GAITHERSBURG, Md.--(BUSINESS WIRE)--Neuraly, a clinical stage biotechnology company pioneering disease-modifying agents for neurodegenerative disorders, today announced publication in the peer-reviewed journal Acta Neuropathologica Communications of preclinical data that contributed to the therapeutic rationale for clinical evaluation of NLY01 in Alzheimer’s and Parkinson’s diseases. The research was conducted in collaboration with Dr. Ted Dawson’s lab at the Johns Hopkins School of Medicine.
The publication, entitled “Blocking microglial activation of reactive astrocytes is neuroprotective in models of Alzheimer’s disease” demonstrated that NLY01, an engineered exendin-4, glucagon-like peptide-1 receptor (GLP-1R) agonist, can selectively block β-amyloid-induced activation of microglia through upregulated GLP-1R, inhibit formation of reactive astrocytes and preserve neuronal viability, resulting in improved spatial learning and memory. NLY01 is entering a Phase 2b trial in Alzheimer’s disease while currently being evaluated in a Phase 2 Parkinson’s disease trial.
“Microglia and reactive astrocytes are a major therapeutic target for neurodegenerative diseases and blocking microglia-astrocyte activation has the potential to reduce neurodegeneration in these conditions,” said Seulki Lee, Ph.D., President and Chief Executive Officer of Neuraly. “To date, we have shown that NLY01 can reduce β-amyloid plaque burden in mouse models of Alzheimer’s and abnormal alpha-synuclein build up in Parkinson’s models. Together, these data suggest that NLY01 has potential as a universal therapy for neurodegenerative diseases.”
In a paper published in Nature Medicine, it was shown that NLY01 binds upregulated GLP-1R, blocking pathological activation of microglia in animal models of neurodegenerative diseases including Parkinson’s. The study also showed that by inhibiting glial activation and subsequent pro-inflammatory cytokine products, NLY01 prevented neuronal cell death and protected against the motor function decline that was observed in the absence of treatment.
“The results published in Acta Neuropathologica Communications add to the growing evidence suggesting that neuroinflammation mediated by microglia and astrocytes contributes to progression and severity in Alzheimer’s disease and other neurodegenerative disorders,” added Viktor Roschke, Ph.D., Chief Scientific Officer of Neuraly. “During progression, resident microglia undergo proinflammatory activation, resulting in an increased capacity to convert resting astrocytes to reactive astrocytes. These results show that targeting upregulated GLP-1R in microglia is a potentially viable therapy for Alzheimer’s and other neurodegenerative disorders.”
NLY01 is a proprietary long-acting analogue of exendin-4, a glucagon-like peptide-1 receptor (GLP-1R) agonist. NLY01 penetrates the blood-brain barrier (BBB) in animal models and its receptor (GLP-1R) is highly expressed on glial cells. NLY01 is being developed as a disease-modifying agent for neurodegenerative disorders including Parkinson’s and Alzheimer’s disease. NLY01 is being evaluated in a Phase 2 trial in patients with Parkinson’s disease and entering a Phase 2b trial in Alzheimer’s disease.
Neuraly is a clinical-stage company whose mission is to translate scientific discoveries in neurology into revolutionary new drugs that can radically improve and prolong the lives of people suffering from the devastating consequences of diseases such as Parkinson’s disease (PD), Alzheimer’s disease (AD) and other neurodegenerative disorders. The company is leveraging a deep understanding of the role of glia biology in neuroinflammation and neuroprotection in advancing a risk-diversified product portfolio for PD and AD. Neuraly is a subsidiary of D&D Pharmatech, a clinical-stage global biotech company that funds the development of revolutionary medicines through disease-specific subsidiary companies founded and guided by top-tier medical research faculty and biotechnology veterans, please visit https://www.neuralymed.com/ and http://www.ddpharmatech.com/