The SCN9A gene encodes the Nav1.7 sodium channel protein, which is primarily expressed in the sensory and sympathetic nerves of the peripheral nervous system and is highly expressed in the dorsal root ganglia. Nav1.7 sodium channels play a crucial role in transmitting positively charged sodium ions within cells, which are essential for generating and transmitting electrical signals. When a person experiences pain, this protein releases sodium ion currents that amplify and stimulate nerve cells, sending electrical signals to the brain, thereby causing the sensation of pain. The SCN9A gene guides the entry of sodium ions into cells and facilitates communication between neurons. Mutations in the SCN9A gene can alter the function of sodium channels in the brain, disrupting neuronal communication and leading to various pain, olfactory, and neurological disorders such as erythromelalgia, paroxysmal extreme pain disorder, Dravet syndrome, small fiber neuropathy, and congenital insensitivity to pain. The abnormal protein function and symptoms resulting from gene mutations are directly related to the severity of the mutations, and different mutation types may lead to completely different conditions.

SCN9A is an excellent target for analgesic drug development. Downregulation of SCN9A expression can alleviate acute pain as well as certain types of inflammatory and neuropathic pain ^[1]. OliPass Corporation, a South Korean biotechnology company, has developed an antisense peptide nucleic acid (PNA) analgesic targeting SCN9A (OLP-1002), which has entered Phase 2a clinical trials. Antisense PNA is an artificially synthesized DNA/RNA mimic that inhibits RNA/DNA transcription and translation by complementary pairing with RNA/DNA sequences. The drug has shown strong analgesic effects and prolonged therapeutic duration in Australian patients with moderate to severe chronic osteoarthritis pain. It is estimated that due to its potent efficacy, excellent safety profile, and broad therapeutic scope, OLP-1002 could generate over $50 billion in market potential annually ^[2-4].

The B6-hSCN9A mouse is a mouse Scn9a humanized model, generated by replacing the mouse Scn9a gene (including the 5' UTR and 3' UTR) with the corresponding human SCN9A gene sequence using gene editing technology. Internal research revealed that during the generation of B6-hSCN9A mice, the murine Scn9a gene was inserted unexpectedly, and its precise genomic insertion site remains undetermined*. This strain is suitable for studying the pathogenic mechanisms of neurological diseases such as erythromelalgia, Dravet syndrome, small fiber neuropathy, and congenital insensitivity to pain, as well as for screening analgesic drug candidates. In addition, based on the independently developed TurboKnockout fusion BAC recombination technology, Cyagen can also provide customized services.