{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,19]],"date-time":"2026-05-19T13:04:03Z","timestamp":1779195843129,"version":"3.51.4"},"reference-count":84,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2026,4,15]],"date-time":"2026-04-15T00:00:00Z","timestamp":1776211200000},"content-version":"vor","delay-in-days":14,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"},{"start":{"date-parts":[[2026,4,1]],"date-time":"2026-04-01T00:00:00Z","timestamp":1775001600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01 NS137595"],"award-info":[{"award-number":["R01 NS137595"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["European Journal of Pain"],"published-print":{"date-parts":[[2026,4]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background and Objective<\/jats:title>\n                    <jats:p>Fatty acid\u2010binding proteins (FABPs) are intracellular lipid transporters. Pharmacological inhibition of FABP5 is analgesic in preclinical visceral, inflammatory, neuropathic and joint pain models. Genetic knockout or knockdown of FABP5 induces analgesia in select visceral and inflammatory pain models. This review explores the current evidence supporting FABP5 modulation in pain.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Databases and Data Treatment<\/jats:title>\n                    <jats:p>We searched PubMed (January\u2013August 2025) for studies relating to FABP5 modulation in pain. We used terms associated with inhibition, genetic ablation, analgesia, pain behaviours, pain models and associated signalling pathways.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      FABP5 inhibition mediates analgesia through various lipid\u2010signalling receptors (cannabinoid receptor type 1 [CB\n                      <jats:sub>1<\/jats:sub>\n                      ], peroxisome proliferator\u2013activated receptor alpha [PPAR\u03b1] and transient receptor potential cation channel subfamily V member 1 [TRPV1]). FABP5 inhibitors upregulate\n                      <jats:italic>N<\/jats:italic>\n                      \u2010acylethanolamines and various other\n                      <jats:italic>N<\/jats:italic>\n                      \u2010acyl amino acids. FABP5 inhibitors also suppress cytokines, chemokines and other inflammatory pathways such as tumour necrosis factor (TNF), interleukin (IL)\u20101\u03b2, IL\u20106, prostaglandin (PG) E\n                      <jats:sub>2<\/jats:sub>\n                      and microsomal PG E synthase\u20101 (mPGES\u20101). We recently found that the potent, peripherally selective, FABP5 inhibitor ART26.12 showed a no observable adverse effect level of 1000\u2009mg\/kg\/day in rats and dogs. FABP5 inhibition may offer a favourable safety profile when compared to currently prescribed pain medications (e.g., opioids, corticosteroids and anticonvulsants).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Whilst preclinical data support the potential of FABP5 inhibitors as novel analgesics, further research into sex differences and chronic dosing in visceral and inflammatory pain models is warranted. Despite this, FABP5 inhibition may hold promise for non\u2010opioid and non\u2010steroidal management of painful conditions.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Significance Statement<\/jats:title>\n                    <jats:p>This review highlights fatty acid\u2013binding protein 5 (FABP5) inhibition as a novel, non\u2010opioid and non\u2010steroidal analgesic strategy with multiple mechanisms of action, broad efficacy in preclinical pain models, and a favourable safety profile. FABP5 inhibition may offer promise for the treatment of complex painful conditions.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/ejp.70267","type":"journal-article","created":{"date-parts":[[2026,4,15]],"date-time":"2026-04-15T13:11:31Z","timestamp":1776258691000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Evaluating\n                    <scp>FABP5<\/scp>\n                    as a Therapeutic Target for Pain Management"],"prefix":"10.1002","volume":"30","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5507-1381","authenticated-orcid":false,"given":"William","family":"Warren","sequence":"first","affiliation":[{"name":"Artelo Biosciences Ltd Alderley Park  Alderley Edge Cheshire UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Myles","family":"Osborn","sequence":"additional","affiliation":[{"name":"Artelo Biosciences Ltd Alderley Park  Alderley Edge Cheshire 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