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ALS pathogenesis involves intricate processes within motor neurons, characterized by dysregulated Ca<jats:sup>2+<\/jats:sup> influx and buffering in early ALS\u2010affected motor neurones. This study proposes the modulation of ryanodine receptors (RyRs), key mediators of intracellular Ca<jats:sup>2+<\/jats:sup>, as a therapeutic target.<\/jats:p><\/jats:sec><jats:sec><jats:title>Experimental Approach<\/jats:title><jats:p>A novel class of novel FKBP12 ligands that show activity as cytosolic calcium modulators through stabilizing RyR channel activity, were tested in the superoxide dismutase 1 (SOD1)<jats:sup>G93A<\/jats:sup> mouse model of ALS. Different outcomes were used to assess treatment efficacy, including electrophysiology, histopathology, neuromuscular function and survival.<\/jats:p><\/jats:sec><jats:sec><jats:title>Key Results<\/jats:title><jats:p>Among the novel FKBP12 ligands, MP\u2010010 was chosen for its central nervous system availability and favourable <jats:italic>in vitro<\/jats:italic> pharmaco\u2010toxicological profile. Chronic administration of MP\u2010010 to SOD1<jats:sup>G93A<\/jats:sup> mice produced preservation of motor nerve conduction, with the 61\u2010mg\u00b7kg<jats:sup>\u22121<\/jats:sup> dose significantly delaying the onset of motor impairment. This was accompanied by improved motor coordination, increased innervated endplates and significant preservation of motor neurones in the spinal cord of treated mice. Notably, MP\u2010010 treatment significantly extended lifespan by an average of 10\u2009days compared to vehicle.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions and Implications<\/jats:title><jats:p>FKBP12 ligands, particularly MP\u2010010, exhibit promising neuroprotective effects in ALS, highlighting their potential as novel therapeutic agents. Further investigations into the molecular mechanisms and clinical translatability of these compounds are needed for their application in ALS treatment.<\/jats:p><\/jats:sec>","DOI":"10.1111\/bph.17448","type":"journal-article","created":{"date-parts":[[2025,2,14]],"date-time":"2025-02-14T00:39:21Z","timestamp":1739493561000},"page":"2466-2486","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Novel FKBP prolyl isomerase 1A (FKBP12) ligand promotes functional improvement in SOD1<sup>G93A<\/sup> amyotrophic lateral sclerosis (ALS) mice"],"prefix":"10.1111","volume":"182","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7277-4318","authenticated-orcid":false,"given":"Laura","family":"Moreno\u2010Martinez","sequence":"first","affiliation":[{"name":"Centro de Investigaci\u00f3n Biom\u00e9dica en Red Sobre Enfermedades Neurodegenerativas (CIBERNED)  Madrid Spain"},{"name":"LAGENBIO, Faculty of Veterinary University of 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