{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T06:02:43Z","timestamp":1791525763592,"version":"4.3.4"},"reference-count":41,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2025,7,21]],"date-time":"2025-07-21T00:00:00Z","timestamp":1753056000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100004312","name":"Eli Lilly and Company","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100004312","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["headachejournal.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Headache"],"published-print":{"date-parts":[[2025,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Objectives\/Background<\/jats:title>\n                    <jats:p>This study was undertaken to assess the therapeutic efficacy of galcanezumab in preclinical models of migraine and cluster headache and to determine potential shared trigeminovascular mechanisms of action. Galcanezumab is a humanized monoclonal antibody that binds to the neuropeptide calcitonin gene\u2010related peptide, preventing its biological activity. It has been approved as a preventive treatment for both episodic and chronic migraine and episodic cluster headache, the most common trigeminal autonomic cephalalgia.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Trigeminovascular and trigeminal\u2013autonomic reflex activation was evoked via electrical stimulation of the dura mater or superior salivatory nucleus (SSN), respectively. Evoked responses were recorded in the spinal trigeminal nucleus along with ongoing spontaneous neuronal and cutaneous noxious\u2010evoked and non\u2010noxious\u2010evoked neuronal activity. Rats received either galcanezumab or human control IgG, and responses were compared between groups.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Galcanezumab robustly reduced spontaneous (maximum decrease in dural\u2010evoked: 73% [\u00b13.5] at 4\u2009h 30\u2009min [\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.002]; in SSN\u2010evoked: 67% [\u00b110.7] at 4\u2009h [\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.01]) and cutaneous non\u2010noxious\u2010evoked (maximum decrease in dural\u2010evoked: 50% [\u00b15.7],\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.004; in SSN\u2010evoked: 47% [\u00b110.5],\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.005, at the last recording time point) neuronal activation in the trigeminocervical complex, highlighting a general inhibition of trigeminal sensory processing. Furthermore, it significantly inhibited cutaneous noxious\u2010evoked (maximum decrease in dural\u2010evoked: 38% [\u00b15.2],\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.005; in SSN\u2010evoked: 34% [\u00b17.6],\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.005, at the last recording time point), durovascular\u2010evoked (maximum decrease 48% [\u00b16] at the last recording time point,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.001), and SSN\u2010evoked responses (maximum decrease: 32% [\u00b12.6] at 4\u2009h,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001), demonstrating a clear reduction of trigeminal nociception, independent of the mode of activation. Galcanezumab did not have any effect on the mean arterial blood pressure.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Galcanezumab likely acts via a shared trigeminovascular mechanism to dampen noxious and nonnoxious sensory stimuli in preclinical models of migraine and trigeminal autonomic cephalalgias. This further supports the clinical efficacy of galcanezumab for migraine and cluster headache, while demonstrating general inhibition that may be of relevance to other facial pain conditions.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/head.15006","type":"journal-article","created":{"date-parts":[[2025,7,21]],"date-time":"2025-07-21T11:34:48Z","timestamp":1753097688000},"page":"1693-1703","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Galcanezumab reduces trigeminal nociception and is effective in preclinical models of migraine and trigeminal autonomic cephalalgias"],"prefix":"10.1111","volume":"65","author":[{"given":"Marta","family":"Vila\u2010Pueyo","sequence":"first","affiliation":[{"name":"Headache Group, Wolfson Sensory Pain and Regeneration Centre Institute of Psychiatry, Psychology, and Neuroscience, King's College London  London 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