Galimedix Therapeutics publishes new data in peer-reviewed International Journal of Molecular Sciences demonstrating disease-modifying capability of GAL-201 in Alzheimer’s disease

• Maintains Brain Connectivity: GAL-201 prevents amyloid-beta (Aβ)–induced synaptic damage by maintaining long-term potentiation, a correlate for learning and memory.
• Improves Memory and Behavior: Preclinical testing shows significant improvements in spatial learning and memory in transgenic models of Alzheimer’s disease.
• Targets Core Pathologies: GAL-201 reduces Aβ-induced neuroinflammation and even lowers the number of toxic Aβ plaques, addressing key drivers of disease progression.

KENSINGTON, Md. and MUNICH and MARTINSRIED, Germany, May 21, 2025 (GLOBE NEWSWIRE) — Galimedix Therapeutics, Inc. (“Galimedix”), a Phase 2 clinical-stage biotechnology company developing novel oral and topical neuroprotective therapies with the potential to revolutionize the treatment of serious brain and eye diseases, today announced the publication of compelling new data on the mechanism of GAL-201 in counteracting the damaging effects of amyloid-beta (Aβ) oligomers – soluble protein aggregates known to disrupt memory circuits and contribute to disease pathology in Alzheimer’s disease (AD). The article, entitled, GAL-201 as a Promising Amyloid-β-Targeting Small-Molecule Approach for Alzheimer’s Disease Treatment: Consistent Effects on Synaptic Plasticity, Behavior and Neuroinflammation, was published in the peer-reviewed International Journal of Molecular Sciences and shows the compound’s disease modifying effect in preclinical models of AD. The article can be found here.

The published experiments demonstrate that the Aβ-aggregation modulator GAL-201, which targets the misfolded (aggregation-prone) Aβ-monomers, is not specific to Aβ_1-42 only, but also targets other subtypes of Aβ. By interfering in the Aβ-aggregation cascade at source, toxic oligomers and protofibrils are not formed, resulting in a better cognitive outcome. Even after a single injection of GAL-201, AD animal models exhibited marked improvements in learning and memory behaviors. Further in vitro experiments showed that this protective effect of GAL-201 is accompanied by beneficial effects on synapse dynamics as well as anti-inflammatory effects. In addition, the compound also led to a measurable reduction in the number of Aβ plaques, further supporting its potential as a disease-modifying drug.

Hermann Russ, MD, PhD, Co-founder and Chief Scientific Officer of Galimedix, said: “These new results strengthen the positioning of GAL-201 as both a symptom-relieving and a disease-modifying therapeutic agent for Alzheimer’s disease. The compound targets core features of the disease, including synaptic dysfunction, neuroinflammation, and Aβ plaque formation, thereby fighting progressive neurodegeneration and cognitive decline. We believe that GAL-201 and Galimedix’s sister program GAL-101 are promising candidates for a patient-friendly oral treatment for this devastating disease.”

GAL-201 is currently in preclinical testing. GAL-101, a compound closely related to GAL-201, is currently under investigation in a Phase 1 study. In addition, GAL-101 eye drops are being investigated in the Phase 2 eDREAM study in patients with dry age-related macular degeneration, an Aβ-associated retinal disease.

About Galimedix Therapeutics, Inc. 
Galimedix is a Phase 2 clinical-stage private company developing novel oral and topical neuroprotective therapies with the potential to revolutionize the treatment of serious eye and brain diseases. Founded by a seasoned and highly dedicated team of bio-entrepreneurs, pharmaceutical executives and scientists, Galimedix’s groundbreaking small molecules offer the hope of changing the course of disease where amyloid beta (Aβ) plays a role, such as in dry age-related macular degeneration (AMD), glaucoma and Alzheimer’s disease – Galimedix’s initial areas of focus.

Contact

Alexander Gebauer, MD, PhD
Galimedix Therapeutics, Inc.
Co-founder and Executive Chairman
info@galimedix.com

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