Study Supports Neuroprotective, Disease-Modifying Effects of Clinical Drug Candidate in the Treatment of Alzheimer Disease

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A study found that a novel pan-Trk positive allosteric modulator may improve cognition, resilience, and neurorestorative processes in patients with Alzheimer disease.

The study focused on the potential neuroprotective and disease-modifying effects of the triazinetrione ACD856 in the treatment of Alzheimer disease.¹ “We have utilized cells recombinantly overexpressing Trk-receptors, cell lines with endogenous expression, primary neurons, or in vivo studies to further addressed the mechanism by which triazinetriones increase the activity of Trk-receptors and downstream signaling,” the authors wrote. “We and others have used the PathHunter assay to demonstrate pharmacological effects on Trk-receptors. The assay measures the interaction between SHC-1 and phosphorylated Y490 on TrkA-receptors.”²

Study results showed that ACD856 has protective effects against amyloid-beta induced nerve damage as well as positive effects on neurite outgrowth and synapses,² thus supporting the drug’s potential to promote neurorestorative processes, improve cognition, and increase resilience in patients with Alzheimer disease.¹

“The results confirm ACD856 as a cognitive enhancer, but more importantly, they provide substantial in vitro and in vivo evidence of neuroprotective and long-term effects that contribute to neurotrophic support and increased neuroplasticity,” the authors wrote. “Presumably, the described effects of ACD856 may improve cognition, increase resilience, and promote neurorestorative processes, thereby leading to a healthier brain in patients with [Alzheimer disease].”²

ACD856 is the leading drug candidate in the NeuroRestore platform, which increases nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) signaling. The drug has shown positive symptom-relieving effects during clinical phase 1 studies.¹ “These new results with ACD856 significantly strengthen the commercial potential of the project, which we now prepare for phase 2 studies,” concluded Martin Jönsson, CEO of ACD856 developer AlzeCure Pharma AB, in a press release.

Two additional drugs—both intravenous antibodies designed to eliminate deposits of beta amyloid from the brain—have also made recent strides in the treatment of Alzheimer disease. Lecanemab (Leqembi) received traditional approval by the US Food & Drug Administration (FDA) for the treatment of Alzheimer disease on July 6, 2023.³ Then, on July 17, donanemab (Eli Lilly and Company) was shown to slow the progression of Alzheimer disease in patients with mild impairment by 60%.⁴

See more coverage on Alzheimer disease treatments at psychiatrictimes.com.

References

1. AlzeCure publishes new disease modifying data with NeuroRestore ACD856 against Alzheimer’s and cognitive disorders. AlzeCure Pharma AB. News release. July 11, 2023. Accessed July 17, 2023. https://www.alzecurepharma.se/en/alzecure-publishes-new-disease-modifying-data-with-neurorestore-acd856-against-alzheimers-and-cognitive-disorders/#:~:text=The%20results%20show%20that%20ACD856,exchange%20of%20information%20takes%20place

2. Parrado Fernandez C, Juric S, Backlund M, et al. Neuroprotective and disease-modifying effects of the triazinetrione ACD856, a positive allosteric modulator of Trk-receptors for the treatment of cognitive dysfunction in Alzheimer’s disease. Int J Mol Sci. 2023;24(13):11159.

3. O’Brien E. FDA grants traditional approval to Leqembi for the treatment of Alzheimer disease. Psychiatric Times. July 6, 2023. Accessed July 18, 2023. https://www.psychiatrictimes.com/view/fda-grants-traditional-approval-to-leqembi-for-the-treatment-of-alzheimer-disease

4. O’Brien E. Experimental drug slows progression of Alzheimer disease in patients with mild impairment by 60%. Psychiatric Times. July 17, 2023. Accessed July 18, 2023. https://www.psychiatrictimes.com/view/experimental-drug-slows-progression-of-alzheimer-disease-in-patients-with-mild-impairment-by-60-