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ATH-1105 mitigates multiple pathologies in ALS models both alone and in combination with riluzole

Title: ATH-1105 mitigates multiple pathologies in ALS models both alone and in combination with riluzole
Authors: Andrée-Anne Berthiaume; Kayla N. Kleist; Sherif M. Reda; Sharay E. Setti; Wei Wu; Jewel L. Johnston; Robert W. Taylor; Liana R. Stein; Kevin J. Church
Source: Frontiers in Neurology, Vol 16 (2026)
Publisher Information: Frontiers Media S.A.
Publication Year: 2026
Collection: Directory of Open Access Journals: DOAJ Articles
Subject Terms: ALS; hepatocyte growth factor; neurotrophic factor; neurofilament light chain; TDP-43; neuroprotection; Neurology. Diseases of the nervous system; RC346-429
Description: IntroductionAmyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized by progressive motor neuron degeneration, muscle atrophy, and paralysis. The complexity of ALS pathology, driven by factors such as TDP-43 pathology, excitotoxicity, and neuroinflammation, has hindered therapeutic development. While riluzole (an anti-excitotoxic agent) is the current standard treatment, additional therapeutics are needed to address the broad spectrum of ALS-related pathology. ATH-1105, a small-molecule positive modulator of hepatocyte growth factor (HGF) signaling, has shown promise in preclinical models of ALS. Given the multifactorial nature of ALS and the growing recognition that combination approaches may represent the best treatment options, we investigated the therapeutic potential of ATH-1105 in a TDP-43-driven mouse model of ALS, by comparing and combining it with the known efficacious treatment of riluzole. Additionally, we characterize the mechanism by which ATH-1105 induces neuroprotective effects, emphasizing its effects on TDP-43 pathology.MethodsIn vivo, the impact of daily oral treatment with ATH-1105, alone and in combination with riluzole, was evaluated in Prp-TDP43A315T hemizygous transgenic ALS mice. In vitro, the impact of ATH-1105 on TDP-43-related pathology was assessed in rat primary spinal motor neurons subjected to glutamate toxicity. To demonstrate target engagement, the neuroprotective effects of ATH-1105 were assessed via siRNA-mediated knockdown of MET (HGF receptor).ResultsIn vivo, ATH-1105 significantly improved neuromuscular function and reduced body weight loss, neurodegeneration, inflammation, and TDP-43 phosphorylation. The combination of ATH-1105 with riluzole led to greater therapeutic effects than either treatment alone. In vitro, the neuroprotective effects of ATH-1105 were shown to be associated with MET activation in motor neurons, which was confirmed via siRNA-mediated knockdown of MET. In motor neurons subjected to glutamate toxicity, ATH-1105 reduced ...
Document Type: article in journal/newspaper
Language: English
Relation: https://www.frontiersin.org/articles/10.3389/fneur.2025.1582765/full; https://doaj.org/toc/1664-2295; https://doaj.org/article/1cef85888c3c4ade80f7f883abe21e04
DOI: 10.3389/fneur.2025.1582765
Availability: https://doi.org/10.3389/fneur.2025.1582765; https://doaj.org/article/1cef85888c3c4ade80f7f883abe21e04
Accession Number: edsbas.6DEF93C2
Database: BASE