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    Athira Pharma Presents Preclinical Data Highlighting Neuroprotective Effects of ATH-1105 in Models of ALS at Motor Neurone Disease Association's 35th International Symposium on ALS/MND

    12/6/24 5:30:00 PM ET
    $ATHA
    Biotechnology: Biological Products (No Diagnostic Substances)
    Health Care
    Get the next $ATHA alert in real time by email

    BOTHELL, Wash., Dec. 06, 2024 (GLOBE NEWSWIRE) -- Athira Pharma, Inc. (NASDAQ:ATHA), a clinical-stage biopharmaceutical company focused on developing small molecules to restore neuronal health and slow neurodegeneration, today presented preclinical data highlighting target engagement and neuroprotective effects of ATH-1105 in human motor neurons at the Motor Neurone Disease Association's 35th International Symposium on ALS/MND, taking place Dec. 6-8, 2024, in Montreal, Canada.

    "The preclinical data presented demonstrate for the first time the neuroprotective effects of ATH-1105 in human models of ALS, including human iPSC-derived motor neurons expressing the SOD1-A4V mutation," said Kevin Church, Ph.D., Chief Scientific Officer of Athira. "These findings add to our significant body of preclinical evidence for ATH-1105 that have previously demonstrated improvements in nerve and motor function, biomarkers of inflammation and neurodegeneration, and survival in animal models of ALS."

    Presentation Details:

    Title: ATH-1105, a small-molecule positive modulator of the neurotrophic HGF system, is neuroprotective in co-culture of human iPSC-derived motor neurons and muscle​

    Poster: # HCB-28

    Date/Time: Friday, December 6, 5:30 p.m. EST

    Presenter: Sherif Reda, Ph.D., Associate Director, Discovery Biology, Athira Pharma

    Highlights of this presentation include:

    • ATH-1105 promoted activation of MET (HGF receptor) in ALS patient-derived motor neurons​.
    • ATH-1105 enhanced motor neuron survival and preserved neurite networks following glutamate challenge in primary rat spinal motor neurons.
    • ATH-1105 demonstrated neuroprotective activity through the MET receptor; following siRNA-mediated knockdown of MET, the neuroprotective effects of ATH-1105 on neuronal survival and neurite networks were abolished.
    • In a neuromuscular junction model consisting of human iPSC-derived SOD1A4V motor neurons and human muscle, ATH-1105 enhanced motor neuron survival and preserved neurite networks following glutamate challenge.

    About ATH-1105

    ATH-1105 is an oral, brain-penetrant, small-molecule positive modulator of the neurotrophic HGF system in development for the potential treatment of amyotrophic lateral sclerosis (ALS) and other neurodegenerative diseases. ATH-1105 is currently in a Phase 1 (NCT 06432647) double-blind, placebo-controlled trial in volunteers to evaluate single and multiple oral ascending doses of ATH-1105. The study is evaluating the safety and tolerability of ATH-1105 and includes measurements of pharmacokinetic outcomes. 

    About Athira Pharma, Inc.

    Athira Pharma, Inc., headquartered in the Seattle, Washington area, is a clinical-stage biopharmaceutical company focused on developing small molecules to restore neuronal health and slow neurodegeneration. Athira aims to alter the course of neurological diseases by advancing its pipeline of drug candidates that modulate the neurotrophic HGF system. For more information, visit www.athira.com. You can also follow Athira on Facebook, LinkedIn, X (formerly known as Twitter) and Instagram.

    Forward-Looking Statements

    This communication contains "forward-looking statements" within the meaning of Section 27A of the Securities Act of 1933, Section 21E of the Securities Exchange Act of 1934 and the Private Securities Litigation Reform Act of 1995. These forward-looking statements are not based on historical fact and include statements regarding: Athira's drug candidates as potential treatments for amyotrophic lateral sclerosis and other neurodegenerative diseases; future development plans; the potential learnings from preclinical studies and other nonclinical data and their ability to inform and improve future clinical development plans; expectations regarding the potential efficacy and commercial potential of Athira's drug candidates; and Athira's ability to advance its drug candidates into later stages of development. Forward-looking statements generally include statements that are predictive in nature and depend upon or refer to future events or conditions, and include words such as "may," "will," "should," "on track," "would," "expect," "plan," "believe," "intend," "pursue," "continue," "suggest," "potential," "target," and similar expressions. Any forward-looking statements are based on management's current expectations of future events and are subject to a number of risks and uncertainties that could cause actual results to differ materially and adversely from those set forth in or implied by such forward-looking statements. These risks and uncertainties include, but are not limited to, the data from preclinical and clinical trials may not support the safety, efficacy and tolerability of Athira's drug candidates; development of drug candidates may cease or be delayed; regulatory authorities could object to protocols, amendments and other submissions; future potential regulatory milestones for drug candidates, including those related to current and planned clinical studies, may be insufficient to support regulatory submissions or approval; whether Athira's trials are sufficiently powered to meet the planned endpoints; Athira may not be able to recruit sufficient patients for its clinical trials; the outcome of legal proceedings that have been or may in the future be instituted against Athira, its directors and officers; possible negative interactions of Athira's drug candidates with other treatments; Athira's assumptions regarding its financial condition and the sufficiency of its cash, cash equivalents and investments to fund its planned operations may be incorrect; adverse conditions in the general domestic and global economic markets; the impact of competition; the impact of new or changing laws and regulations; risks related to Athira's exploration of strategic alternatives; as well as the other risks detailed in Athira's filings with the Securities and Exchange Commission from time to time. These forward-looking statements speak only as of the date hereof and Athira undertakes no obligation to update forward-looking statements. Athira may not actually achieve the plans, intentions, or expectations disclosed in its forward-looking statements, and you should not place undue reliance on the forward-looking statements.

    Investor & Media Contact:

    Julie Rathbun

    Athira Pharma

    [email protected]

    206-769-9219

    Corporate Development Contact:

    Maya Kneip

    Program Manager, Portfolio & Program Management

    [email protected]

    (206) 412-9078



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    Q&A

    New
    • What data did Athira Pharma present at the ALS/MND symposium?

      Athira Pharma, Inc. presented preclinical data on ATH-1105, which demonstrates its neuroprotective effects in human motor neurons at the ALS/MND symposium.

    • What were the key findings related to the effects of ATH-1105 on motor neurons?

      The preclinical data showed that ATH-1105 enhanced motor neuron survival and neural connections after a glutamate challenge, particularly in human model systems.

    • How does ATH-1105 exert its neuroprotective effects in motor neurons?

      ATH-1105 activates the MET receptor in motor neurons, and its neuroprotective effects depend on this receptor, as demonstrated by reduced effects after MET knockdown.

    • What is the current status of ATH-1105's clinical development?

      ATH-1105 is currently undergoing a Phase 1 clinical trial focusing on its safety, tolerability, and pharmacokinetic outcomes, which is a double-blind, placebo-controlled study.

    • What is Athira Pharma's broader goal with its drug candidates like ATH-1105?

      Athira aims to reposition the treatment of neurological diseases through its drug candidates that target the neurotrophic HGF system and seeks to alter the course of neurodegeneration.

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