2021/01/01 by Robert A. Neff, Alan D. Wickenden · 1 citation
Biochemistry, Genetics and Molecular Biology · #Venomous Animal Envenomation and Studies #Ion channel regulation and function #Nicotinic Acetylcholine Receptors Study
paper · pdf · doi:10.1080/19336950.2020.1860382
openalex publication_date 2021/01/01 · openalex created_date 2025/10/10 · openalex updated_date 2026/07/29
A fundamental mechanism that drives the propagation of electrical signals in the nervous system is the activation of voltage-gated sodium channels. The sodium channel subtype Nav1.7 is critical for the transmission of pain-related signaling, with gain-of-function mutations in Nav1.7 resulting in various painful pathologies. Loss-of-function mutations cause complete insensitivity to pain and anosmia in humans that otherwise have normal nervous system function, rendering Nav1.7 an attractive target for the treatment of pain. Despite this, no Nav1.7 selective therapeutic has been approved for use as an analgesic to date. Here we present a summary of research that has focused on engineering peptides found in spider venoms to produce Nav1.7 selective antagonists. We discuss the progress that has been made on various scaffolds from different venom families and highlight the challenges that remain in the effort to produce a Nav1.7 selective, venom-based analgesic.