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Neurimmune Therapeutics Announces Advancement of Alzheimer's Program into Preclinical Development
"Neurimmune's unique Reverse Translational Medicine (RTM(TM) ) technology platform combined with in-depth expertise in neuroscience played a critical role in moving the program forward. The fact that we could reach all preclinical milestones in such a short period of time shows that our RTM(TM) technology can significantly accelerate the transition from discovery to development of human monoclonal antibodies," said Jan Grimm, Chief Scientific Officer of Neurimmune Therapeutics.
"The rapid advancement into preclinical development demonstrates the progress and productivity of our collaboration with Biogen Idec - we are very happy to work with a partner that has such extensive and valuable experience in the development of biopharmaceuticals. The significant milestone payments also provide Neurimmune with additional financial stability to support the sustainable future development of our company," said Michael Salzmann, COO and General Manager of Neurimmune Therapeutics.
"Biogen Idec is globally recognized as a leader in the development of innovative therapies for neurologic diseases, and this program is an important entry into Alzheimer's disease for us," said Kenneth Rhodes, PhD, Vice President, Discovery Neurobiology, Biogen Idec. "The rapid progression of this antibody is the result of a very effective joint collaboration, which capitalized on Neurimmune's novel RTM(TM) approach and our proven expertise in neuroscience and the development of therapeutic antibodies."
Alzheimer's disease is the most prevalent age-related neurodegenerative disease affecting more than 15 million patients worldwide. There are currently no treatments approved to slow or stop the progression of the disease. Patients with Alzheimer's disease experience the progressive loss of cognitive functions, particularly those related to memory, followed by death eight to 15 years after a progressive decline in their disease. The pathology of Alzheimer's disease is characterized by distinctive features, including the deposition of Abeta in the form of senile plaques and the loss of specific neuronal populations in the brain.
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