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 eye and brain diseases, announces encouraging data with orally available small molecule GAL-201, showing its neuroprotective and symptomatic alleviation potential in models of Alzheimer’s disease (AD). These new findings strongly support previous studies where GAL-201 was characterized as a promising development candidate for the treatment of AD (Russ et. al. 2022). The data was presented this week at the International Conference on Alzheimer’s and Parkinson’s Diseases and related neurological disorders (AD/PD™ 2024: advances in science and therapy).
“The small molecule GAL-201 belongs to a new pharmacological class of amyloid beta aggregation modulators that acts upstream of other known Aβ-targeting agents,” explained Hermann Russ, M.D., Ph.D., Co-founder, and Chief Scientific Officer of Galimedix. “The positive results presented at AD/PD™ 2024 demonstrate how treatment with GAL-201 has a potential neuroprotective effect and may also improve cognitive function. Furthermore, they validate that toxic Aβ oligomers and protofibrils are a major underlying cause of this devastating disease, and not the deposited forms of Aβ. We look forward to advancing this promising new drug candidate into the clinic.”
Data from the poster, entitled “The amyloid beta aggregation modulator GAL-201 is under development for oral AD treatment: Cognitive improvement in a transgenic AD model”, showed a high affinity of GAL-201 to misfolded Aβ monomers, the precursors of the neurotoxic forms of Aβ oligomers and protofibrils. Binding of GAL-201 to the Aβ monomers significantly prevented Aβ-induced suppression of long-term potentiation (LTP), considered a neuronal correlate of learning and memory. These results mirrored morphological changes observed in neuronal cells (dendrites), where Aβ-induced spine loss was also prevented. Preserving dendritic spines is essential, as they are correlated with synaptic plasticity. Additionally, in behavioral experiments using AD animal models, a single injection of GAL-201 resulted in improved cognitive performance, both in duration (escape latency) and accuracy (left and right decisions) performing a task (water-cross maze) and were comparable to healthy mice.
The presented results further substantiate GAL-201’s role as a promising future Aβ-targeting treatment for AD, with an advanced mechanism of action and a patient-friendly application route as an oral tablet. The next step is to move GAL-201 towards IND submission and clinical development.
The poster can be accessed here:
“The amyloid beta aggregation modulator GAL-201 is under development for oral AD treatment: Cognitive improvement in a transgenic AD model”
