ArticleHeadache
Galcanezumab reduces trigeminal nociception and is effective in preclinical models of migraine and trigeminal autonomic cephalalgias.
Article in Headache. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- From bench to bedside: relevant animal models across the migraine attack phases.The journal of headache and pain · 2026Review
- Non-neuronal targets for migraine therapy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Review
- Extremely low dose norepinephrine in treatment of refractory chronic cluster headache: two case reports and literature review.Frontiers in neuroscience · 2026Article
- Article
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4 authors.
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Abstract
OBJECTIVES/
backgroundThis 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-related 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.
methodsTrigeminovascular and trigeminal-autonomic 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-evoked and non-noxious-evoked neuronal activity. Rats received either galcanezumab or human control IgG, and responses were compared between groups.
resultsGalcanezumab robustly reduced spontaneous (maximum decrease in dural-evoked: 73% [±3.5] at 4 h 30 min [p = 0.002]; in SSN-evoked: 67% [±10.7] at 4 h [p = 0.01]) and cutaneous non-noxious-evoked (maximum decrease in dural-evoked: 50% [±5.7], p = 0.004; in SSN-evoked: 47% [±10.5], p = 0.005, 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-evoked (maximum decrease in dural-evoked: 38% [±5.2], p = 0.005; in SSN-evoked: 34% [±7.6], p = 0.005, at the last recording time point), durovascular-evoked (maximum decrease 48% [±6] at the last recording time point, p = 0.001), and SSN-evoked responses (maximum decrease: 32% [±2.6] at 4 h, p < 0.001), 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.
conclusionGalcanezumab 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.
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