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Nav1.9 (SCN11A)

Gene sequencing, cell culture and mouse studies suggest antagonizing Nav1.9 could help treat congenital analgesia. Sequencing of patients identified a missense gain-of-function mutation in SCN11A, which encodes the voltage-gated sodium ion channel Nav1.9. In a dorsal root ganglion neuronal cell line, expression of mutant Nav1.9 decreased the depolarization required to activate or inactivate voltage-dependent sodium currents compared with wild-type Nav1.9 expression. In heterozygous knock-in mice expressing the mutant Scn11a allele, thermal and mechanical stimuli produced fewer pain responses and less protective activity than what was seen in mice expressing wild-type Scn11a. Next steps include testing Nav1.9 inhibitors in congenital analgesia and testing whether compounds mimicking mutant channel behavior could help suppress pain.

SciBX 6(41); doi:10.1038/scibx.2013.1166
Published online Oct. 24, 2013

Patent application filed; available for licensing

Leipold, E. et al. Nat. Genet.; published online Sept. 15, 2013;
Contact: Ingo Kurth, Institute of Human Genetics, Jena University Hospital, Jena, Germany