hSCN10A(Nav1.8)(SD) Rat

The SCN10A gene, which encodes the sodium channel Na(v)1.8, is a susceptibility factor for cardiac conduction block and severe ventricular arrhythmias. Genetic variations in ion channel genes are associated with hereditary arrhythmias, such as Long QT Syndrome, Short QT Syndrome, Brugada Syndrome (BrS), and conduction abnormalities. These variations are also linked to sudden unexplained death (SUD) in young adults and children. Several studies have identified common variants of SCN10A as potential regulators of human PR and QRS durations, with SCN10A being a major susceptibility gene for BrS ^[1-2]. The Nav1.8 protein is expressed in small-diameter sensory neurons of the trigeminal ganglion and dorsal root ganglion (DRG), as well as in some medium- and large-diameter neurons and in layers I and II of the spinal dorsal horn ^[3]. The SCN10A/Nav1.8 voltage-gated sodium channel is crucial in pain management. Studies have shown that Nav1.8 channel inhibitors have the potential to become a new class of effective analgesics suitable for multimodal pain treatment in postoperative patients. Additionally, the low expression of SCN10A in the brain suggests a lower likelihood of adverse effects, including dependency and abuse, within the central nervous system ^[4]. In early 2025, the FDA approved Suzetrigine, a Nav1.8 inhibitor developed by Vertex Pharmaceuticals, marking a breakthrough in the pain management field previously dominated by opioid drugs. As the first non-opioid acute pain medication in two decades, the success of Suzetrigine is a significant milestone.

hSCN10A(Nav1.8)(SD) rats are a Scn10a humanized model created by inserting the human SCN10A gene's coding sequence (CDS) and 3'UTR into the rat Scn10a gene. This model can be used for mechanistic studies of acute pain and diabetic peripheral neuropathic pain and the development, screening, and evaluation of analgesic drugs in preclinical research. During the production of this rat strain, scratching behavior was observed after weaning and cage separation, resulting in skin lesions. Trimming the nails at the time of cage separation effectively prevents such skin damage. For long-term prevention, nail trimming should be repeated every 2 weeks.