unwanted effects including hypotension, the selective drug candidate VX548 targeting NaV1.8 recently yielded positive results in two phase 2 clinical trials for acute pain after abdominoplasty or bunionectomy without important side effects.
Source: The Journal of Pain - Category: Materials Science Authors: Source Type: research