{"id":2111,"date":"2025-09-17T15:50:09","date_gmt":"2025-09-17T15:50:09","guid":{"rendered":"https:\/\/blogs.bmj.com\/jmg\/?p=2111"},"modified":"2026-02-22T00:49:37","modified_gmt":"2026-02-22T00:49:37","slug":"six-at-sixty-no-gain-no-pain-medical-genetics-taking-nav1-7-from-target-to-pharmacy","status":"publish","type":"post","link":"https:\/\/blogs.bmj.com\/jmg\/2025\/09\/17\/six-at-sixty-no-gain-no-pain-medical-genetics-taking-nav1-7-from-target-to-pharmacy\/","title":{"rendered":"Six at Sixty. \u2018No gain, no pain\u2019: medical genetics taking Nav1.7 from target to pharmacy (Contributed by Pu Xia)"},"content":{"rendered":"<p>Chronic pain affects millions, but opioid painkillers bring addiction, tolerance and fatal breathing risks. The voltage-gated sodium channel Nav1.7, encoded by <em>SCN9A<\/em>, is key in pain signaling. 2004 research linked its gain-of-function mutations to primary erythromelalgia, and 2006 work connected loss-of-function mutations to congenital insensitivity to pain, making it a therapeutic target. Though Nav1.7 inhibitor development faced challenges, 2025\u2019s FDA approval of Nav1.8 inhibitor suzetrigine, a milestone in non-opioid analgesia, showing genetics&#8217; role in advancing medicine. (<a href=\"https:\/\/jmg.bmj.com\/content\/early\/2025\/09\/11\/jmg-2025-111174\">https:\/\/jmg.bmj.com\/content\/early\/2025\/09\/11\/jmg-2025-111174<\/a> )<\/p>\n<p><a href=\"https:\/\/blogs.bmj.com\/jmg\/2025\/09\/17\/six-at-sixty-no-gain-no-pain-medical-genetics-taking-nav1-7-from-target-to-pharmacy\/group-photo-2\/\" rel=\"attachment wp-att-2112\"><img loading=\"lazy\" decoding=\"async\" class=\"alignnone size-medium wp-image-2112\" src=\"https:\/\/blogs.bmj.com\/jmg\/files\/2025\/09\/group-photo-300x152.jpg\" alt=\"\" width=\"300\" height=\"152\" srcset=\"https:\/\/blogs.bmj.com\/jmg\/files\/2025\/09\/group-photo-300x152.jpg 300w, https:\/\/blogs.bmj.com\/jmg\/files\/2025\/09\/group-photo-1024x518.jpg 1024w, https:\/\/blogs.bmj.com\/jmg\/files\/2025\/09\/group-photo-768x389.jpg 768w, https:\/\/blogs.bmj.com\/jmg\/files\/2025\/09\/group-photo-1536x777.jpg 1536w, https:\/\/blogs.bmj.com\/jmg\/files\/2025\/09\/group-photo-2048x1036.jpg 2048w, https:\/\/blogs.bmj.com\/jmg\/files\/2025\/09\/group-photo-640x324.jpg 640w\" sizes=\"auto, (max-width: 300px) 100vw, 300px\" \/><\/a><\/p>\n<p>Group Photo of the Genetic Skin Disease Center, Jiangsu Key Laboratory of Molecular Biology for Skin Diseases and STIs<!--TrendMD v2.4.8--><\/p>\n","protected":false},"excerpt":{"rendered":"<p>Chronic pain affects millions, but opioid painkillers bring addiction, tolerance and fatal breathing risks. The voltage-gated sodium channel Nav1.7, encoded by SCN9A, is key in pain signaling. 2004 research linked its gain-of-function mutations to primary erythromelalgia, and 2006 work connected loss-of-function mutations to congenital insensitivity to pain, making it a therapeutic target. Though Nav1.7 inhibitor [&#8230;]<\/p>\n<p><a class=\"btn btn-secondary understrap-read-more-link\" href=\"https:\/\/blogs.bmj.com\/jmg\/2025\/09\/17\/six-at-sixty-no-gain-no-pain-medical-genetics-taking-nav1-7-from-target-to-pharmacy\/\">Read More&#8230;<\/a><\/p>\n","protected":false},"author":123,"featured_media":0,"comment_status":"open","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[1],"tags":[],"class_list":["post-2111","post","type-post","status-publish","format-standard","hentry","category-uncategorized"],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v27.6 - https:\/\/yoast.com\/product\/yoast-seo-wordpress\/ -->\n<title>Six at Sixty. \u2018No gain, no pain\u2019: medical genetics taking Nav1.7 from target to pharmacy (Contributed by Pu Xia) - JMG Contact blog<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/blogs.bmj.com\/jmg\/2025\/09\/17\/six-at-sixty-no-gain-no-pain-medical-genetics-taking-nav1-7-from-target-to-pharmacy\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Six at Sixty. \u2018No gain, no pain\u2019: medical genetics taking Nav1.7 from target to pharmacy (Contributed by Pu Xia) - JMG Contact blog\" \/>\n<meta property=\"og:description\" content=\"Chronic pain affects millions, but opioid painkillers bring addiction, tolerance and fatal breathing risks. The voltage-gated sodium channel Nav1.7, encoded by SCN9A, is key in pain signaling. 2004 research linked its gain-of-function mutations to primary erythromelalgia, and 2006 work connected loss-of-function mutations to congenital insensitivity to pain, making it a therapeutic target. 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