Our Science

The rationale for targeting Nav1.7: 

•  Nav1.7 controls the passage of sodium ions into sensory neurons.  Hyperactivity in Nav1.7 is associated with increased firing in pain-sensing neurons—and thus agony even in the absence of painful stimuli—while deletion of the channel appears to cause pain insensitivity. (The Scientist Magazine)

•  Nav1.7, a major sodium receptor in the nociceptive system, is not located in the brain, thus preventing any side effects associated with depression of CNS excitability.  (Zakrzewska et al; Trials. 2013;23(14):402.)

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Nav1.7 repressors are designed to bind to the DNA promoter region of the SCN9A gene, which encodes the Nav1.7 channel protein, and prevent its transcription into mRNA.

The Nav1.7 repressors work at the DNA level by binding to specific sequences in the promoter region of the SCN9A gene, thereby preventing the recruitment of RNA polymerase and other transcription factors that are necessary for transcription to occur. As a result, the Nav1.7 channel protein is not produced, and the transmission of pain signals through this ion channel is reduced.

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We are developing a treatment to suppress the Nav1.7 channel incorporating novel delivery platforms. Such a treatment, when it is realized, will allow for the commercialization of a first-in-class product to address systemic pain, including neuropathic and lower back pain.