ALTERITY THERAPEUTICS LIMITED MELBOURNE, AUSTRALIA AND SAN FRANCISCO, USA - 16 November 2023: Alterity Therapeutics (ASX: ATH, NASDAQ: ATHE) ("Alterity" or "the Company"), a biotechnology company dedicated to developing disease modifying treatments for neurodegenerative diseases, today announced promising new data related to ATH434 was presented at the Society for Neuroscience that took place November 11-15, 2023, in Washington, D.C.
The poster entitled, "Potent Antioxidant and Mitochondrial-protectant Effects of ATH434, a Novel Inhibitor of α-Synuclein Aggregation with Moderate Iron-binding Affinity," presents new data indicating that ATH434 can preserve mitochondrial function after oxidative injury and exert direct anti-oxidant activity independent of its iron binding properties. These features were not observed with another iron binding agent approved for treating iron overload that was also investigated. The study was run under the direction of Dr. Daniel J. Kosman, Distinguished Professor of Biochemistry at the State University of New York at Buffalo.
David Stamler, M.D., Chief Executive Officer of Alterity, commented, "These exciting new data underscore the potential of ATH434 as a treatment for neurodegenerative diseases, including Parkinson's disease and related disorders. We have long known that ATH434 is able to reduce labile iron which, when elevated, can drive oxidative stress. The demonstrated mitochondrial protection may reveal additional mechanisms that augment its ability to slow disease progression. We are grateful for the valued contributions from our collaborators in Dr. Kosman's laboratory at SUNY-Buffalo."
The study, authored by Dr. Danielle Bailey, investigated the efficacy of ATH434 and comparator agents as mitochondrial protectants using a menadione-induced model of oxidative stress in a neuronal cell line. A suite of in-solution assays detailed the mechanisms underlying ATH434's direct antioxidant capacity. The poster presentation is attached and can be accessed on Alterity's website under The Science page.
About ATH434
Alterity's lead candidate, ATH434, is an oral agent designed to inhibit the aggregation of pathological proteins implicated in neurodegeneration. ATH434 has been shown preclinically to reduce α-synuclein pathology and preserve neuronal function by restoring normal iron balance in the brain. As an iron chaperone, it has excellent potential to treat Parkinson's disease as well as various Parkinsonian disorders such as Multiple System Atrophy (MSA). ATH434 successfully completed Phase 1 studies demonstrating the agent is well tolerated and achieved brain levels comparable to efficacious levels in animal models of MSA. ATH434 is currently being studied in two clinical trials: Study ATH434-201 is a randomized, double-blind, placebo-controlled Phase 2 clinical trial in patients with early-stage MSA and Study ATH434-202 is an open-label Phase 2 Biomarker trial in patients with more advanced MSA. ATH434 has been granted Orphan drug designation for the treatment of MSA by the U.S. FDA and the European Commission.
About Alterity Therapeutics Limited
Alterity Therapeutics is a clinical stage biotechnology company dedicated to creating an alternate future for people living with neurodegenerative diseases. The Company's lead asset, ATH434, has the potential to treat various Parkinsonian disorders and is currently being evaluated in two Phase 2 clinical trials in Multiple System Atrophy. Alterity also has a broad drug discovery platform generating patentable chemical compounds to treat the underlying pathology of neurological diseases. The Company is based in Melbourne, Australia, and San Francisco, California, USA. For further information please visit the Company's web site at www.alteritytherapeutics.com.
Authorisation & Additional information
This announcement was authorized by David Stamler, CEO of Alterity Therapeutics Limited.
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Alterity Therapeutics Ltd. published this content on 16 November 2023 and is solely responsible for the information contained therein. Distributed by Public, unedited and unaltered, on 15 November 2023 22:52:57 UTC.
