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Discovery of a Selective, State-Independent Inhibitor of NaV1.7 by Modification of Guanidinium Toxins
[article]
2019
biorxiv/medrxiv
pre-print
The voltage-gated sodium channel isoform NaV1.7 is highly expressed in small diameter dorsal root ganglion neurons and is obligatory for nociceptive signal transmission. Genetic gain-of-function and loss-of-function NaV1.7 mutations have been identified in select individuals, and are associated with episodic extreme pain disorders and insensitivity to pain, respectively. These findings implicate NaV1.7 as a key pharmacotherapeutic target for the treatment of pain. While several small molecules
doi:10.1101/869206
fatcat:rib5avthjrbc7kxqi7bdeascpq