Alzheimer’s Disease (AD) is a complex and progressive neurodegenerative disease which is characterized by memory loss and cognitive impairment. It is one of the most prevalent neurodegenerative diseases and it is estimated that the number of patients will increase dramatically in the coming years. Despite decades of research there is still no treatment available that can cure or even slow down the progression in AD.
Mitochondrial dysfunction and neuroinflammation are present in AD. Although the underlying mechanisms of these pathologic changes remain unclear, possible links between these phenomena have been reported, and it is increasingly recognized that mitochondria or mitochondrial components may contribute to neuroinflammation. Therefore, compounds that improve mitochondrial function during the pathogenesis of AD are an innovative therapeutic strategy. SUL-138 is such a compound.
We are happy to announce that a new scientific manuscript detailing the efficacy of SUL-138 in preclinical models for AD, was recently published in Alzheimer’s Research & Therapy. Christina de Veij Mestdagh and Rob Henning from respectively the Free University Amsterdam (VU) and the University Medical Center Groningen (UMCG) investigated the therapeutic effects of SUL-138 in the APP/PS1 and wildtype mice.
Treatment with SUL-138 improves mitochondrial function and reduces disease progression in a preclinical model for AD.
In this study both wildtype and APP/PS1 mice received chronic oral treatment with either SUL-138 or vehicle for 12 weeks starting at approximately 3 months of age. The effects of SUL-138 were assessed by evaluating mitochondrial protein expression, synaptic plasticity, memory and amyloid plaque depositions in the hippocampus.
It was shown that chronic treatment with SUL-138 increases synaptic plasticity and memory function compared to vehicle treatment. Interestingly, synaptic plasticity and memory function were improved in both the APP/PS1 and wildtype mice treated with SUL-138. Treatment with SUL-138 also significantly reduced the number and size of amyloid plaque depositions in the hippocampus. Last, proteomic analysis showed that SUL-138 increases mitochondrial protein expression of proteins involved in metabolism indicating rescue of mitochondrial impairments typically observed in AD.
Preclinical development SUL-138 and FIH
SUL-138 is an orally available small molecule compound which is part of the mitochondrial platform technology developed by Sulfateq. The compound is designed to improve mitochondrial function during disease. Mitochondria play a key role in the pathophysiology of Alzheimer’s Disease.
Sulfateq in collaboration with GEN İlaç ve Sağlık Ürünleri Sanayi ve Ticaret A.Ş. (GEN) are currently finalizing the last preclinical studies to enable a First in Human (FIH) clinical trial. In this trial the safety, tolerability and pharmacokinetics of SUL-138 will be investigated.
The new publication is available through this link, would you like to receive more information about our compounds or discuss possibilities? Please contact us, we are happy to answer your inquiry!